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Annual Report 2006
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01 > Overview // AR 2006
Our vision >>
>> to your health
The Westmead Millennium Institute will continue to grow as
a world leader in medical research with the power to improve
the health of all mankind.
Our “Bench to Bedside” philosophy will ensure that
our research outcomes are rapidly translated into better
prevention strategies, treatments and healthcare for all.
The Westmead Millennium Institute is one of the largest
medical research institutes in Australia with over 400 staff
conducting research into a wide range of important human
disorders affecting both adults and children.
Our research spans infectious and immune diseases; cancer
and leukaemia; liver and metabolic diseases; eye and brainrelated
disorders and heart and respiratory disorders.
Closely affiliated with both Westmead Hospital and
the University of Sydney, our research extends from the
laboratory to the patient, using the basic tools of molecular
and cell biology, genetic epidemiology, imaging technology
and clinical research.
This ‘Bench to Bedside’ approach enables greater translation of
research from biomedical discovery to the development of new
prevention strategies, diagnostics and more effective treatments.

02 03 > Overview // AR 2006
Contents
Chairman’s Report
OVERVIEW
RESEARCH REPORT
Medical research is driven by a hypothesis. A scientist begins
their project with a critical assumption or idea. While science
Furthermore WMI researchers devised a test which assists in
identifying the appropriate treatment for multiple sclerosis
can be serendipitous, presenting unanticipated results, it is
patients. They have created a quick and non-invasive
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Chairman’s Report – 3
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Director’s Report – 4
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Messages – 5
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Research Highlights – 6
Infection and Immunity – 10
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Cancer – 14
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Liver and Metabolic – 16
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Neuroscience and Vision – 18
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N59 Cardio-respiratory – 20
International collaborations – 22
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Infection & Immunity – 30
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Cancer – 37
Liver and Metabolic – 43
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Cardio-respiratory – 48
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Staff – 50
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Publications 2006 – 54
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the researchers dogged pursuit of knowledge that advances
our medical frontiers.
Like any investigation, medical research, is a step-by-step
process. It can be painstaking, entailing the collection and
interpretation of endless data, over many years. A researcher
will test, and re-test results before announcing an outcome.
Research at the Westmead Millennium Institute (WMI) is
focused on outcomes; outcomes, which will directly benefit
patients and assist health care practitioners provide better
treatments and prevention strategies.
This year the Institute celebrated its tenth anniversary. It
has been a decade of outstanding achievement. The diverse
research work conducted at the Institute and its contribution
to better healthcare outcomes is recognized internationally.
Since its formal establishment just over a decade ago the
Institute’s researchers have lead or contributed to a number
of significant medical research breakthroughs. WMI is widely
acknowledged for its contribution to the discovery of the first
gene found to cause melanoma. WMI researchers are world
leaders in HIV research, tracing and trying to prevent the
way HIV enters the body. Australia’s only successful clinical
islet cell transplantation unit for curing Type 1 diabetics, was
established by WMI researchers and this unit is still one of
only a few in the world.
diagnosis for brain infections, including brain abscess and
meningitis and worked tirelessly to understand the nature of
a liver disease now commonly known as NASH.
Through its longitudinal, Blue Mountains Eye Study, WMI
researchers have identified the most common causes of
blindness in the elderly. And this year the Institute established
Australia’s first major collaborative breast cancer tissue bank
– a central library of both clinical and molecular data for use
by all Australian researchers.
Support of this high caliber medical research is critical.
Without it researchers cannot continue to look for cures and
better treatments.
I would like to thank those who do support and continue to
support the Institute including the Millennium Foundation
Board and its staff, the WMI Advisory Board and Council
of Governors, Sydney West Area Health Service and the
University of Sydney.
Finally I would like to congratulate the Institute staff on
their achievements over the past decade and wish them every
success in 2007.
Mr Paul Bell
Advisory Board and Council of Governors – 24
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Organisation Structure – 25
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Westmead Millennium Institute at a glance – 60
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Funding – 26
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Science is a process.
Director’s Report
< 04 05 > Overview // AR 2006
Messages
This year, the Westmead Millennium Institute reached a
significant milestone celebrating a decade of excellence in
medical research.
Ten years ago, we were a small group of 60 researchers,
covering four major research areas. Since then we have grown
to be one the largest medical research institutes in Australia,
with five primary research divisions and over 400 staff and
postgraduate students.
Over the past ten years, our researchers have competed with
the best biomedical research in the world but still maintained
a focus on outcomes. The Institute’s motto ‘bench to bedside’
remains at the core of our work. Our research utilizes the
common and rapidly advancing technologies of cell biology
and genetic epidemiology. We share ideas and technology,
collaborating on new research directions for new diagnostics,
treatment and therapies. Many of our discoveries are being
transferred to the frontline of health care services and new
biotechnology.
As Director of the Institute, I am privileged to acknowledge
the efforts of all of the Centres’ leaders and their staff who
conduct both basic and clinical research and are recognized
internationally in both endeavours. This year the Institute
received 14 NHMRC project grants in addition to our three
ongoing NHMRC Program Grants and 3 NHMRC Centres
of Clinical Research Excellence. The breadth of the research is
impressive, interactive and covers a diverse range of disorders
and diseases. The funded projects will examine the molecular
determinants of progression and treatment in melanoma,
genes underlying dermatitis and asthma, transport of
Herpes Simplex virus in nerve cells, host factors affecting
hepatitis C, nuclear receptors in liver disease, the molecular
mechanisms of scarring of kidneys, the mechanisms of
induction of high blood pressure by snoring, amongst others
and eye disease in children. There is an encouraging degree
of cross collaboration in the use of biomedical and genetic
epidemiologic research techniques amongst the groups
involved in these apparently diverse topics.
In addition Associate Professor Philip O’Connell led a team
which was awarded $16M over 4 years to establish the
Australian Centre for Pancreatic Islet Transplantation. This
is a translational centre which has already cured selected
patients with diabetes through transplantation of islets, a
perfect example of bench to bedside research.
The expertise of the Brain Dynamics Centre, under the
leadership of Associate Professor Lea Williams was recognized
this year when they received a Clinical Centre of Research
Excellence award to establish a Centre for Anxiety and
Neuroscience and an Australian Research Council grant to
conduct further research into the risk markers for depression.
These successes are based on the legacy of the research
pioneers of Westmead Hospital. In particular Professor Peter
Castaldi who we recognized this year with the inaugural
’Castaldi Oration’. Professor Castaldi was a driving force
behind the establishment of this Institute and I would like to
reiterate the Institute’s appreciation of his continuing support
and guidance. Professor Peter Doherty, Nobel Laureate
and Patron of the Institute gave a most erudite entertaining
oration on “The continuing threat of infectious diseases”.
Finally, to Mr Paul Bell, Chairman of the WMI Advisory
Board and Mr Pat Wilde, The Millennium Foundation
President, thank you. Both Boards whom you represent
operate on a volunteer basis, and have worked tirelessly over
the past decade to raise much-needed funds and support
for the institute. Your efforts are appreciated by not only the
Executive but all here at WMI.
Professor Tony Cunningham
From the Chief Executive,
Sydney West Area Health Service
The vision of Sydney West Area Health Service is to provide
quality health care to the people it serves. Fundamental to
this objective is the support and enhancement of medical
research and innovation.
From the outset medical research has been a key part of the
Westmead campus. The campus was developed on a highly
effective model - a tertiary teaching hospital, combining first
class clinical care with teaching and medical research.
Over the past decade the Westmead Millennium Institute has
grown to become one of Australia’s leading research institutes.
Its primary objective of translating research outcomes in to
improved diagnostics and more effective prevention and
treatment strategies assists SWAHS in meeting our goal of
improving the health of our community through excellence
in healthcare.
I applaud the dedication and innovation of Westmead
Millennium Institute researchers and wish them every success
in the next decade.
Professor Steven Boyages
From the Vice-Chancellor,
University of Sydney
The University of Sydney has been allied with Westmead
since it was established in the late nineteen seventies. As a
university teaching facility it is a first class campus. For almost
three decades it has displayed an unrivalled ability to blend
academia with the practicalities of healthcare delivery.
From the outset its professors and doctors have embraced
both basic science and clinical medicine while at the same
time emphasising the translation of research into better
health outcomes. When the Institute was formally established
ten years ago, this research philosophy was firmly entrenched
Since then WMI researchers have contributed to the field
of medical research in a number of different ways. Not
only does their work contribute enormously to medical
knowledge, but their mentoring and support of PhD,
Masters and Honours students ensures the continued growth
of a critical mass of research excellence.
Over the past decade the University of Sydney has been
proud to support the world-class medical research at
Westmead and as we continue our partnership, wish its staff
every success.
Professor Gavin Brown AO FAA CorrFRSE

06 07 > Overview // AR 2006
Research Highlights
In July, the Institute celebrated ten years of research. The
centrepiece of the celebration was the Inaugural Castaldi
Oration delivered by 2005 Australian of the year and
Nobel Laureate, Professor Peter Doherty. The oration, was
established to honour former Area Health Service Board
Chairman and WMI Advisory Board Member, Emeritus
Professor Peter Castaldi AO. More than 200 guests attended
the event including the Right Honourable Gough Whitlam
and NSW Health Minister John Hatzistergos.
The Institute received more than $14 million in NHMRC
funding during 2006, the largest amount awarded to
any medical research institute in NSW. Thirteen highlycompetitive
grants were awarded to the institute’s diverse
range of projects including research covering diagnosis,
treatment and prevention of liver disease, paediatric eye
disorders, ovarian, breast and colon cancer, renal and kidney
failure, serious viral infection, cardiac arrhythmia and
respiratory disorders including asthma and sleep apnoea.

08 09 > Overview // AR 2006
Research Highlights
Infection and Immunity
The Nuclear Magnetic Resonance spectroscopy team, lead by
Professor Tania Sorrell had an extremely successful year with
funded by both the federal government and the JDRF aims
to identify factors that cause graft damage and to develop a
safer immunosuppressive regimen.
Liver and Metabolic
Dr Poustchi was the recipient of a Young Investigator
award at the Asia Pacific Digestive Disease Week in Cebu,
The Brain Dynamics Centre capped a successful year with
the opening of their newly refurbished facilities. The Baroness
Susan Greenfield officially opened three new laboratories.
the completion of studies showing that biochemical profiles
of different fungi can be identified using NMR spectroscopy
and which can be used for their clinical diagnosis. The work
also showed that resistance to medicines used in therapy can
also be rapidly determined using this technology.
Institute researchers together with Professor Adrian Mindel
conducted the first nationwide survey of adult infection
with Herpes Simplex viruses types 1 and 2 (which cause
oral and genital herpes respectively) conducted outside the
USA. Such studies will provide the baseline information for
future deployment of vaccines against genital herpes expected
within the next five years.
Responding to the urgent national need for knowledge on
avian flu, infectious diseases researchers investigated ways
to rapidly and accurately identify the presence of the avian
virus in people. The virus researchers received two NHMRC
strategic grants to work on a portable diagnostic system that
could show the presence of flu virus H5N1 in a human
sample within two hours. A highly sensitive technique for
detection of potential resistance to antiviral drugs was also
developed.
The pioneering immunological clinical research of the
pancreatic islet cell transplantation group resulted in
them being chosen to lead an Australian wide research
consortium. The aim of the research is to develop pancreatic
islet transplantation as a mainstream therapy for patients
with difficult to control diabetes. The new study, which was
The Molecular Genetics of Allergy Group, lead by Dr
Graham Jones made significant process in the understanding
of the genetics and function of a new gene, PHF11, and
its involvement asthma and eczema. The group identified
genetic variants in PHF11 that increase the risk of developing
asthma and eczema. It also showed for the first time that
PHF11 controls the expression of other genes expressed in a
subset of immune cells called T-cells.
Cancer
Melanoma researchers lead by Professor Rick Kefford
and A/Professor Graham Mann commenced a research
program investigating the molecular determinants of the
risk, progression and treatment response in melanoma. The
NHMRC funded program will be conducted over the next
five years.
The Genomics and Genetic Epidemiology group completed
the Australian Melanoma Family Study (AMFS), with
the University of Melbourne’s MEGA Centre and the
Queensland Cancer Fund Epidemiology Research Unit.
This is one of the world’s largest population-based studies
of melanoma. Approximately 1100 people who developed
melanoma before age 40 or unaffected controls were enrolled
in the study, plus thousands of their family members.
The Breast Cancer Tissue Bank, a simple but vital research
tool, began sample collection this year. Patients operated on
in NSW hospitals were invited to donate tissue to the bank.
Researchers across Australia are able to access the bank.
Philippines 2006, for related research on insulin resistance
and responses to antiviral therapy in patients with Chronic
hepatitis C.
In the area of insulin resistance and liver disease, Dr Ian
Cua a Clinical Research Fellow won the Unit’s second
Young Investigator Award at the Asian Pacific Association
for the Study of the Liver meeting (March 2006) in Manila,
Philippines, for his studies on the role of adipokines in
mediating insulin resistance in hepatitis C.
Neuroscience and Vision
Researchers in the Centre for Vision Research in conjunction
with the University of Sydney, used data from the Blue
Mountains Eye Study to investigate dietary fat and its
relationship to this eye disease. They found that people who
consumed one serve of fish a week had a 40% lower risk of
developing the early form of age-related maculopathy (ARM)
and people who consumed three serves of fish a week had a
75% lower risk of developing the more severe form of ARM.
A PhD project titled: Conscious and Nonconscious Emotion
processing: An integration of fMRI and ERPs was recognized
by the award of best PhD thesis for this year (winning the
Tasman Lovell medal in Psychology). It identified the neural
signature of conscious and nonconscious processing of fear
and happiness.
Cardio-respiratory
During 2006 LECRR researchers completed a major
epidemiologic study that identified heavy snoring as a risk
factor for the presence of carotid artery wall atherosclerosis
(plaque). Since dislodgement of carotid artery wall plaque is a
cause of stroke, this finding suggests that heavy snoring alone
poses a significant health threat.
A project conducted by the Centre for Heart Research
involved the creation of a chronic ovine (sheep) model of
atrial flutter using purely percutaneous (through the skin)
means. Previous models required open heart surgery. With
the aid of new 3D electro-anatomical imaging, the group was
able to reliably induce atrial flutter in sheep, similar to the
abnormal heart rhythms experienced by humans. Gene and
stem cell therapy to treat such disorders of the conduction
system of the heart will commence in late 2007.

10 11 > Overview // AR 2006
Infection and Immunity
We are examining important viruses and bacteria and how they interact
with the immune system. We are also looking at how to manipulate the
immune system for transplantation.
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The Infection and Immunity division is investigating serious
infectious diseases and pathogens, oral infection, organ
transplantation, autoimmunity and other immune disorders.
The Centre for Infectious Diseases and Microbiology
conducts research on the identification, treatment and
prevention of serious infectious diseases. It also provides
training and education to health care professionals, patients
and the community in managing the spread of these diseases.
A major research area is concentrating on Cryptococcus,
a fungus that causes meningitis and other brain and lung
infections. Researchers aim to define how the organism enter
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Peptide C
the body and triggers the disease to develop new treatments
against it.
Work over the past year has provided further insight into
how a recently discovered enzyme, phospholipase B (PLB),
enables Cryptococcusto to penetrate a patient’s tissue.
As investigations progress, researchers hope to use PLB
as a target for new drug treatments that may eliminate
cryptococcal infection and several other important fungibased
diseases.
Research in new antifungal drug treatments has led to the
identification of three classes of drugs that may inhibit the
effect of PLB. One of these drugs, Miltefosine, is already
being used in developing countries to kill a parasite that causes
leishmaniasis. Laboratory tests have also shown Miltefosine to
kill a number of fungi, including those resistant to available
drugs. The centre aims to improve Miltefosine’s effect while
reducing some of its current side effects. Collaborations are
being sought overseas to conduct a trial of Miltefosine to
treat cryptococcosis, which has become a major problem for
patients with AIDS in developing countries.
B
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With the support of a five-year NHMRC Centre of Clinical
Research Excellence (CCRE) grant (2005-09), research
continues to improve outcomes for immunocompromised
patients with blood malignancies. One new strategy aimed
at bone marrow transplant patients is investigating the effects
of vaccinating bone marrow donors’ cells so that immunity
can develop before the transplant takes place, reducing the
recipient’s risk of infection following the procedure.
This year, the centre began the Community Respiratory Virus
Project to understand how coughs, flu, colds, bronchitis or
pneumonia are being transmitted in the hospital wards to
patients with blood malignancies or who are undergoing
transplants. Results so far have been very positive with some
transmission patterns being identified between patients, their
families and staff. This has led to strict protocols being set
(including a flu vaccination program for patients and their
families) to prevent the spread of flu and other respiratory
viruses. An education program developed for patients and
their families has successfully incorporated information about
the impact of these infections upon the patients.
Over the past year, researchers working in rapid diagnostics
have characterized a new antibiotic resistant gene relevant to
serious infections in Australian intensive care units (ICUs).
Using newly created procedures for analysis, researchers
hope to simultaneously identify bacteria causing disease and
the genes associated with their resistance. These advanced
diagnostic methods will mean strategies can be implemented
faster than currently possible to prevent bacteria from
being transmitted to ICU patients, and treatments can be
administered more rapidly in the event of infection.
The Centre for Transplant and Renal Research is
internationally reputed for its investigations into causes,
treatments and cures for progressive renal disease and
transplantation.
More than 150,000 Australians have Type 1 diabetes (also
known as juvenile or insulin-dependent diabetes). These
patients are at risk of developing serious complications
including kidney failure. If diabetic control can be improved
then the incidence of these complications can be reduced.
The centre proposes a radically new treatment where blood
sugar levels are nomalised by transplanting the insulin
producing cells, rather than using the imperfect treatment of
insulin injections.
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The centre is continuing to make important breakthroughs
in this field of study, which includes investigations of
human pancreatic islet cell transplantation to patients and
the production of alternative sources of islet cells through
xenotransplantation – the transplantation or grafting of cells,
tissues and organs from one species to another.
Researchers at the centre were the first to establish a successful
clinical pancreatic islet cell transplant program in Australia
proving that infusing patients with these cells provides
much better control of diabetes than the traditional insulin
injection therapy.
COOH

12 13 > Overview // AR 2006
The positive benefits lasted only a few years, and the
centre is now leading a larger Australian consortium, with
substantially increased Federal Government funding, which
is being administered by the Juvenile Diabetes Research
Foundation. The aim is to examine anti-rejection treatments
that may reduce the risk of islet cell grafts failing. The
researchers hope to develop safer and more effective processes
for islet transplantation and to have a better understanding of
what happens to the graft after it has been transplanted.
Dovetailing this field of research is the centre’s pioneering
work aimed at creating a limitless supply of insulin producing
cells using modified pigs as the source. In collaboration with
a numbers other researcher groups the centre is investigating
ways to design pancreatic islet cells that can be taken from
pigs that will be more resistant to the human immune system.
The Centre for Virus Research is a world leader in research
on human immunodeficiency virus (HIV) and the herpes
group of viruses including herpes simplex virus (HSV),
cytomegalovirus (CMV), and Varicella Zoster virus. The
Centre’s main focus is to identify how these viruses infect
patients to develop ways to diagnose, treat or prevent them and
their transmission in the international and local community.
In 2006 an estimated 40 million people were infected with
HIV worldwide. The centre has helped identify how HIV
infects patients via host cells called dendritic cells, which are
found in the lining of the genital tract. In women, this lining
is thinner and less protected than in men. Understanding
how these early interactions occur is encouraging the
development of ‘microbicides’ or decoys, which may stop
the virus from entering cells of the genital tract. The Centre
is now collaborating with a biotechnology firm to develop
novel candidate microbcides.
Centre researchers are also using sophisticated techniques
to study how HIV induces changes in hundreds of human
genes that simultaneously occur within a single infected
dendritic cell. Other important work is directed at how a
group of people infected with a weaker strain of HIV have
been able to naturally control it. Recently, this work has
led to the discovery of defensive proteins, which appear to
control HIV in these patients.
Cytomegalovirus affects about 60 per cent of the population.
It is usually controlled in healthy people, but can be fatal
in immunosuppressed people such as those who have
undergone bone marrow or solid organ transplants.
Researchers have been defining the mechanisms that keep
CMV dormant and the chemical interactions that trigger its
activation. This work has led to the discovery and patent of a
type of interleukin-10, a protein that inhibits key functions
of immune cells.
Shingles is a painful condition affecting many elderly
individuals caused by re-emergence of dormant Varicella
virus years after causing chicken-pox. An exciting research
project is underway that may provide insight into the
molecular immune processes which allow this and then
control the re-emergence. With ethics permission, autopsy
material from patients who have passed away at the time of
a shingles episode are being used to identify such immune
mechanisms in the hope of improving the success rate of
current vaccine (about 60 per cent).
The centre has already pioneered work showing how herpes
simplex virus travels in nerves between the site of infection
on the skin and the site of dormant infection near the spinal
cord. When the virus is activated, it travels back to the skin
surface to present as cold sores or genital herpes. The Centre
is unraveling mechanisms that trigger this viral activity to
produce blocks that may stop the outbreaks. Negotiations
with a US biotechnology firm are underway to fund this
research in return for licensing one of the centre’s patents.
Research into HSV type 2 is significant because it causes
genital herpes and enhances HIV by up to three times. The
vaccine Simplirix, which was developed some years ago
based on discoveries made by the centre, is being retrialled
in the US with availability forecast within about three years.
Simplirix has shown to be about 75 per cent effective against
genital herpes infection in women who have never previously
had HSV. Centre researchers are examining how immune
processes control virus infection in an attempt to improve the
vaccine to protect previously infected women and also men.
In particular, work on how immunity to HSV type 1 (which
usually causes cold sores) can control HSV type 2 is about to
be patented.
The Institute of Dental Research investigates the causes
of major oral diseases to design new and better treatment
options for patients. As both tooth decay and chronic gum
infection (periodontal disease) are major health burdens for
Australian communities, the Institute’s work is critical.
Ongoing research into the microbiology of progressive tooth
decay has identified a particular group of bacteria that attack
the tooth nerve in the final stages of decay. Researchers are
currently investigating new diagnostic methods that can be
used in the dental surgery to predict the invasion by these
bacteria, so that more conservative approaches to treatment
may be applied. For the patient this may mean retaining
the living tooth rather than undergoing more complex and
invasive therapies, which often leave the tooth susceptible to
fracture leading to even more complicated treatments at a
later stage.
The Institute is also developing a new anti-bacterial
compound that may be able to target specific diseases or
bacteria in the mouth and gums so that protective bacterial
flora (good bacteria) are not destroyed during treatment.
Current therapies still rely on broad-spectrum antiseptics or
antibiotics, which wipe out good and bad bacteria present
in the mouth. While tests are at an early stage, the eventual
outcome may see low-cost treatments such as toothpastes or
mouthwashes containing the specific anti-bacterial available
in supermarkets.
The Institute for Immunology and Allergy Research
investigates diseases caused by abnormal functioning of the
immune system. This includes many major unsolved diseases
that plague communities worldwide. The Institute’s research
programs focus on three main themes: autoimmune disease
such as multiple sclerosis (MS); allergy disorders such as
eczema and asthma, and why individuals vary so much in
their response to infection with HIV and hepatitis C viruses.
Collaborative research on the genetics of severe eczema and
asthma in children has led to the discovery of a link between
these diseases and several genes that are important for normal
immune function called TIM-1, TIM-3 and PHF11.
Researchers know TIM-1 and TIM-3 are expressed on the
surface of specific types of immune cells and relay messages
inside the cell, leading to cell activation through the turning
on or off of specific genes. The Institute has now made
important advances in understanding how PHF11 operates,
showing that it is present deep inside a cell and directly
controls the switching of genes on or off. Researchers are
now investigating whether these genes interact to influence
susceptibility to disease. Although still at an early stage,
this research may guide the development of new drugs and
topical therapies.
Major research is also being conducted on a gene crucial to
the immune system’s healthy functioning called Interleukin
7 receptor alpha chain or CD127. In 2003, the Institute was
the first to publish findings that a genetic variant of CD127 is
important in the development of MS. The researchers believe
this is due to its role in generating regulatory T cells, which
stop the immune system from attacking the body’s own
tissue and have submitted at patent application for improved
therapy based on this discovery. Three international research
groups have recently confirmed this discovery making
CD127 only the second clearly established genetic risk factor
in MS after HLA (a cell’s identification markers). As a result,
CD127 has become one of the hottest areas of research into
MS strengthened by the potential to design treatments to alter
the abnormalities found in the gene’s function.
In other research, the Institute was awarded an Australian
Research Council Linkage Project grant to collaborate with
the pharmaceutical company Biogen IDEC to investigate
why up to one-third of MS patients fail to benefit from
interferon, the disease’s main treatment therapy.
NHMRC grant funding is also supporting research between
the Institute and the Storr Liver Unit to investigate the
genetics of hepatitis C. About 35 per cent of individuals fully
recover from the hepatitis C infection due to their immune
system clearing the virus from their body. The remaining
65 per cent of patients fail to clear the virus and may go
on to form cirrhosis and liver cancer. Based on these data,
researchers are examining the factors in patients’ genetic
makeup that determine disease outcomes when infected by
the virus.

14 15 > Overview // AR 2006
Cancer
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The Cancer division conducts groundbreaking laboratory
and clinical investigations into cancers common to
Australians to improve prevention and treatment strategies
and to establish new cures.
The Westmead Institute for Cancer Research bases its
research on the notion that if discoveries can be made to
understand the faults in the wiring of cancer at a molecular and
cellular basis - and how this differs from the make up of healthy
cells - then medical science can develop ways to correct the
defects.
One of the difficulties researchers face is a lack of suitable
human cancer research models. An outstanding success this
year has been the development of a three-dimensional model
of normal breast tissue. This model is enabling researchers
to grow tiny spheres of cells taken from breast tissue in a
highly organised structure, which is more closely aligned
physiologically to the human system than traditional cell culture
or animal models.
In using the model, researchers are unraveling the process of
how breast cells become cancerous through the actions of
the ovarian hormones oestrogen and progesterone. Major
advancements are already in play with researchers identifying
pathways these hormones control within the normal breast
cells. As work progresses, researchers hope to identify the
normal breast cell targets that control the interaction between
the ovarian hormones and cancerous cells to produce suitable
prevention strategies.
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The Institute hosts the newly opened Breast Cancer Tissue
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Bank. The bank has begun collecting breast cancer tissue
samples from hundreds of women with breast cancer across
NSW. This is a major achievement made possible through the
cooperation of clinicians and patients. Data from the samples
will be carefully linked back to the women’s follow up treatment
and outcomes and researchers from all over Australia will have
access to the bank to improve investigations into the disease.
Cancer researchers Rick Kefford and Graham Mann are the
determine the genetic signatures that make particular melanoma
tumours behave aggressively using modern gene expression
and microarray technology. Researchers hope to develop new
treatments that target molecular faults within the cells to improve
diagnosis and prognosis of this disease, enabling clinicians to give
patients better treatment and advice.
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Of all human cancers melanoma is most resistant to current
therapies and it is an area where researchers are also using gene
expression analysis (examining how genes operate within a cell)
to produce better treatment outcomes for patients. The Institute
is investigating features in the few melanomas that are sensitive
to treatment as a basis for developing techniques to breakdown
the disease’s resistance to chemotherapy.
Ovarian cancer is the most lethal gynaecological cancer. Each
year, more than 1,000 women in Australia are diagnosed and
more than 800 women die from the disease. Overall survival
rates are low with only about 45 per cent of women free of the
malignancy after five years.
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Most ovarian cancers are initially sensitive to chemotherapy.
However, the most common outcome for women with this
disease is for it to return within a couple of years and, when
the patient relapses, the cancer is most often resistant to
chemotherapy. There are however, a small group of patients
that respond extremely well to chemotherapy and are essentially
cured. Researchers in the Gynaecological Cancer Research
Group are trying to identify why some patients respond so
much better to treatment than others in the hopes of developing
new therapies based on gene targeting.
They have already identified one gene that may be used to
increase response to chemotherapy and this work has led to an
international patent. The researchers have found tumours that
express a lot of this gene tend to do worse, and that this gene
is over-expressed in ovarian cancer cells which are resistant to
treatment. (Expression is the process of a gene’s DNA sequence
being converted to proteins within cells.) The group is now
investigating methods to decrease the gene’s expression using
a novel technique called siRNA, which specifically targets the
Most cancers are due to genetic changes that accumulate in the cells with
leading chief investigators on a five-year NHMRC Program gene. The aim is to then apply conventional chemotherapy
age, but in 5 to 10 per cent of cases, patients have a family history of multiple
Grant and a Cancer Institute NSW Translational Program grant, to improve a patient’s response to treatment. Pre-clinical
cases of early-onset cancer. Many patients are enrolled in collaborative,
both of which commenced in 2006. These cement long-standing experiments are underway with a commercial partner being
00.005.0491 00.005.0492 00.005.0488 00.005.0489 00.005.0460 00.005.0461 collaborations with 00.005.0468 the Sydney Melanoma Unit 00.005.0469 – the largest sought to 00.005.0516 develop methods to target this 00.005.0517 gene. The group is also 00.005
genetic-epidemiological studies investigating the familial aspects of cancer.
28 26
melanoma treatment centre in the world. The programs aim to investigating other genes with similar characteristics to possibly
extend the treatment base.
00.005.0464 00.005.0515

16 17 > Overview // AR 2006
Liver and Metabolic
HO
3
A
5
The Liver and Metabolic division researches aspects of
liver disease that affect patients in Australia with a focus
on hepatitis B and C, fatty liver disease and liver cancer.
The Storr Liver Unit researchers conduct many exciting
projects. The unit has been investigating the molecular causes
of fatty liver disease (FLD) and ways to reduce its increasing
prevalence. Of all liver disease, FLD is the most common
in Australia. It occurs through an accumulation of fat in the
liver and is closely linked to overweight, obesity and diabetes
- about 70 per cent of Australians are overweight or obese
and diabetes affects about one in five Australians.
Researchers have been examining the importance of bile acids
to the origin and progression of FLD. The molecule NF-kB
has also been shown to trigger inflammation and damage in
patients with FLD. Importantly, the unit has also established
a link between obesity and hepatic fibrosis (liver scarring),
B
6
C
Cholestorol
D
17
which can eventually lead to cirrhosis or end stage liver
disease. Patients with FLD have increased levels of leptin, a
hormone secreted by fat cells and attributed to have a major
role in regulating the appetite and metabolism. The Unit
has now identified how leptin acts on certain cells found in
the liver called Kupffer cells, to release proteins, which then
activate the cells responsible for fibrosis.
The Storr Liver Unit is also conducting a two-year Lifestyle
Intervention study for fatty liver disease, which is the world’s
first and largest clinical trial aimed at reducing overweight
and obesity levels in these individuals. The study is based
on a behaviour modification program designed to break
down the psychological barriers that prevent patients from
maintaining a healthy lifestyle. More than 170 patients have
been recruited for the trial. Results at three months already
show improvements in physical activity, weight, liver tests and a
reduced risk of diabetes in those who received the intervention.
not being screened, rendering the trial redundant. Despite
professional concerns over the stress that diagnostic screening
may cause, patients preferred this to not knowing if they had
cancer. A screening protocol has now been implemented.
It has shown that malignant tumours were detected at an
earlier stage when they were smaller and easier to treat,
suggesting that screening protocols are appropriate for this
disease.
In other research, the Storr Liver Unit has been looking
at the role of bile acids in drug metabolism. There is huge
individual variation in how patients respond to drugs.
Traditionally, drug doses in treatments such as chemotherapy
are administered using the same dose for all persons.
However, while one patient may have little response another
may develop serious side effects. Exploring molecules called
nuclear receptors within the liver, researchers have been
trying to understand differences in individual variations
in these drug responses, in an effort to develop more
‘personalised’ medicine.
The unit is also conducting novel work in the area of human
genome mapping in individuals who have been treated for
hepatitis C. Researchers are in the preliminary stages of
understanding how to scan the entire genetic code of these
individuals to work out why some respond to hepatitis C
treatments and others do not. These investigations seek to
identify whole genome differences between the two groups
of individuals with the ultimate aim of reading a patient’s
molecular signature to administer better treatment regimens.
If successful, this technology could eventually be used for
many disease treatments.
Propionyl-CoA
NADP + H +
O 2
7`-hydroxylas
NADPH + H +
O 2
2 CoA-SH
The rate at which drugs are cleared from the body can vary substantially
between individuals and have a major influence on the effectiveness and
toxicity of treatments. Researchers are exploring molecules called nuclear
receptors within the liver trying to understand differences in individual
drug responses.
In another world first, the unit recently abandoned a
OH
proposed randomised controlled trial to address doubts over
the benefits of liver cancer screening. An overwhelming
majority (95 per cent) of patients chose to be screened over
C – S – CoA
O

18 19 > Overview // AR 2006
Neuroscience and Vision
Our researchers have commenced studies on the genetic epidemiology
of psychiatric disorders. The ultimate aim of these studies is to identify a
genetic predisposition to various brain disorders at a very early stage.
The Neuroscience and Vision division is investigating the
causes of emotional disorders, mental illness and visual
disorders, using a combination of imaging technology,
molecular biology and epidemiology.
The Brain Dynamics Centre is a world leader in
interdisciplinary brain and mental health research.The centre
focuses on major mental illnesses including schizophrenia,
depression, attention deficit hyperactivity disorder (ADHD)
and related behavioural disorders (such as conduct disorder),
anxiety disorder, particularly post traumatic stress disorder
(PTSD), and more recently conversion disorders.
Finding suitable treatments for these disorders has been
difficult for clinicians since their origins are still largely
unknown. This has motivated researchers to make use of all
available diagnostic techniques - genotyping, EEG, MRI,
psychometrics - to quantify brain dysfunction at all scales.
This, in turn, informs quantitative and conceptual models
of disorders. Researchers at the centre have also developed
new methods to analyse the data. For the first time they
have a complete map or model showing how the brain
functions physically and chemically to be able to navigate
abnormal changes in the brain. Researchers can use the
brain map to understand how individuals may respond to
different therapies, ultimately leading to more accurate and
personalised treatments being prescribed faster.
In another breakthrough this year, research has identified
key cognitive and biological markers of ADHD. They have
also identified which of these markers are improved with
stimulants such as Ritalin. These are important findings
because they provide an objective test to assess which children
are likely to respond best to stimulants. A new trial is now
underway to test which children may respond to nonstimulant
medication.
Researchers have also shown that biological changes in the
brain occur with PTSD and predict response to psychological
treatments. In addition, researchers have learnt biological
changes in the brain are a major factor in anorexia nervosa,
a chronic eating disorder affecting mostly young women.
Testing pre and post treatment is again determining which
biological markers improve with medical treatment. This
research also offers insights into whether medication may be
of help for some individuals with anorexia.
While the causes of schizophrenia are still unknown, the
researchers have identified candidate cognitive and biological
markers of this condition. Cognitive remediation is being
trialled for the first time in Australia to target specific
problems such as poor memory or information processing.
The Centre for Vision Research investigates the causes of
vision impairment to reduce the impact these conditions
have on people’s lives. The centre has been conducting visual
impairment studies in older and younger people for more
than a decade. Researchers are concentrating on several
themes including the genetic and nutritional influences on
eye diseases.
Recently, a 10-year examination on a group of more than
3,650 people was completed as part of the landmark Blue
Mountains Eye Study. Using baseline photographs taken of
patients’ retinal vessels, researchers have been able to show
the diameter of retinal arteries is strongly related to blood
pressure levels now and into the future, making it a strong
marker for cardiovascular disease risk. Researchers have also
confirmed the retinal veins are markers associated with disease
such as diabetes, and can also indicate if a patient smokes and
whether they have generalised inflammatory problems.
Researchers involved in the Blue Mountains Eye Study have
also investigated the role fish high in omega-3 fatty acids play
in affecting factors leading to cardiovascular disease. Those
who ate moderate amounts of fish had better retinal factors
at the study’s commencement and had reduced risk of heart
attack and stroke 10 years on.
A separate study has shown individuals who ate a diet with
a higher glycaemic index (the speed of which glucose is
absorbed in the blood) are more prone to cataracts and
macular degeneration. Similarly, those with signs of macular
degeneration who ate higher amounts of fish high in omega-
3 fatty acids could slow the disease’s progression.
The centre has expanded its investigations into the causes of
short-sightedness to include children from Singapore. Myopia
levels in south-east Asian countries have grown exponentially
in the past 50 years. Ninety per cent of university graduates
in Singapore are short sighted as are young people joining the
armed forces. A study comparing myopia levels in children
in Sydney and Singapore with similar Chinese backgrounds
and age-related profiles showed the Sydney children had very
low rates of the condition (3 per cent), while the children in
Singapore had much higher rates (29 per cent). Researchers
believe the time children generally spend playing outdoors
directly correlates to myopia levels.

20 21 > Overview // AR 2006
Cardio-respiratory
Laboratory and clinical studies are combined by respiratory researchers
hoping to identify breathing and sleep disorders linked to or resulting from
a disease or injury.
The Cardio-respiratory division combines laboratory
research and clinical studies to enhance our understanding
of common cardio and respiratory disorders like abnormal
heart rhythms and sleep disorders.
The Centre for Heart Research is focused on finding better
treatments for patients with abnormal heart rhythms and to
cures these conditions.
Ventricular trachycardia (VT) is a debilitating condition that
causes the heart to beat rapidly, affecting the heart’s pumping
chambers or ventricles. It usually occurs when the heart
muscle has sustained damaged from previous heart attacks
and can cause sudden death.
VT is treated using a defibrillator, a device which triggers a
painful electric shock to normalise the heartbeat. A therapy
can be applied which modifies abnormal electrical activity
responsible for VT, reducing the need for patients to undergo
the electric shocks. This method uses radiofrequency ablation
to heat the heart tissue using electrical energy to destroy
small regions responsible for VT. To locate these areas more
effectively, researchers are working on a three-dimensional
mapping system, which is based on satellite navigation
technology, to guide clinicians directly to the scarred areas.
Researchers are also developing a novel catheter, which
is positioned within the patient’s heart to indicate where
abnormal electrical activity is originating from. This can be
done from a single abnormal heartbeat, which is a major
improvement on previous methods. The ultimate aim for
researchers is to perfect these innovations so patients with VT
may be cured of the condition.
Researchers have also been working on improving outcomes
for patients with atrial fibrillation (AF), rapid heart-beating in
the upper heart chamber, which leads to stroke in about 15
per cent of people aged over 75 years.
Technology developed in France to isolate electrical triggers that
cause AF is being offered to Westmead Hospital patients as an
alternative to medication or open-heart surgery. Researchers at
the centre are working to improve the 70 per cent efficacy of
this treatment and to improve the procedure’s success rate.
Among other projects, researchers have begun collaborating
with Westmead Hospital’s cardiothoracic unit to investigate
ways of refining the artificial mitral valve used to replace the
diseased valve in patients.
The Ludwig Engel Centre for Respiratory Research aims to
improve the quality of life for patients with respiratory and
sleep-related respiratory diseases.
The centre primarily researches the causes, consequences
and potential new treatments of the obstructive sleep apnoea
syndrome, a disorder affecting about 800,000 Australians.
Other research areas include cystic fibrosis, asthma and
chronic obstructive pulmonary disease.
Patients with sleep apnoea experience repeated episodes
of throat blockage during sleep, which stops them from
breathing for short periods of time. The disorder results
from snoring and obstructed breathing and is linked to
hypertension, heart failure, heart attacks as well as stroke.
Over the past year, researchers have been looking at the
role heavy snoring may play in triggering stroke. Vibrations
caused from heavy snoring travel in tissues surrounding
the airways to the carotid arteries found in the neck, which
supply blood to the brain. Researchers are investigating
whether this may exacerbate atherosclerosis (hardening) in
the carotid arteries eventually leading to stroke.
Clinical studies yet to be published on a group of 110
patients with varying degrees of heavy snoring and mild sleep
apnoea showed heavy snoring was associated with a 10- to
17-fold increase in the risk of carotid artery vascular disease.
As research continues, approaches to treatment may alter to
include more regular screening of carotid arteries in patients
who snore heavily and increased research into preventative
therapies for the condition.
Studies over the past year have also assessed the efficacy of
a rehabilitation program designed to minimise hospital
admissions and improve quality of life and wellbeing in
patients with chronic obstructive lung disease. The program
uses a combination of aerobic exercise, education, clinical
support and medication optimization. This successful
combination has been shown to add 60 metres to patients’
walking distance and reduce hospital admission rates over
two years following completion of the program and improve
general wellbeing.

22 23 > Overview // AR 2006
International Collaborations
Medical research today is an international activity and some
research projects like the sequencing of the human genome
are only made possible by international co-operation.
From the outset the Institute has formed international links
and partnerships with research institutes, hospitals and
universities across the globe.
UNITED KINGDOM
Cambridge
Dundee
Glasgow
Leicestershire
London
Manchester
In 2006, our research projects span the world’s continents,
from Moscow to Manila to Minneapolis. These
collaborations allow our researchers to contribute and gain
valuable research knowledge.
While we participate on this international stage we also
work closely with our Australian based research partners.
Together this assists us in achieving our goal of better
prevention strategies, treatments and healthcare for all.
MIDDLE EAST
Taran - Iran
Tel Hashomer (near Tel Aviv)
ASIA
Beijing
Manila
Singapore
Tokyo
USA
Baltimore
Boston
Cambridge (Massachusetts)
Chicago
Denver
Houston
Michigan
New York
Philadelphia
San Diego
San Francisco
Seattle
Washington DC
EUROPE
Geneva
Hamburg
Madrid
Moscow
Nijmegen (Netherlands)
Paris
Perugia
Rome
Rotterdam
Wuppertal (Germany)
Zurich
SOUTH AFRICA
Alberton
Durbinw
Sydney
NEW ZEALAND
Auckland

24 25 > Overview // AR 2006
Advisory Board and Council of Governors
Organisation Structure
WMI ADVISORY BOARD
ADVISORY BOARD
GOVERNORS
Chair – Mr Paul Bell
DIVISIONS AND GROUPS
INFECTION & IMMUNITY
Mr Paul Bell
Chairman
R2
Professor Gavin Brown AO
Vice-Chancellor, University of Sydney
Professor Peter Castaldi AO
57
57
57
57
8
8
8
Professor Tony Cunningham
Director, Westmead Millennium Institute
8
8
57
8
05
N53
R2
57
Mr Philip Chronican
57
57
Group Executive, Westpac Institutional Bank
8
57
X
57
57
N53
N53
57
57
57
57
57
8
57
57
57
57
57
57
57
Professor Jeremy Chapman
Network Director, Acute Interventional Medicine
Sydney West Area Health Service
Mr David Greatorex AO
Mr Jim Bosnjak OAM
Chairman, Bosnjak Investment Group
N59
57
57
Dr Peter Farrell
Chief Executive Officer, ResMed Australia
Professor Ian Gust AO
N53
DIRECTOR
Prof Tony Cunningham
CHIEF OPERATING OFFICER
Mr Mark Dado
OPERATIONS
Manager, Mr Glenn Holden
FACILITIES AND
GRANT ADMINISTRATION
Manager, Mr Mark Smith
FINANCE
Manager, Mr Mark Wissam
Centre for Infectious
Diseases and Microbiology
Director, Professor Tania Sorrell
Centre for Transplant and
Renal Research
Director, Transplantation
A/Prof Phillip O’Connell
Director, Nephrology
Prof David Harris
Centre for Virus Research
Director, Prof Tony Cunningham
Institute of Dental Research
Director, Prof Neil Hunter
Institute for Immunology
and Allergy Research
Director, Prof Graeme Stewart
LIVER & METABOLIC
Storr Liver Unit
Co-Acting Director,
Prof Jacob George
Co-Acting Director,
Prof Christopher Liddle
NEUROSCIENCE & VISION
Brain Dynamics Centre
Director, A/Prof Lea Williams
Centre for Vision Research
Director, Prof Paul Mitchell
PR2
N59
PR2
57
Mr James Wakim
Managing Director, Arab Bank Australia
Mr Patrick Wilde
President, The Millennium Foundation
R4
N59
R2
R2
OR6
R2
R2
57
Professor Janice Reid
Vice-Chancellor, University of Western Sydney
R2
HUMAN RESOURCES
Manager, Ms Amanda Clout
PR AND COMMUNICATIONS
Manager, Ms Gayle McNaught
Information Technology
CANCER
Westmead Institute for
Cancer Research
Director, Prof Rick Kefford
CARDIO-RESPIRATORY
Centre for Heart Research
Director, Dr Pramesh Kovoor
Ludwig Engel Centre for
Respiratory Medicine
Director, A/Prof John Wheatley
N53
R4
OP4
R2
R2
OR6
Manager, Mr Ian Magee
Science Council
Chair, A/Prof Christine Clarke
R4

26 27 > Overview // AR 2006
Funding
Infrastructure Grants 2,651,483
Funding Organisations
During 2006 the Institute received research funding from the following major organisations. We thank them for their support.
Allergan Australia Pty Ltd
Leukaemia Foundation
National Health and Medical Research Council Grants 7,814,750
Other Grants 8,412,863
Other Income 2,055,313
Total 20,934,409
American Health Assistance Foundation
Anthony Rothe Memorial Trust
Australia and New Zealand Intensive Care Foundation
Australian Centre for HIV and Hepatitis Virology Research
Australian Cystic Fibrosis Research Trust
Australian Dental Research Foundation
Australian Health Ministers’ Advisory Council
Australian Research Council
Australian Rotary Health Research Fund
Australian Society for Psychiatric Research
Biogen Idec Australia
Cancer Institute NSW
Cure Cancer Foundation
Eli Lilly Australia Pty Ltd
Janssen-Cilag Pty Ltd
Juvenile Diabetes Research Foundation
Juvenile Diabetes Research Foundation International
Kidney Health Australia
Multiple Sclerosis Research Australia
National Breast Cancer Foundation
National Health and Medical Research Council
National Heart Foundation of Australia
National Institutes of Health (USA)
NSW Office of Science and Medical Research
Pfizer Australia Pty Ltd
Red Cross Blood Transfusion Service
Robert W Storr Bequest
Roche Products Pty Ltd
Sanofi-aventis Australia Pty Ltd
Schizophrenia Research Institute
The Australian Lung Foundation
The Cancer Council New South Wales
The Cardiac Society of Australia and New Zealand
The Millennium Foundation
University of Sydney
University of Sydney Cancer Research Fund

28 29 >
Research Report // AR 2006
Research Report

.
< 30 31 > Research Report // AR 2006
Infection and Immunity
Centre for Infectious Diseases and Microbiology
Fungal pathogenesis
The group has shown that specialised lipid domains
(“rafts”) in the cell membrane of the fungus Cryptococcus
neoformans, which causes severe meningitis, serve as sites
of attachment of a key enzyme, phospholipase B (PLB).
This enzyme is attached to the raft by an anchor. When
released from the anchor, free PLB1 facilitates penetration
of Cryptococcus into lung and brain. We are now studying
how the production and release of PLB1 is regulated and
the mechanism by which it is released from the membrane.
This fundamental knowledge will lead to new understanding
of cryptococcal biology and help us to identify new
target molecules for development of drugs to treat fungal
infections. This work was received with great interest by the
international cryptococcal research community.
Antifungal drug development
The group has an NHMRC project grant to make and test
new chemical compounds that act on enzymes produced by
fungi, which are important in virulence (and hence initiation
of disease). Led by synthetic chemist, Dr Kate Jolliffe, 50
novel compounds in 2 chemical classes have been made and
tested against a range of fungi that cause disease in humans.
Particular interesting is one class of compound related to
a marketed drug, miltefosine, which was developed as an
anti-cancer drug and is now used for treatment of a parasite
infection (leishmaniasis). We will be undertaking further
modification and testing of the most promising compounds
in 2007.
Bacterial pathogenesis, antibiotic resistance and
novel diagnostics
The group was the first to identify and have since
characterised the genetic basis of newly arrived transmissible
resistance to carbapenem antibiotics and the CTX-M
type ESBLs newly arrived in Australia, including novel
gene variants. The group has defined the basis for most
major antibiotic resistance genes relevant in ICU in
Australia, and begun to incorporate these into novel highspeed
multiplexed assays in collaboration with industry
partners. Assays developed for rapid detection of S. aureus,
MRSA, and influenza (including H5N1 “bird flu”) are
now entering clinical trials. Our work has been presented
in major international conferences (eg ICAAC) and
journals (eg Lancet Infections Diseases, Nature Reviews
Microbiology). New areas include bacteriophage therapeutics
(in collaboration with industry), novel immunofluorescence
methods (funded by ARC, in collaboration with Macquarie
University) and quorum-sensing inhibitors (funded by ARC,
in collaboration with BioSignal/ UNSW).
Nuclear magnetic resonance spectroscopy
This has been a very successful year, with the completion of
studies showing that biochemical profiles of different fungi
can be identified by NMR spectroscopy and hence be of
diagnostic value, and that resistance to medicines used in
1
NH 2
1
2
2
therapy can also be rapidly determined using this technology.
The work has been published in the top international
antibiotics journal and was presented at the leading
international meeting on mycology (ISHAM), in Paris, in
June 2006.
Improved outcomes in immunosuppressed
haematology patients
This is a large Centre of Clinical Excellence Program now
in its second year. So far research highlights have included
a study of the occurrence, transmission and prevention of
community respiratory virus infections in patients with
cancer of the blood. Importantly the group has shown that
protection of patients is improved by routine vaccination
against influenza and education of patients, their carers,
and staff about the importance of hand washing and other
infection control measures. Several important ethics studies
are underway, assessing patients understanding of informed
consent for treatments that they receive, their response to
living with cancer, and the effect of isolation during times of
very low function of the immune system (in order to prevent
serious infections). Other key programs are proceeding
in vaccine research and the development of faster tests for
diagnosis of infections, in order prevent, or to improve
outcomes of serious infections through more rapid diagnosis
and thus commencement of treatment.
3
6
s
s
s
10
Centre for Transplant and Renal Research
Pancreatic islet cell transplantation
Following the units pioneering clinical trial of pancreatic islet
transplantation they have been chosen to lead an Australia
s
11
Peptide C
wide consortium with the aim of developing pancreatic islet
transplantation as a mainstream therapy for patients with
difficult to control diabetes. The original trial involved six
patients with severe metabolic complications from their
diabetes. Five of the six had marked improved metabolic
outcomes after successful pancreatic islet transplantation
and three patients no longer required insulin injections for
substantial periods of time. This trial identified progressive
loss of islet graft function and complications from the
anti-rejection drugs as the major impediments to it more
widespread application. The new study, which has been
funded by the Federal Government and the JDRF aims to
identify factors that cause graft damage and to develop a safer
immunosuppressive regimen.
Pancreatic islet xenotransplantation research
Currently pancreatic islet cell transplantation is the only
known cure for Type 1 diabetes. If this therapy is to be
more effective sources of insulin producing cells other than
B
A
organ donors needs to be found. In collaboration with
researchers in Melbourne and Adelaide we are investigating
the use of pig pancreatic islet cells for future transplantation
in human patients. The group’s current research is focused
on understanding the mechanisms of early islet cell loss.
This appears to be due to a combination of clotting and
early cellular rejection. Our data suggests that producing
pigs whose islet cells express several human proteins that
regulate clotting and rejection may be sufficient to allow
this tissue to be used safely in patients. This information
has been used to develop a new line of pigs that have been
genetically modified so that they may be better suited to
clinical transplantation. Australia is the world leader in pig
transgenesis and this ambitious collaborative project between
four research institutes is making substantial progress in the
development of pig islet cell xenotransplantation.
Transplantation immunity and tolerance
The aim of this group is to better understand the
mechanisms of rejection of pancreatic islet xenografts
and to develop novel strategies for suppressing this
immune response. The group has made several findings in
understanding the role macrophages play in the rejection
of pig islet grafts. In particular they have shown that
macrophages have a surprisingly specific and sophisticated
recognition response for identifying pig tissue. At present
work in this area is focusing on understanding the molecular
mechanisms responsible for this recognition. In particular
we have focused on a group of macrophage receptors called
toll receptors and have found that they have an important
role in regulating macrophage recognition of pig tissue.
The group is also investigating novel strategies to induce
tolerance to transplanted islet tissue and to further reduce
the requirement for long-term immunosuppression. In
particular they are focusing on the role of a regulatory T cell
called CD4CD25+ T cells. They have found that these cells
are capable of inducing tolerance to islet allografts and have
begun investigating their role in maintaining tolerance to pig
islet cells.
Chronic allograft nephropathy research
The aim of this group is to increase knowledge about the
mechanisms for the long-term loss of renal transplant.
Current treatment strategies are very good at preventing
acute cellular rejection but over time renal transplants are
s
20
s
21
still lost to a complex process known as Chronic Allograft
Nephropathy. The group has been at the forefront of this
research internationally and by studying protocol biopsies
has identified several novel factors responsible for this
chronic graft loss. The focus of the group is to understand
the molecular mechanisms responsible for this loss
using a genome wide analysis of biopsy specimens using
genomics or gene chips. This had allowed us to identify
early mechanisms of graft fibrosis and glomerulosclerosis.
Which in turn has allowed us to understand better the
early pathology that ultimately leads to chronic allograft
nephropathy. Ultimately it will assist us to develop a
diagnositic test that predicts those patients that will develop
this condition and to design new treatments. In the last 6
months we have been successful in obtaining funding from
the National Institutes of Health in the US to take part in
a large multicentre study that will identify the genomics of
Chronic Allograft Nephropathy.
COOH

32 33 > Research Report // AR 2006
Renal failure research
include using soluble receptors as decoys binding to the virus
role in subverting human gene machinery in different cell
partially effective vaccine candidate has been developed
This research is focused on novel therapies for reducing
as well as direct antagonism of the HIV binding receptors.
types. The Retroviral Genetics lab also runs services for drug
(partly based on our previous work) but is not yet licensed.
kidney inflammation in chronic kidney disease. New
approaches to treatment that are currently being tested
in animal models of human kidney disease include the
administration of protective cells (regulatory macrophages
and regulatory T lymphocytes) which reduce inflammation
and structural and functional injury. In addition, vaccination
using genes of molecules that drive the inflammatory
response is also being tested. We have exciting preliminary
results in models of diabetic nephropathy, suggesting that
this approach not only slows the progression of diabetic
kidney disease, but also reduces the severity of diabetes itself,
and also reduces diabetic complications occurring in other
organs including eyes and heart. These novel approaches are
bringing new understanding to the processes that underlie
the progressive nature of kidney disease, and have the exciting
potential of use for treating human kidney disease.
Centre for Virus Research
HIV molecular pathogenesis
The HIV molecular pathogenesis group’s primary focus is to
understand the very early interactions of the HIV virus with
host cells of the body, predominantly human dendritic cells
(DCs). These are the first cells to come into contact with
HIV within the genital tract.
In 2006 our group revealed that HIV induces partial
maturation of DC and in doing so the virus may utilise
the migratory capacity of DC to gain access to T cells in
the lymph nodes. The group continues to investigate the
mechanisms by which HIV subverts the maturation of
DC and the effect this may have on the initiation of an
appropriate immune response.
The global gene changes that HIV induces in dendritic
cells continue to be investigated using DNA microarray
technology, and investigations are now being broadened to
include the effects that HIV has on the proteins regulating
the expression of interferons.
Other investigations conducted in the laboratory involve
investigating ways to prevent infection of DCs particularly
those in skin and genital mucosa. The methods employed
Preliminary studies indicate that these can be effective
inhibitors. The ultimate goal is to reduce or even prevent viral
trafficking at a very early stage of infection.
HIV protein functions and interactions group
The main interest of this group is to understand the function
of several HIV proteins and their interaction with cellular
proteins on a molecular level. The long-term aim is to
identify novel antiviral therapeutics.
During 2006, the research projects conducted by the group
included understanding the role and function of the small
HIV protein Vpr in viral isolates from AIDS patients,
investigation of the role of the cytoplasmic tail of the
envelope HIV glycoprotein 41, and a collaborative study to
determine the role of DNA methylation in HIV replication.
Retroviral genetics laboratory
The Retroviral genetics laboratory focuses on several different
aspects of HIV pathogenesis. We are working on the innate
and adaptive immune factors which are found in untreated
HIV+ patients with non-progressive disease.
The main goal of this group is to understand what guides
the path to non-progressive HIV disease in a subset of HIV+
individuals and can these natural factors, which provide them
protection, find some use as therapeutic agents/vaccines.
We are adopting a variety of immunological, virological,
proteomic and protein chemistry techniques to identify and
characterize these novel factors from patients who have lived
with HIV for more than 20 years.
Another aspect of this study is genomics where we are
gathering information based on the cell surface markers
and whole human genome (>47,000 genes) to understand
how HIV guides different stages of HIV disease in different
hosts and in different cell types within the same host at the
level of manipulating cellular phenotype and human gene
machinery.
Other studies in the lab are also directed at understanding
HIV infection of the brain in relation to cellular infiltration
across the blood brain barrier, HIV recombination,
emergence of novel HIV strains, their pathogenesis and their
resistance and epidemiologic testing of HIV in Australia.
Cytomegalovirus research
Human cytomegalovirus (CMV) is a medically important
virus which infects 50-90% of the population. Whilst
infection is usually mild in healthy individuals, it is a frequent
cause of serious, life-threatening disease in neonates and
immunosuppressed individuals such as solid organ and bone
marrow transplant recipients, and in people with HIV AIDS.
After initial (primary) infection, the virus is not completely
cleared by the host’s immune system. Rather, the virus is
able to establish a life-long latent infection, during which
time the virus remains in the body but does not grow or
cause disease. Periodically, the virus may reawaken from this
latent state by a process called reactivation, resulting in the
production of new infectious virus. Reactivation from the
latent state in immunosuppressed individuals is thought to be
the major cause of serious disease in these people, but despite
the importance of latency and reactivation to the success of
this virus as a human pathogen, these areas of the life cycle of
CMV remain very poorly understood.
The CMV research group is working to discover how the
virus operates during the latent phase of infection. The
group has applied a variety of molecular and cell biology
approaches, including the use of microarray technologies,
to identify both viral genes and human genes that play
important roles during CMV latent infection of human cells.
These studies have provided important insights into how
the virus functions during latency. Identifying the critical
virus and host cell components of latency and reactivation
will provide a rational basis for the design of drugs and
therapies to limit the consequences of CMV disease in
immunosuppressed individuals.
HSV immunology
Herpes Simplex virus (HSV) causes two common infections,
cold sores (HSV1) and genital herpes (HSV2). Its infection
can sometimes result in encephalitis and neonatal herpes.
Genital herpes enhances acquisition up to threefold. A
The HSV immunology group is focused on discovering
and developing new vaccine candidates and has also been
studying the interaction between HSV and immune cells like
dendritic cells (DC) and T lymphocytes.
Dendritic cells (DC) are the most potent antigen presenting
cells to stimulate T lymphocytes and classified as myeloid
dendritic cells (mDC) and plasmacytoid dendritic cells
(pDC). Langerhans cells are another type of DC residing
in epidermis, which are presumed to play a primary role in
herpes lesions. Such Langerhans cells have been shown to be
infected in herpes lesions. How HSV infects these cells in
vitro and alters their function is now being studied. pDCs
are supposed to be restricted to blood and lymph nodes.
However during 2006, the group used confocal microscopy,
to identify pDC in the skin of genital herpes lesions but are
not infected by HSV2.
In herpes lesions CD4 lymphocytes are the first to enter
and partly control HSV infection preparing the way for
later infiltration by CD8 lymphocytes which clear up the
infection. Some peptides in glycoprotein D (gD) of HSV2
were identified as strong immunostimulatory antigens for
CD4 T lymphocytes. Some of these “epitopes” are recognised
by CD4 lymphocytes of people infected with HSV1 as well
as HSV2, providing a rationale for why infection with one
of these two viruses can protect against the other. Some of
these peptides were conjugated to lipid (in collaboration with
Professor David Jackson, University of Melbourne). The
immunogenicity of the lipopeptides were improved 2-3 fold.
We are currently examining the mechanism of these effects.
Viral transport and assembly
Herpes Simplex virus (HSV) enters the body via the skin
before entering the termini of nerve cell processes. It is
transported along these processes to the body of the nerve
cell. HSV lies dormant within these nerve cell bodies near
the spinal cord in most people. Intermittently the virus
reactivates and is transported back down the nerve cell
processes to the skin where it causes blisters and ulcers or is
shed without causing symptoms.

34 35 > Research Report // AR 2006
One aim of the group is to determine how HSV is assembled
on to identify the first VZV encoded anti-apoptotic gene
Oral bacteria and infective endocarditis
porphyrin macrocycle and therefore must obtain this from
within cells at the molecular level. Recent work has identified
ORF63. To further our understanding of VZV with human
Streptococcus gordonii is a primary coloniser of oral
tissue sources, usually from haem-proteins that may also
crucial molecular interactions required for viral assembly.
nerve cells the group has developed a novel model of VZV
microbial biofilms. This organism is considered to be
supply iron. Research at the institute has identified the so-
Such information on viral assembly will allow development
infection of intact human explant ganglia. The group has
beneficial in the oral environment but pathogenic when it
called HA2 receptor as a porphyrin receptor important in the
of inhibitors of this process which may be candidates for use
shown for the first time that VZV can infect intact human
colonises heart valves as this results in infective endocarditis.
acquisition and surface storage of haem. In recent work this
as antivirals for control of recurrent herpes simplex.
ganglionic cells and this is a novel way of studying the
There is considerable interest in attempting to engineer
receptor mechanism was effectively used to selectively target
The group also aims to examine the mechanism(s) involved in
the entry, axonal transport, assembly and exit of HSV-1 from
neurons. The group’s studies have shown how HSV can travel,
assemble and exit from specialized sites along human nerves.
Another aim of the group is to determine how HSV and
HIV are transported within cells at the molecular level.
Recent discoveries have shown how virus transport in cells
is dependent on interactions between specific viral proteins
and cellular “motor proteins” and how in the case of HSV
the virus escapes from nerves to infect skin and cause disease.
Such information on viral transport will allow development
of inhibitors of this process which may be candidates for use
as antivirals for control of recurrent herpes simplex or HIV.
Varicella zoster virus
Despite its significant impact on the community, little is
known about the molecular basis of the Varicella zoster
virus (VZV), due in part, to VZV only infecting humans.
To more closely examine the interaction of VZV with host
cells, the group has established several models of infection
using human cell-types which are targets for infection and
are relevant to those that suffer from either Varicella or herpes
zoster/PHN because each of these cell types are likely to play
different, but essential roles in the disease process. These
include human fibroblasts (skin cells), neurons (nerve cells)
and specialized immune cells (T cells and dendritic cells).
The group has recently shown that human nerve cells
infected with VZV do not undergo programmed cell death
(apoptosis). This is an important finding because it suggests
the nerve cell damage observed when VZV reawakens from
its “silent” state in nerve cells to cause shingles is not due
to programmed cell death. Another implication from this
observation is that VZV encodes a function to interfere with
the death response in human nerve cells, thus providing
a possible mechanism by which the virus can establish
and maintain its life-long dormant infection. We went
interaction of this virus with human nerve cells.
These features of intact ganglionic infection can now be
studied in further detail to better define the molecular
mechanisms that underlie VZV infection of ganglionic cells.
For example, this model provides a means to rapidly test
viral gene mutant viruses and new candidate vaccine strains
containing targeted gene disruptions to define viral genes that
may play critical roles in VZV neurotropism and to examine
in detail the outcome of infection of both neurons and nonneuronal
cells with respect to apoptosis and cell function.
Institute of Dental Research
Proteomics and structural genomics of oral pathogens
The difficulty in preventing dental caries results from the
need to devise a strategy to eliminate key cariogenic species
without disrupting the overall complexity of the protective
biofilm community on teeth. Solving this problem is at
the forefront of research at the institute. The completion of
a comprehensive series of comparative proteome studies,
involving both planktonic and biofilm grown cells, has
highlighted a number of biochemical events that are unique
for the survival of the cariogenic pathogen, Streptococcus
mutans, that proliferates under acidic conditions in dental
plaque. Genes implicated in these adaptive responses,
including alteration in acid tolerance and biofilm formation,
are being systematically examined using a functional
genomics approach. By defining the critical events associated
with the survival and proliferation of S. mutans under
conditions that lead to enamel dissolution, researchers at
the Institute are gaining the necessary knowledge to develop
a comprehensive strategy for intervention, thus allowing
appropriate susceptible biochemical events to be targeted to
control or eliminate disease.
this bacterium to be both non-pathogenic and to resist
displacement by oral pathogens such as Streptococcus
mutans. In vitro gene expression technology has identified the
gom locus comprising a regulon of 15 open reading frames
implicated in bacterial growth, beneficial adhesion to the tooth
surface, and pathogenic colonisation of heart valves. Analysis
of this locus by researchers at the institute has focused on a
group of novel glycosidases within the gom locus with the
3D-structure of the first of these, GcnA, recently having being
solved at high resolution. Current research is directed at the
selective inhibition of this glycosidase as well as to determining
the structure and function of other products of the gom locus
including two related glycosidases that are also implicated in
infective endocarditis.
Polymicrobial aetiology of caries progression
In studies at the institute, some eighty bacterial species
were detected within the polymicrobial consortia of carious
dentine that overlies the pulp following an extension of the
enamel lesion of dental caries. However, recent studies have
shown that pulpal infection, arising from end-stage disease, is
far more selective. By using fluorescence in situ hybridisation
(FISH), the complex consortia of bacteria associated with
carious dentine has been shown to mass at the periphery of
the soft tissue, with only a few species invading. Currently,
the structural framework and spatial arrangement of bacterial
invasion is being mapped. While clinically important from
a dental perspective, this process also provides a rare insight
into the dynamics of polymicrobial infections that impact
severely on human health, particularly chronic infections.
Targeted control of oral pathogens
Competition for iron is considered to be a central event in
many infections. A number of pathogenic bacteria have
acquired complex mechanisms to sequester iron, often from
haem. The periodontal pathogen, Porphyromonas gingivalis,
is unusual in that it has lost the capacity to synthesise the
and inhibit this bacterium with custom synthesised modified
porphyrin-antibiotic conjugates. More recently, a number of
other haem binding proteins that are located on the surface
of the organism have been identified and are being studies
in order to expand the range of targets for inhibition by
exploiting those aspects of porphyrin storage and transport
that are unique to P. gingivalis.
Determinants of oral infection in high-risk
aboriginal communities
Anaerobic Gram negative bacteria have been determined
to be numerically important in relation to the early onset
and high incidence of periodontal disease in an Aboriginal
community. Research at the institute has suggested that
early mucosal colonisation of infants with pathogenic
porphyromonads act as release sites for transmission of these
organisms within families. Biotyping of Porphyromonas
gingivalis strains based on variations in the lysine-gingipain
gene indicated skewing of biotype distribution in the
Aboriginal community compared with that observed in
metropolitan cohorts. Further evidence for the presence
of characteristic discriminatory flora within the Aboriginal
community was obtained by microbial population analysis
based on molecular phylogeny. These observations have
provided a basis for ongoing dissection of the microbial risk
factors for oral infection that prevail in such a high risk group
and underpin proposed strategies to break the cycle of disease
by preventing transmission to infants. Additionally, there is
no information to determine whether disease susceptibility
amongst Aborigines reflects organisms that have been
associated with Aboriginal people for millennia or if there
is a pathogenic influence from organisms acquired, most
probably, from Anglo-Saxon settlers. As there is little genomic
information for these mucosal pathogens, assessment of the
origin and heterogeneity of organisms within communities
is being assessed by analysis of a matrix of highly conserved
house-keeping genes. This will both establish the relative

36 37 > Research Report // AR 2006
diversity of strains of the organism within the community
the optimal design of vaccines that require T lymphocyte
the expression of genes in Th1 cells. Furthermore, genetic
and also probe the question of separation or overlap with
responses, and for using lymphocytes for immunotherapy.
polymorphisms in PHF11 that are highly associated with
similarly studied organisms from Anglo-Saxon sources, with
isolates from other ethnic groups providing outlier controls.
Role of oral bacteria in immune development in marsupials
At birth, the highly under-developed Tammar wallaby,
Macropus eugenii, climbs through a saliva coated channel
in the fur of its mother from the urogenital tract to the
pouch which has also been cleaned by the licking action of
the mother. For the first three months of its development
the neonate is attached to a teat in the pouch and is
totally dependent on its surrounding environment for
immunological protection since it does not possess mature
lymphoid tissue and therefore lacks immune competence.
It is well recognized in eutherian mammals that bacteria
play a pivotal role in maintaining the health of mucosal
surfaces and in aiding immune development. While
preliminary studies have shown that the bacterial microflora
of the Tammar wallaby pouch young changes with time,
the exact nature of these microbial changes, has not been
elucidated. In collaboration with Macquarie University,
researchers at the Institute are engaged in using advanced
molecular phylogenetic methods to identify those bacteria
that are transmitted to the neonate and the role oral bacteria
play in both protecting the neonate from infection and in
influencing mucosal development and maturation of the
immune system.
Institute for Immunology and Allergy Research
Immunobiology and apoptosis
The group has discovered a key role for death-inducing
cytokines (Tumour Necrosis Factor, TRAIL and Fas Ligand)
in controlling these processes. Understanding how death
cytokines control lymphocyte homeostasis is important as it
provides information about how autoimmune diseases such
as Multiple Sclerosis (MS) arise, and provides key insights
into how immunomodulatory therapies exert their efficacy.
Death cytokines like TRAIL are already being developed
for use in humans with cancer, but our findings may open
the way for their expanded use in new therapy regimes
for diseases like MS. Our findings are also important for
Death cytokines are also part of the immune response to
virus infection, and consequently most viruses have evolved
specific mechanisms by which they evade the effects of these
cytokines. Smallpox, for example, controls these processes
through the production of a viral death-receptor homologue.
Our research on the poxvirus death receptor protein has
revealed a completely new mechanism of evasion of TNFreceptor
signalling. The minimal domain in this protein that
is required for inhibiting TNF-receptor signalling is also
present in TRAIL-Receptors, and a mini protein encoding
only this domain can ameliorate arthritis in mice. For this
reason, we are currently investigating how the expression
of this domain by TRAIL-receptor proteins alters TRAIL
biology, and how it might be used to prevent autoimmune
inflammation in diseases such as Multiple Sclerosis.
Molecular genetics of allergy
The goal of this group is to establish a research program
that links genetic studies with functional molecular and
cell biological assays to understand how heritable genetic
polymorphisms change gene function in human allergic
disorders.
To investigate the molecular genetics of human allergy, the
group has assembled a well-characterised family-based cohort
of children affected by severe atopic eczema. Researchers are
now investigating the genetics and function of genes that are
involved in T-cell activation.
In an NHMRC supported project, the group has confirmed
that the PHF11 gene at chromosome 13q14 is a major
gene associated with asthma, eczema and atopy and has
now completed the first functional study of PHF11. They
found that PHF11 is localised to the nucleus and the
expression of PHF11 was several fold higher in Th1 T-cells
cells when compared to Th2 cells. Knock-down of PHF11
using shRNA resulted in a significant decrease in the basal
expression of interferon-gamma and interleukin-2 in Th1
cells, both of which are critical Th1-type genes. Further
functional analysis has identified an interaction between
PHF11 and the NF-_ B transcription factor in modulating
atopic eczema in our cohort reduce PHF11 RNA in Th1
cells. This suggests that genetic variation in PHF11 may
contribute to the imbalance between Th1 and Th2 cells that
characterises atopic disorders. In another project the group
published an association study linking genetic variants in
the Th2-specific TIM-1 gene and childhood atopic eczema.
They are following this study up with additional genetic and
functional studies of the related Th1-specific T-cell receptor,
TIM-3.
Multiple sclerosis genetic research
This group was the first to identify common polymorphisms
in the gene CD127 and test their association with MS.
They have subsequently shown a variant was associated
with the primary progressive form of the disease. Two
international groups, using very large cohorts, have now
confirmed CD127 as the first non-HLA region gene to have
its association with MS widely replicated. The group has
studied the functional significance of the CD127 haplotypes
and demonstrated they have different splicing features and
respond differently to stimulation in different immune cell
types. Manipulation of immune cells using this information
is part of a provisional patent application for MS treatment
held by the institute.
The group has continued its international collaborations with
Cambridge University and through them the International
MS genetics consortium, which is shortly to publish the
largest ever genome screen in MS. It has also begun an
Australian MS genetics collaboration, called ‘Ausgene’, with
researchers in Victoria, Queensland and NSW.
The group continues to develop links with Industry and has
an ARC Linkage Grant (2006-2008) in combination with
BiogenIdec, to investigate pharmacogenomic aspects of the
use of interferon beta. It also provides Australia’s neutralizing
antibody testing service for this drug.
Cancer
Westmead Institute for Cancer Research
Breast cancer research
The Breast cancer research group is investigating the role of
the ovarian hormones oestrogen and progesterone in the
development of the normal breast, and in breast cancer.
Ovarian hormones are fundamental regulators of normal
cell growth and differentiation and are also crucial to the
development and progression of breast cancer. Progesterone
has a pivotal role in normal female reproduction in the
uterus, ovary, mammary gland and brain, and the number
of cellular pathways regulated by progesterone reflects the
complexity of its physiological role.
The progesterone receptor (PR), which mediates the effects
of progesterone in target tissues, is expressed as two proteins,
which have very different activities. Progesterone receptors
transduce the signals of cyclically fluctuating progesterone
levels in the body. For four decades or more of reproductive
life, alternating peaks of progesterone and oestrogens exert
profound effects on reproductive function, especially on the
development and function of the breast.
Some years ago the Breast Cancer Research Group identified
a change in expression of two forms of the progesterone
receptor, PRA and PRB, in cancer. Their work in 2006 has
focused on further identifying the cellular consequences of
this change. Gene expression profiles have shown a distinct
shift in the ability of a cell to respond to progesterone
when the two forms of the PR are imbalanced, and this
is associated with clear changes in signalling pathways
important in maintenance of normal cell biology.
These studies are being extended by the development of new
culture systems, in which these signalling pathways in the
normal human breast can be interrogated. Normal breast
tissue in this culture system maintains the ability to respond,
in physiologically relevant ways, to progesterone, and the
pathways by which this hormone influence the normal breast
are now being unravelled in ongoing studies.

38 39 > Research Report // AR 2006
0.005.0484
0.005.0486 research facilities 00.005.0459 at Westmead. The Bank 00.005.0458
was created to
provide a resource of breast cancer biospecimens and clinical
46
0.005.0489
26
The mechanisms through which PR controls gene expression
have also been explored in 2006, with the demonstration
that receptors aggregate with other key components of
transcriptional machinery when they are activated. Studies in
2006 demonstrated that these aggregations were functionally
significant, and identified some of the key functional
components of these aggregates. This aggregation process
is disrupted in human cancers, and ongoing studies in the
group are aimed at identifying the functional consequences
of its disruption in cancer. Most breast cancers are thought to
be initiated at puberty, and develop throughout reproductive
life. Although the vast majority of breast cancers are detected
after menopause, the influence of cyclical ovarian hormones
on their biology is profound. The studies from the Breast
Cancer Group aim to throw new light on the fundamental
question of how ovarian hormones influence breast cancer
initiation and progression.
Breast cancer tissue bank
WMI has led the establishment of the Breast Cancer Tissue
Bank with funding from the NHMRC, Cancer Institute
NSW and the National Breast Cancer Foundation. The
headquarters of the Bank are located within the clinical and
data to support breast cancer research throughout Australia.
Under the management of WMI a network of centres from
across New South Wales collected tissue for the Bank during
2006.
Materials in the bank are processed and stored using
international best practice methodologies to preserve the
integrity of the specimens and increase their value to research
scientists. Access to human tissue is essential for translating
00.005.0463
46
00.005.0482 00.005.0481
00.005.0465 00.005.0466
51
00.005.0462
has important implications for determining the risk of genetic-epidemiological studies investigating the familial
developing melanoma and possibly the treatment strategy aspects of cancer. As many high-risk individuals have now
for patients carrying altered copies of the p16INK4a protein. been identified, the group established a risk-management
Furthermore, it is likely that unidentified p16INK4a clinic in 2006 that facilitates co-ordinated, multidisciplinary
functions (other then regulation of cell proliferation) may care of women at high risk of breast and ovarian cancer, as
add to its role as melanoma susceptibility gene. The Cell well as providing further opportunities for research. The
Cycle research group is investigating the role of p16INK4a in study of Magnetic Resonance Imaging of the breasts of highrisk
women in NSW has commenced at Westmead and the
novel biomolecular pathways.
group is now accumulating data to determine its usefulness
The BRAF oncogene is switched on in most melanomas
in comparison to standard mammographic screening. The
but intriguingly also in 80% of benign moles. Most moles
Service has completed the collaborative study of breast ductal
never transform into melanomas and their melanocytes are
lavage specimens, investigating its use as a surveillance tool in
normally growth arrested. Thus, although aberrant activation
women at high risk of breast cancer.
of BRAF plays a role in melanoma, normal melanocytes
apparently respond to active BRAF by growth arrest and The group continues to participate in the international
only additional genetic alterations allow these cells to become GOG-199 study, aimed at assessing the usefulness of
malignant. The Cell Cycle research group is exploring the screening versus preventive surgery in women at increased
mechanisms responsible for this BRAF-induced growth risk of cancer of the ovary and fallopian tubes. The group
arrest, which is clearly critical in protecting against melanoma has also continued its role in the study of tamoxifen in breast
formation. These investigations will also resolve the molecular cancer prevention for those at higher risk based on family
events necessary to transform a normal melanocyte into a history. In addition, the group has continued to collaborate
melanoma.
in the investigation of the psychosocial aspects of genetic
Melanoma cancers are notoriously resistant to chemotherapy.
00.005.0464 00.005.0515 00.005.0467 00.005.0514
Through its research, the Cell Cycle team has confirmed
that cells in which p14ARF and p16INK4a are active are
more sensitive to chemotherapy. The impact of activated
BRAF on chemosensitivity is currently being investigated.
All these molecules are critical in the genesis of melanoma.
Therefore defining each of their functions is essential to the
development of a rational approach to targeted therapy for
this destructive disease.
Familial cancer research
Most cancers are due to genetic changes that accumulate in
00.005.0460 00.005.0461 00.005.0468 00.005.0469 00.005.0516 00.005.0517 00.005.0518
current research knowledge into clinical practice and in turn
basic researchers can utilise information derived from human
specimens to drive further investigation into the molecular
basis of disease.
Data and specimens stored in the Bank are available to
all Australian researchers following scientific review of the
proposed project.
Cell cycle research
In Australia, melanoma is the third most common cancer
in men and women with over 3,000 cases per year and an
overall lifetime risk of 3.7%. We know now that cancer is
caused by genetic changes, or mutations, in cells. However,
the precise sequence of mutations required to transform a
dormant melanocyte into a melanoma remains unresolved.
In recent years the group’s work has contributed to the
identification of several critical pathways crucial to this
process. In particular, the p16INK4a/p14ARF locus, which
encodes the tumour suppressor proteins p16INK4a and
p14ARF, is altered in 39% of melanoma-prone families and a
single base change that activates the BRAF oncogene is found
in 50-70% of melanomas. The Cell Cycle Research Group
is investigating how these proteins work and which cellular
targets they interact with.
This team recently proposed that the p14ARF protein
mediates the attachment of the small modifying protein,
SUMO, to a number of target proteins in a process called
sumoylation. Sumoylation regulates cellular activity of
these target proteins by altering their function. The group is
exploring the effects of p14ARF induced sumoylation, and
the consequences of p14ARF mutation on the functioning of
these proteins.
Some studies have reported that p14ARF can induce
programmed cell death, known as apoptosis, possibly by
activating the master apoptosis gene p53. The Cell Cycle
group has clarified that p14ARF induces apoptosis only
when co-expressed at normal physiological levels in cells
with a functional p53 gene; it cannot induce apoptosis by
itself. p14ARF is also known to stabilize proteins such as p53
by blocking the attachment of the small modifier protein
ubiquitination which acts as a degradation signal. The
effect of melanoma associated p14ARF mutations on the
degradation of essential proteins is also being investigated.
The p16INK4a tumour suppressor is frequently altered in
high risk melanoma families, and these altered p16INK4a
proteins may affect the function of the remaining
normal copy of p16INK4a. This important hypothesis is
currently being investigated by the Cell Cycle group and
the cells with age, but in 5 to 10 per cent of cases, patients
have a family history of multiple cases of early-onset cancer,
that suggests the presence of an inherited gene mutation that
greatly increases their risk of cancer.
The clinical arm of the Familial Cancer Research Group
operates a service where individuals with a strong family
history of breast, ovary, bowel cancer or melanoma, can be
assessed for genetic susceptibility. In conjunction with this
clinical service, many patients are enrolled in collaborative,
testing for cancer susceptibility by participating in studies of
decision aids and counselling tools for patients considering
genetic testing.
In 2006 the group established pilot telemedicine programs in
several rural centres to evaluate the usefulness of this clinical
tool to improve rural genetic health services.
The group’s laboratory provides a testing service for
individuals in the families described above, primarily
for mutations in the BRCA1 and BRCA2 breast cancer
susceptibility genes. In addition, there is some screening
for susceptibility to melanoma. The laboratory’s research
program has been successfully directed towards improved
screening for BRCA1 and BRCA2 mutations and
continues to focus on improvements to screening and the
understanding of the gene mutations that are detected by
screening.
Gene expression in cancer
Mutations in the tumour-suppressor gene BRCA1 are a
common factor in many breast cancers. The Gene Expression
laboratory is studying the effect of cancer mutations on

40 41 > Research Report // AR 2006
specific proteins in the cell, with emphasis on cellular
and to improve our understanding of the mechanisms that
clinical outcome and, eventually, improve the survival of
disease in patients with haematological malignancy.
alterations that lead to breast and colon cancer. The group
is investigating how such mutations disrupt the normal
function of the BRCA1 protein.
determine how a patient will respond to chemotherapy.
The normal process of ovulation is known to play a part
in early events leading to ovarian cancer. The Group has
patients with ovarian cancer. In all, more than 1800 patients
have been recruited to the study, surpassing expectations and
data analysis is underway.
In the last 12 months, the group has continued to develop
its clinical program of cytomegalovirus (CMV) specific
cytotoxic T cell administration to patients with impaired
The BRCA1 protein senses DNA damage. It monitors
dividing cells, and in response to DNA damage, initiates
gene repair processes in the cell nucleus so the errors are not
transmitted to new cells. BRCA1 has a partner, BARD1;
their interaction helps facilitate the DNA-repair process.
Previously the group discovered that the BRCA1 and
BARD1 proteins, in their unbound state, are normally free to
shuttle between the nucleus and cytoplasm, but when bound
together they become confined to the nucleus, an essential
step in activating the complexed proteins for their crucial role
in DNA-repair and cell-survival.
They have also identified a class of BRCA1 gene mutations
that display an unexpected influence on the BRCA1 proteins
that carry this mutation. The mutant BRCA1 proteins are
positioned differently inside the cell, and are prevented from
entering the nucleus and complexing with BARD1. This
finding provides another mechanism for changes in DNA
repair elicited by BRCA1 gene mutations in breast cancer.
In 2006 the laboratory discovered that the BARD1 protein
locates at cellular mitochondria, implicating a pathway for
control of cell death or cell survival.
The group is also investigating two genes that appear to
play key roles in colorectal cancer: beta catenin and the
tumour-suppressor gene APC. A very large protein, APC
- like BRCA1 - shuttles between the cytoplasm and the
nucleus, where it performs its tumour-suppressor function.
The ultimate aim of this research is to discover new pathways
that control the action of proteins like BRCA1 and APC
in normal cells, and to develop drugs or other reagents that
correct defects in these pathways in cancer cells.
Gynaecological cancers
Ovarian cancer is the most lethal gynaecological malignancy.
The Gynaecological Cancer Research Group has a program
of research which aims to improve our understanding of the
progression from healthy ovarian epithelial cells to cancer
used laser capture micro-dissection to dissect out individual
epithelial cells from normal ovaries, to studying normal
patterns of gene expression during the ovulatory cycle, using
mice as a model system. They used expression microarrays
to identify all active genes in normal cells, and then use
changing patterns of normal gene expression as a standard to
detect aberrant gene expression patterns in malignant human
ovarian cells. Genes that normally regulate cell proliferation
and apoptosis (programmed cell death) are obvious suspects
for contributing to malignant transformation. The group has
identified several novel candidate genes that may be involved
in the initial steps leading to ovarian cancer.
Most ovarian cancers are initially sensitive to chemotherapy,
but eventually develop resistance. Currently there was no
way to predict which ovarian cancers would become resistant
to chemotherapy, nor any way to modulate gene expression
to restore drug sensitivity. The group has identified a set of
genes whose expression levels differ between resistant and
drug-sensitive cells. They have found that one of these genes
is higher in tumours from patients that have a worse clinical
outcome. The Institute has a patent on the discovery, and is
now seeking compounds to reduce expression of this gene,
that could be used in combination with platinum drugs to
treat ovarian cancer.
The Australian Ovarian Cancer Study is a major
collaborative project involving WICR, the Queensland
Institute of Medical Research (QIMR), and Melbourne’s
Peter McCallum Cancer Centre (PeterMac), and over 20
hospitals across the country. It aimed to recruit 1000 ovarian
cancer patients and create a library of biospecimens at the
PeterMac, for analysis to identify genes involved in ovarian
cancer. QIMR researchers have collected comprehensive
epidemiological data on patients to help identify
environmental and life-style risk factors, while the WICR
group are monitoring the individual patients for a minimum
of five years, recording all details of their treatment and its
outcome. The data will be correlated with risk-factor data
and tumour-gene profiles to identify factors that will predict
Leukaemia cell biology group
The Leukaemia Cell Biology Group is investigating the
role of bone marrow stromal cells in acute lymphoblastic
leukaemia (ALL). ALL is the most common childhood
cancer. Although responsive to chemotherapy 25% of
children and 65% of adults will relapse following treatment
and less than 10% of relapsed patients will survive for 5 years.
New treatments for ALL are necessary to improve outcomes
for these patients.
ALL arises in the bone marrow from cells that normally
develop into B cells (antibody producing cells). ALL cells
are highly dependent on the bone marrow stroma for their
growth and survival and bone marrow stroma protects ALL
cells from the effects of chemotherapy. The leukaemia cell
biology group has been investigating ways in which the bone
marrow supports ALL cells with the aim of disrupting this
supportive and protective function.
The group has identified SDF-1 as a major factor that
supports ALL cells. Drugs that can block the effects of SDF-
1 move ALL cells out of the bone marrow making them
more susceptible to chemotherapy. These drugs inhibit the
growth of ALL cells in the laboratory and in a mouse model
of human leukaemia. These drugs were particularly effective
at minimizing the spread of ALL to other tissues including
the liver and kidney.
The group has also studied the way in which SDF-1
tells ALL cells to grow and survive. By targeting these
mechanisms, even more potent agents have been identified.
It is anticipated that these drugs will enhance the effectiveness
of currently used chemotherapy agents with minimal toxicity.
If successful, these agents will decrease the total dose of
chemotherapy required to treat standard risk patients and
help increase the cure rates in patients with a poor prognosis.
Leukaemia cell therapies
The Cell Therapies group focuses on investigating the use of
targeted cells for the treatment of infectious and malignant
immune systems. The group is currently running its
second clinical trial of CMV specific T cell administration
for patients recovering after allogeneic bone marrow
transplantation. The initial trial using a CMV peptide to
stimulate donor T cells accrued 9 patients. No acute adverse
events were observed and increases in CMV specific T cells
in circulation following infusion were observed. No patient
in the trial required pharmacotherapy for CMV infection or
reactivation.
A considerable amount of effort has been expended in the
last 12 months on gaining approval for a gene therapy trial
of CMV that will expand entry criteria into the trial and will
result in a broader target specificity of CMV antigens. The
trial commenced accrual late in 2006 and has already accrued
8 patients with 4 patients receiving T cell infusions from
their donors. No adverse events have been noted and no
pharmacotherapy for CMV has been required as yet in any
patient receiving T cells.
We are also studying the generation in vitro of T cells
specific for the viral illness varicella zoster that commonly
affect immunocompromised individuals. Using a clinical
vaccine preparation for antigen stimulation, the group has
been able to stimulate growth of a population of T cells
whose specificity is currently being assessed. It is hoped that
this process can be incorporated into generation of CMV
specific T cells to give a tri-virus specific culture product that
will recognise CMV, adenovirus (derived from the vector
encoding the CMV protein pp65) and varicella zoster virus.
Translational oncology
The aim of the Translational Oncology group is to focus
research on clinically important issues in oncology and to
assist clinical application of basic laboratory research through
examination of information and samples from patients with
cancer.
In 2006, the group continued to work to identify measures
that may assist determination of optimal chemotherapy

42 43 > Research Report // AR 2006
doses for patients. This is an important issue since the rate at
which drugs are cleared from the body can vary substantially
between individuals and have a major influence on the
effectiveness and toxicity of treatment.
In a collaborative project with the Family Cancer group and
the Kathleen Cuningham Consortium for Research into
Familial Breast Cancer (kConFab), Translational Oncology
also reported a study in 2006 that described the pathology
features of breast cancer in carriers of variants in a gene that
has been implicated in increased breast cancer risk; ataxia
telangiectasia mutated (ATM). This was of interest because
certain types of familial breast cancer are associated with
particular pathologic features although these were not seen in
carriers of ATM variants.
Another major project that Translational Oncology is
involved with is establishment of a Breast Cancer Tissue
Bank in centres across New South Wales that will make
breast cancer tissue specimens available for research Australiawide.
Supported by funding from the National Health
and Medical Research Council, National Breast Cancer
Foundation and Cancer Institute NSW this initiative will
form important infrastructure for future translational breast
cancer research.
Genomics and genetic epidemiology
The Genomics and Genetic Epidemiology Group focuses
on identifying the genes that strongly affect cancer risk
and discovering how that genetic risk interacts with the
environment to cause cancer. Hundreds of families of people
with a strong family history of melanoma have supported the
groups projects over the last twenty years and their samples
continue to be used intensively to identify new melanoma
genes. Over 2006 they were used in three searches involving
22 research groups of the international melanoma genetics
consortium (GenoMEL) and several million dollars’ funding
from the European Union and the US National Institutes of
Health. They cover each of the main high-throughput ways
of identifying new disease genes: genetic linkage, genetic
association and candidate gene analysis.
The group also completed the Australian Melanoma Family
Study (AMFS), with the University of Melbourne’s MEGA
Centre and the Queensland Cancer Fund Epidemiology
Research Unit. This is one of the world’s largest populationbased
studies of melanoma, enrolling over 1100 people who
developed melanoma before age 40 in Melbourne, Sydney
and Brisbane, or unaffected controls, plus thousands of their
family members. Early-onset melanoma can be indicative of
increased susceptibility, but little is known about what genes
contribute to risk in this setting. The AMFS has shown that
HO
3
A
5
B
6
C
in at least some cases (2%) a gene that is commonly mutated
in familial melanoma is responsible: the CDKN2A (p16)
tumour suppressor gene. The group has also showed that
the risk caused by these mutated genes in the population is
not as high as it is in people with a strong family history of
melanoma.
As part of her successful PhD Nadine Kasparian reported
some of the first research anywhere in the world that has
Cholestorol
studied perception of melanoma risk and the psychological
consequences of high melanoma risk in melanoma families.
These are collaborations with Prince of Wales Hospital and
the University of Sydney.
Both the NHMRC and Cancer Institute NSW Program
Grants have enabled the group to start wide-ranging studies
with collaborators at the Sydney Melanoma Unit, directed
at understanding the genetic abnormalities in melanomas
themselves. The goals of these high-throughput studies
of gene and protein expression are to understand how
apparently similar melanomas can have such different clinical
behaviour, whether a greater propensity to relapse after
surgery, or differing responsiveness to drug and biological
treatment, for example. Since the SMU is the largest
melanoma treatment and clinical research centre in the
world, these are intended to be benchmark studies of these
issues and will be the main focus of the group in 2007-8.
HO
H
17
D
OH
OH
Liver and Metabolic
Storr Liver Unit
The role of leptin in the pathogenesis of hepatic fibrosis
The mechanisms by which the hormone leptin, which
Propionyl-CoA
NADP + H +
circulates in increased concentrations in obese individuals,
exerts its pro-fibrogenic (scarring) effects on the liver are
O 2
NADPH + H +
currently unclear. In this project we examined the expression
of pro-fibrogenic genes and proteins in cultured rat hepatic
7`-hydroxylase
stellate cells (HSCs; the main cellular source of scar tissue
in the liver) following exposure to leptin. We were able
to demonstrate that leptin did not directly enhance HSC
activation. In contrast, there were remarkable increases in
pro-fibrogenic gene and protein expression in HSCs after
these cells were cultured in the medium of Kupffer cells that
had been previously exposed to leptin. Furthermore, we
found that the effect of leptin on Kupffer cells was mediated
by increasing the production of connective tissue growth
O
factor (CTGF) and transforming growth factor beta. 2 Both
C – S – CoA
O
2 CoA-SH
these cytokines are potent stimulators of fibrosis in hepatic
stellate cells. We have taken these data further and have now
characterized the intracellular molecular basis by which leptin
exerts its affects. This project has demonstrated that Kupffer
cells play an important role in leptin-mediated liver fibrosis
and provide a novel molecular mechanism by which obesity
causes scarring of the liver and cirrhosis.
Molecular mechanisms for the development of fatty liver
disease in humans
Non-alcoholic fatty liver disease (NAFLD) is the commonest
cause of progressive liver damage in Australia leading to
cirrhosis and liver cancer in some individuals. To date,
altered lipid (fat) homeostasis has been shown to contribute
to the accumulation of liver fat, but the mechanisms by
which a fatty liver is converted to one with liver damage
(steatohepatitis) has not been fully elucidated. In this project,
researchers from the Storr Liver Unit sought to identify
the molecular determinants leading to the progression to
steatohepatitis. We therefore examined the expression of
a number of critical nuclear receptors (NXRs) and key
genes regulating carbohydrate, cholesterol and bile acid
metabolism, synthesis and transport within the liver. In
addition, we examined the expression of key inflammatory
cytokines and pro- and anti-apoptotic cell death genes.
This study was unique in that it was conducted on minute
quantities of human liver tissue removed at the time of liver
biopsy. Our results indicated that several nuclear receptors
NADP +
(LXR, PXR, FXR and CAR) which regulate key genes for
bile acid synthesis and export were up-regulated in patients
with steatohepatitis compared with healthy controls.
Likewise, the expression of key cell death genes (BAD, BID,
BAX) and those which mediate liver inflammation, were
increased in livers from patients with steatohepatitis. These
data are consistent with our novel proposal that alterations
in nuclear receptor expression are a critical mediator of liver
HO
damage in patients with non-alcoholic steatohepatitis.
The role of bile acids as a mediator of liver injury in an
animal model of fatty liver disease
In this study, we attempted to further characterise the
several steps
OH
7-Hydroxychole
molecular and cellular basis for the development of nonalcoholic
steatohepatitis (NASH) by studies using an animal
model that was developed at the Storr Liver Unit. NASH
is characterized by the presence of hepatic steatosis (fat),
liver injury, inflammation and variable fibrosis (scarring).
The mechanisms which initiate hepatitis in a fatty liver
are important, and at present unknown. In this research,
analogous to our human studies, we sought to examine the
role of nuclear receptors and key genes regulating bile acid and
cholesterol metabolism, synthesis and transport within the
liver of animals with NASH. Our results demonstrated that
bile acids were significantly increased early in the development
of NASH in mice. By day 5, we noted major changes in
nuclear receptors and their downstream targets and of genes
which regulate bile acid synthesis and export. Taken together
these data strongly suggest that nuclear receptors and their
ligands (bile acids and oxysterols) may be important mediators
of liver injury in our nutritional model of NASH. It is hoped
that linking these molecular studies in animals with a fatty
liver, to that in humans with NASH will permit a better
understanding of NAFLD and suggest novel treatments.
NADP
O
2 CoA
Prop
Cholyl-CoA

44 45 > Research Report // AR 2006
Dysregulation of normal muscle function and its
contribution to the development of fatty liver disease.
The liver plays a central role in processing macronutrients
in response to the influx of nutrients and hormones such
as insulin. While the liver maintains fasting blood glucose
concentrations, skeletal muscle and fat tissue are the major
sites of insulin stimulated glucose disposal. Furthermore,
muscle is intricately involved in whole body lipid (fat)
homeostasis. In these additional studies, we examined
changes in the expression of key genes regulating energy
uncoupling, lipid oxidation and glucose transport in the
muscle and liver of mice that develop NASH when fed a
diet deficient in the compounds methionine and choline
(MCD). Our results indicated that lipid oxidation in muscle
is reduced during MCD feeding, thereby delivering a higher
lipid load to the liver and contributing to the development
of hepatic steatosis. Thus, there appears to be a complex and
intricate link between the liver and muscle with regard to
lipid homeostasis that may in part explain lipid accumulation
in the livers of persons who develop fatty liver disease.
The role of the hormone adiponectin and its receptors in
hepatic fibrosis
Liver injury from any cause can lead to hepatic fibrosis, a
process which is mediated by the hepatic stellate cell (HSC).
Adiponectin, a recently characterised hormone secreted
by fat cells with anti-inflammatory and anti-atherogenic
properties may serve as a novel protein in the modulation
of liver fibrosis. Researchers at the Storr Liver unit became
interested in this protein when we noted that low levels
of adiponectin were associated with the development of
NASH in humans. In contrast, high levels of this hormone
appear to be protective for the development of a fatty
liver. We therefore sought to characterise the modulation
of adiponectin receptors which mediate the function of
adiponectin during the activation of HSCs to a profibrogenic
cell type. While this project is in its infancy, we have
demonstrated significant decreases in the expression levels
of the AdipoR1 but not the AdipoR2 receptor during the
activation of HSCs. In contrast, when HSCs were treated
with the cytokine transforming growth factor beta, the
expression of AdipoR2 was up-regulated. Our results indicate
that differential modulation of adiponectin receptors occurs
in vitro during HSC culture and in response to profibrogenic
cytokines. These changes in receptor expression may play
an important role in modulating the fibrogenic response
of the liver to chronic injury. Further studies are therefore
underway to determine the molecular basis of these effects
and to determine if modulation of these receptors in the liver
can lead to reductions in hepatic fibrosis in patients with fatty
liver disease.
Molecular pharmacology research
The Molecular Pharmacology group, lead by Professor Chris
Liddle is engaged in research into the mechanisms regulating
the metabolism and transport of both xenobiotic compounds
(such as therapeutic drugs) and endobiotics (such as lipids,
cholesterol and bile acids) within the liver. Nuclear receptors
are key intracellular proteins that “sense” the presence of
these molecules and they have been working to exploit these
receptors as targets to develop new treatments for a range
of liver diseases. Parts of this work are being performed in
collaboration with the laboratory of Professor Ron Evans at
the Salk Institute, La Jolla, California. In collaboration with
the Cancer Pharmacology Unit at Concord Hospital we
have been investigating the altered metabolism of drugs that
frequently occurs in patients with advanced cancer with a
view to developing interventions that will allow such patients
to be able to receive the benefit of full doses of vital cancer
chemotherapy. Our recent work in the field of regulatory
mechanisms in drug metabolism has led to the generation
of two patents, which have been successfully licensed to the
pharmaceutical industry. Royalties arising from these patents
now provide significant ongoing funding for research projects
with the Storr Liver Unit.
Neuroscience and Vision
Brain Dynamics Centre
Brain connectivity projects
These projects are focused on understanding the mechanisms
of how the brain binds information into a coherent whole,
and determines what is significant and important, and what
is not. Understanding the mechanisms of integrative brain
function is important for identifying the causes of disorders
of mental health.
A second focus of these projects is on the role of age and
sex differences. Major psychiatric disorders have striking
differences in their prevalence in males versus females, and
peak ages of onset, such that understanding these factors is
important for understanding the processes of mental illness.
A PhD thesis on this topic will be completed this year.
Towards a continuum of orienting and defensive responses
This ARC Discovery project is focused on identifying the
neural mechanisms underlying how we determine what is
significant in the environment, and process it accordingly.
The ability to discriminate what is significant and important
from what is not is crucial to effective information processing.
Thus, a breakdown in the mechanism of significance
processing may underlie major psychiatric disorders.
PhD research in this area was awarded the Tasman-Lovell
medal this year for the best project.
Development of integrative markers of brain function
This is another ARC linkage project and is focused on
integrating genetic information with cognitive, emotional
and neuroimaging measures to identify evidence-based
biological markers of complex brain function. Biological
markers are important tools for identifying predisposing
factors to disease, diagnosis, treatment evaluation, and the
monitoring of disease progression.
Emotion processing in adolescence and application to
conduct disorder
This project is focused on understanding the biological
basis of emotion processing in adolescence, which is a peak
period for the onset of emotional and behavioural disorders.
These results will provide a platform for identifying specific
disturbances in emotion-related brain function in children
and adolescents with conduct disorder.
Results to date show a striking change in brain function
profile for salient emotions of fear and happiness from
childhood (6-7 years) to adolescence (8-13) years to later
teenage years (14-15 years), when the profile becomes more
like that of an adult
Identifying the ‘signature’ for ADHD and
treatment predictions
This project has used tests of emotion cognition and brain
function to identify objective markers of ADHD and
response to stimulants in ADHD. These markers were found
to classify over 80% of ADHD adolescents.
Posttraumatic stress disorder (PTSD) biological markers
and treatment response
This project aims to develop the most effective treatments for
acute and chronic PTSD. Cognitive behavioural treatments
(CBT) are the current first line treatment of PTSD, but
response can be heterogeneous. This project aims to identify
the most effective elements of CBT treatment of PTSD.
The group conducted a randomized controlled trial on
103 participants with PTSD to examine the most effective
combination of treatment elements for PTSD. Specifically,
the group examined whether cognitive therapy (CT)
enhanced treatment response to exposure-based therapies
(prolonged (PE) and invivo (IV) in an 8-week CBT program
conducted in the Clinic for Traumatic Stress at BDC.
Acute stress disorder treatment efficacy
This study examined the relative efficacy of cognitive therapy
(CT) and exposure treatments in acute trauma populations
(within 3-4 weeks of trauma) in a randomized controlled
trial. Results indicate that early intervention following trauma

46 47 > Research Report // AR 2006
is highly effective in reducing PTSD symptoms. Importantly,
both cognitive therapy and exposure-based therapies are
highly successful in reducing PTSD symptoms compared to a
wait-list control, but PE has greater treatment gains than CR.
Markers of PTSD
The research team is continuing to explore the relationships
between autonomic arousal and neural function in response
to emotional signals and in the context of cognitive tasks.
They have pioneered new integrative analysis techniques
for SCR-fMRI data. They are also examining responses to
positive facial signals in PTSD to explore the integrity of
the reward/approach systems in PTSD. We are examining
structural MRI data to identify specific impairments in brain
regions (particularly anterior cingulate and hippocampus) in
PTSD. Finally, we are integrating autonomic, genetic, spatial
and temporal neural measures (fMRI and EEG) to examine
integrative theoretical models of PTSD.
Depression - objective markers for depression
In Australia, it has been estimated that depression costs
our economy $3.3billion in lost productivity each year,
highlighting the urgent need for valid markers of the illness
and successful treatment. This research, funded by NHMRC
and ARC, is focused on using measures of emotion,
cognition and brain function to identify objective markers
of depression and response to anti-depressant treatment.
Results to date identify distinct brain changes that predict
development of depression.
Pfizer fellowship and NISAD: “Missing links: connectivity
and schizophrenia”
The Centre has focused on young people who have recently
experienced their first-episode of psychosis. The ultimate aim
is to identify the causes of the disorder, and how it might be
prevented or better treated in the future. The project
of normal connectivity revealed in the project reported
under the Cognitive Neuroscience Unit. Schizophrenia
patients showed a reversal of the normal connectivity
between amygdala-frontal networks for processing
stimulus significance.
The inability to ‘bind’ perceptions and cognitions into
a coherent whole in schizophrenia may involve the
networks for determining significance. The findings
support the Centre’s model of schizophrenia as a disorder
of neural connectivity.
Structural brain alterations in schizophrenia
This is a PhD research project which used high-resolution
(~1mm3) images of the brain provided by structural MRI
(sMRI). The same first episode group was studied to provide
a means to link information across projects.
First episode schizophrenia patients showed a loss of grey
matter in the frontal, parietal and temporal cortices, as well
as cerebellum, at the time of their first presentation to mental
health services, relative to matched healthy controls.
In addition, these reductions in grey matter followed a
different pattern of relationship to neural activity to that in
healthy controls. In healthy subjects, grey matter declined
slightly (consistent with neural pruning) and EEG activity
(indexing neural activity) followed a similar pattern. In
schizophrenia, however, there was a preservation or even
increase of EEG activity, particularly for the slow wave Theta
band. This dissociation in schizophrenia is consistent with a
disorganization of pruning, and may be a factor in the cause of
schizophrenia in late adolescence. The increase in EEG activity
may reflect increases in synchronized activity in particular.
Centre for Vision Research
The Blue Mountains eye study
The Blue Mountains Eye Study is a benchmark populationbased
study in ophthalmology. As well as defining the
prevalence, incidence and risk factors for eye diseases, many
novel systemic associations have been explored. The 10-
year mortality and cause of death information from this
Blue Mountains population has been explored in relation
to information derived from grading photographs taken of
the retina at the back of the eye. Retinal vessels may carry
information about the circulation system in the brain and
in other end organs of the body. Our data have shown
that retinal photographs provide information on structural
changes in small vessels of the retina. These signs may
be independent sub clinical markers for vascular disease,
predicting subjects at higher risk of future vascular events,
including the development of stroke, stroke-related death,
cardio-vascular death and high blood pressure in older
people. The Centre has also led to data analyses pooling Blue
Mountains Eye Study and Beaver Dam Eye Study (USA)
data to investigate less frequent retinal vascular lesions such as
retinal emboli and retinal vein occlusion.
Retinal vessel signs in acute stroke patients
This multi-centre clinical cohort study has recruited acute
stroke patients from three centres (stroke units at Westmead
Hospital, Royal Melbourne Hospital and Singapore General
Hospital) to assess whether retinal vessel signs can help to
determine the prognosis for different clinical stroke subtypes,
in collaboration with the Retinal Vascular Imaging Centre
(RetVIC) in Melbourne and stroke specialists in Singapore.
So far, more than 1300 patients have been recruited
following acute stroke. Retinal photographs were taken and
the assessment of these signs is currently underway.
Cataract surgery and risk of age-related macular Degeneration
Age-related Macular Degeneration (AMD) is the leading
cause of blindness in older people. Previous populationbased
studies have suggested at least a 3-fold higher risk of
progression to late-stage AMD in eyes after cataract surgery.
This project aims to confirm these findings in a much larger
sample of older people having cataract surgery and also to
look at cataract surgery outcomes, including the impact on
quality of life.
Almost 2,000 patients undergoing cataract surgery at
Westmead Hospital and from private ophthalmologist rooms
have been recruited, with over 1200 patients being reexamined
6 months post-operatively. We plan to follow these
patients for up to 5 years to assess both short-term (2-3 years)
and long-term risks of AMD after cataract surgery.
The Sydney childhood eye study
This project has assessed the frequency and risk factors
associated with myopia and other common eye conditions
in school children aged 6 or 12 years. The project examined
1740 6-year-old and 2353 12-year-old children from almost
60 primary and secondary schools across Sydney.
Reports from this study have identified that reduced outdoor
activity, rather than increased close work, may predict
myopia (short-sightedness). The study also showed that other
common childhood eye conditions like amblyopia (reduced
vision in one eye) and strabismus (squint) are relatively well
detected at present, but identified new risk factors, particularly
modest levels of lower birth weight or prematurity.
The new phase (Sydney Paediatric Eye Disease Study) is now
examining a large sample of children aged less than 6 years
to determine factors associated with the development of
amblyopia and its detection in very young children.
compared first episode schizophrenia patients to the pattern

48 49 > Research Report // AR 2006
Cardio-respiratory
Ludwig Engel Centre for Respiratory Research
Sleep disordered breathing
The centre has a particular emphasis on sleep disordered
breathing with an international reputation for researching
the mechanisms underlying the obstructive sleep apnoea
syndrome (OSAS). In this disorder, patients experience
repetitive episodes of throat blockage during sleep leading
to complete cessation of breathing for short periods of
time. In the short term, this leads to daytime fatigue, poor
concentration, and an increased risk of motor vehicle
accidents. In the long term it has been linked to the
occurrence of heart disease, high blood pressure and stroke.
LECRR researchers are working to understand the processes
associated with the occurrence of obstructed breathing
during sleep in order to improve the treatments available for
this important disorder.
LECRR researchers have also conducted an important study
examining the interaction between sleep apnoea and daytime
blood pressure. A large cohort of Samoan OSAS patients
has shown significant and progressive reductions in daytime
blood pressure following treatment of their OSAS.
Cystic fibrosis
Cystic fibrosis (CF) is the most common lethal inherited
disease affecting Australians. In CF, altered salt transport
across the lining of the airways leads to drying of the airway
surface which impedes the processes which remove mucus
from the lungs. Mucus retention makes the lungs very
susceptible to bacterial infections. People with CF experience
repeated chest infections requiring constant medical care.
During 2006 the group’s researchers continued to provide
a diagnostic service using the nasal potential difference
technique to assist in the diagnosis of CF in patients
referred from physicians in Sydney, Melbourne, Adelaide
and Brisbane. The centre researchers also studied pancreatic
enzymes which are present in the blood to determine the
pancreatic status of CF patients.
Centre for Heart Research
Development of treatments for atrial tachycardias
There are two current research projects being performed. The
first involves the creation of a chronic ovine model of atrial
flutter using purely percutaneous means. Previous models
have required open heart surgery which is far more invasive
and painful for the animal. With the aid of new 3D electro
anatomical imaging, the group has now been able to reliably
induce atrial flutter in sheep that is similar to that found in
humans.
The next step is to attempt to cure this by performing
microwave ablation of the cavotricuspid isthmus using a
novel percutaneous microwave catheter. An ARC funded
collaboration with the University of Technology began
to investigate alternative energy sources for treatment of
abnormal heart rhythms.
The other project aims to develop a chronic ovine model
of atrial fibrillation by inducing heart failure in sheep using
rapid ventricular pacing using implanted pacemakers. Unlike
previous models, the group hopes to be able to develop
ventricular scarring and electrophysiological parameters and
validated a novel approach of electroanatomical mapping of
ventricular scar using non-contact mapping.
Ventricular tachycardia originating from within deep tissue
of the septum is complex and difficult to ablate due to the
limited scope of current ablation technologies, and due to the
inability of current mapping techniques in identifying sublayer
activation of myocardium. Using non-contact mapping
the group has been able to distinguish between deep tissue
and superficial origins of focal ventricular tachycardia. All
aspects of the abovementioned research will be incorporated
into further studies using dual chamber simultaneous noncontact
mapping aimed to identifying successful target sites for
radiofrequency ablation of complex ventricular tachycardia.
Further research is also being undertaken to evaluate an
in-house developed percutaneous deployable catheter which
is more efficient at heating tissue than conventional radio
frequency ablation catheters, and is capable of detecting tip
contact with myocardium.
During 2006 LECRR researchers completed a major
epidemiologic study that identified heavy snoring as a risk
factor for the presence of carotid artery wall atherosclerosis
(plaque). Since dislodgement of carotid artery wall plaque is a
cause of stroke, this finding suggests that heavy snoring alone
poses a significant health threat. Other studies undertaken in
2006 include a large study examining relationships between
cranio-facial structure and OSAS, measurements of the
surface tension of the upper airway lining liquid in healthy
subjects and OSAS patients, studies examining the impact
of snoring on blood pressure control, and the development
of a computer model aimed at defining the relationships
between peri-pharyngeal tissue pressure and upper airway
patency. In collaboration with the University of Sydney,
Asthma and chronic obstructive pulmonary disease
Asthma now affects the lives of over 2 million Australian
children and adults. Despite decades of research into the
causes and treatment of asthma the prevalence of asthma in
the population continues to rise. A major research interest of
the centre is the influence of mouth versus nose breathing on
the occurrence of asthmatic symptoms. The centre’s research
recognised that asthmatic subjects have altered perception of
nasal obstruction, leading them to switch to mouth breathing
more readily than healthy individuals, and that this switch
may contribute to the development of an asthma episode.
Future research will investigate whether nasal breathing can
help to resolve an episode of asthma.
a model of atrial fibrillation that is electrophysiologically
similar to chronic atrial fibrillation as seen in humans. If
successful, this would enable us to trial ablation techniques to
treat this disorder.
Development of treatments for ventricular tachycardia
The project aims to understand how post-myocardial
infarction substrate precipitates ventricular tachycardia
and to develop novel strategies of mapping and ablation
of ventricular tachycardia using non-invasive, non-contact
electrophysiological mapping.
Clinical evidence suggests that ventricular tachycardia often
precipitates at the border zone of scarred and non-scarred
myocardium. In an ovine model of chronic myocardial
infarction the group assessed the association between

50 51 > Research Report // AR 2006
Staff
Infection and Immunity
Centre for Infectious Diseases
and Microbiology
Director
Prof Tania Sorrell
Laboratory Manager
Mr Gary Martinic
Bacterial Pathogenesis
Research Group Leader
A/Prof Jon Iredell
Senior Research Officer
Dr Sally Partridge
Scientific Officer
Ms Damla Power
Mrs Belinda Roychoudhry
PhD Students
Ms Deborah Blanckenberg
Mr Andrew Ginn
Mr Bjorn Espedido
Ms Jubelle Valenzuela
Mr Zhiyong Zong
Masters Student
Mrs Lee Thomas
Fungal Pathogenesis
Research Group Leader
Dr Julianne Djordjevic
Senior Research Officer
Dr Alfred Widmer
Scientific Officer
Dr Catherine Wu
Research Assistant
Ms Sue Dowd
Ms Namfon (Beth) Pantarat
Mrs Ganendren Ranjini
Ms Christabel Wilson
PhD Students
Dr Methee Chayakulkeeree
Ms Orla Morissey
Dr Geoffrey Playford
Ms Rosemary Siafakas
Miss Kylie Turner
Molecular Mycology
Research Group Leader
A/Prof. Wieland Meyer
Post-doctoral Fellow
Dr Clement Tsui
Research Assistant
Ms Krystyna Maszewska
PhD Students
Dr Azian Harun
Miss Sirada Kaocharoen
Mr Popchai Ngamskulrungraj
Miss Luciana Trilles
Mycology
Senior Scientific Officer
Dr Catriona Halliday
Research Officer
Ms Jessie Lay
Public Health
Staff Specialist
Dr Vitali Sintchenko
Research Epidemiologist
Ms Heather Gidding
Research Officer
Dr Qinning Wang
Education Officer
Ms Judith Holford
Technical Officer
Ms Ping Zhu
Centre for Virus Research
Director
Prof Tony Cunningham
Deputy Director
Dr Barry Slobedman
Admin Assistant
Ms Janine Murray
Lab Manager
Ms Rebecca Howard
Clinical Research Officer
Ms Janette Taylor
Cytomegalovirus Research
Research Group Leader
Dr Barry Slobedman
Research Associate
Dr Josh Stern
Research Assistant
Miss Winnie Garcia
PhD Student
Mr Selmir Avdic
Mr Allen Cheung
Mr Michael Godwin
Ms Joanne Tan
Honours Student
Mr John Cao
Mr Brad Webster
Herpes Immunopathogenesis
Research Group Leader
Professor Tony Cunningham
Research Officer
Dr Min Kim
Dr Monica Miranda-Saksena
Ms Lidija Bosnjak
Research Assistant
Mr Bibing Tijono
PhD Student
Mrs Anupriya Aggarwal
Honours Student
Miss Fay Roberson
Herpes Protein Chemistry
Research Group Leader
Dr Russell Diefenbach
PhD Student
Ms Debbie Ko
Ms Branka Mijatov
Ms April Morton
Honours Student
Mr Jin Lee
HIV Molecular Pathogenesis
Research Officer
Dr Andrew Harman
Dr Najla Nasr
Post-doctoral Fellow
Dr Heather Donaghy
Research Assistant
Mr Joey Lai
Miss Valerie Marsden
Miss Sarah Mercier
PhD Student
Miss Kerrie Dunstan
Dr Susan Maddocks
HIV Protein Function and Interaction
Research Group Leader
Dr Sabine Piller
Research Assistant
Miss Eleanor Hitchen
PhD Student
Miss Judy Edmonds
Ms Vicki Kassouf
Honours Student
Miss Suzanah Philipsz
Miss Sarah Sherwood
HIV Retroviral Genetics
Research Group Leader
Dr Nitin Saksena
Postdoctoral Fellow
Dr Bin Wang
Staff Specialist
Dr Dominic Dwyer
PhD Student
Ms Da’ed Haddad
Mr Shwen Ho
Ms Katherine Lau
Ms Megan Steain
Ms Jingqin Wu
Ms Julie Zhou
Varicella Zoster Research
Research Group Leader
Dr Allison Abendroth
Research Assistant
Miss Elizabeth Sloan
PhD Student
Mr Joshua Bowles
Ms Kavitha Gowrishankar
Ms Jennifer Huch
Honours Student
Mr Rodney Henriquez
Centre for Transplant and
Renal Research
Director - Transplantation
A/Prof Philip O’Connell
Director – Nephrology
Prof David Harris
Director - Renal Medicine
Prof Jeremy Chapman
Visiting Medical Officer
Dr Brian Nankivell
Laboratory Manager
Mr Gary Martinic
Business Manager
Ms Lara Stretton
Research Administrator
Ms Debra Tucker
Islet Transplantation
Senior research fellow
Dr Wayne Hawthorne
Scientific Officers
Mr Denbigh Simond
Mrs Tina Patel
Ms Lindy Williams
Technical Officers
Ms Jennifer O’Hara
Ms Kelly Hucker
Ms Kay Waite
PhD student
Dr Satoshi Akima
Mr Chiomad (Chi) Abili-Morris
Visiting Scholar
Mrs Xuehong Lu
Xeno Transplant Group
Senior Scientist
Dr Shounan Yi
Scientist
Miss Elvira Jimenez-Vera
PhD Student
Mr Matthew Vittalone
Mr Moses Wavamuno
Visiting scholar
Miss Jing Jing Wu
Miss Yiling (Elise) Fu
Renal Medicine
Renal Medicine
Director
Prof David Harris
Scientist
Dr Deepika Mahajan
Dr Yiping Wang
Dr Guoping Zheng
PhD Student
Mr Vincent Lee
Mr Alvin Tan
Dr Ying (Cindy) Wang
Mr Dong Zheng
Research Assistant
Ms Zolaikha Rahimi
Kidney Regeneration
Research Group Leader
Dr Gopala Rangan
PhD Students
Mr Jason Coombes
Miss Lena Succar
Institute for Dental Research
Director
Prof Neil Hunter
Deputy Director
Prof Neil Jacques
Honorary Research Associate
A/Prof John Gibbins
Honorary Research Fellow
Dr Bettine Webb
Senior Lecturer
Dr Liz Martin
Senior Research Scientist
Dr Derek Harty
Post-doctoral Fellow
Dr Ping Ye
Research Fellows
Dr Roy Byun
Dr Cherly Chapple
Dr Mangala Nadkarni
Dr Cathy Rathsam
Dr Peter Yun
Research Assistant
Miss Gina Browne
Miss Ruth Eaton
Technical Officer
Mrs Mara Cvejic
Ms Mary Simonian
PhD Student
Ms Kim Chhour
Ms Hongya Xie
Masters Student
Dr Kersten Angner
Dr Nazilla Babapoor
Admin Assistant
Ms Tracey Bowerman
Institute for Immunology
and Allergy
Research Director
Prof Graeme Stewart
Lab Manager
Mr Stephen Schibeci
Clinical Research Leader
Dr David Fulcher
Dr Rob Heard
A/Prof Connie Katelaris
Genetics of Multiple Sclerosis
Research Group Leader
Dr David Booth
Hospital Scientist
Dr Fiona McKay
Research Assistant
Mrs Najwa Marmash
Immunogenetics
Scientific Officer
Dr Marc Buhler
Immunology
Registrar
Dr Lucinda Berglund
Molecular Genetics of Asthma and
Allergy
Research Group Leader
Dr Graham Jones
Research Assistant
Ms Emily Clarke
PhD Student
Ms Nusrat Rahman
Molecular Immunology
Post-doctoral Fellow
Dr Salvador Gala
Viral Immunobiology and Apoptosis
Research Group Leader
Dr Lisa Sedger
Research Assistant
Mrs Sarah Osvath
PhD Student
Ms Arna Katew
Masters Student
Ms Nuruliza Roslan
Honours Student
Miss Maha Mahmassani
B cell Immunobiology
Research Group Leader
Dr David Fulcher
Research Assistant
Shreya Malik
Cancer
Westmead Institute for Cancer Research
Director
Prof Rick Kefford
PA to Rick Kefford
Ms Annette Arkell
Deputy Director
A/Prof Ken Bradstock
Lab Manager
Dr Greg Kaplan
Flow Cytometry
Senior Scientific Officer
Ms Mary Sartor
Technical Assistant
Mrs Alicia Smith-Wildey
Admin Assistant
Ms Carol Godson
Miss Rozanne Kazminski
Breast Cancer
Research Group Leader
A/Prof Christine Clarke
Postdoctoral Fellow
Dr Dinny Graham
Dr Patricia Mote
Research Assistant
Miss Adrienne Hanson
Ms Usha Salagame
Mrs Ornella Tolhurst
Technical Assistant
Ms Jadranka Tomas
PhD Student
Ms Hazel Hill
Breast Cancer Tissue Bank
Project Manager
Mrs Jane Carpenter
Tumour Bank Officer
Ms Virginia James
Database Administrator
Mr James Miller
Mr Eftaker Molla
Cell Cycle Research
Research Group Leader
Dr Helen Rizos
Research Officer
Dr Therese Becker
Dr Lyndee Scurr
Research Assistant
Ms Ana Ayub
Mrs Malama Irvine
PhD Student
Miss Prerna Badhwar
Mr Stuart Gallagher
Mr Sebastian Haferkamp
Ms Heather McKenzie
Cellular Therapies
Research Group Leader
A/Prof David Gottlieb
Senior Scientific Officer
Ms Vicki Antonenas
Research Officer
Dr Anita Gamvrellis
Research Assistant
Mr Leighton Clancy
PhD Student
Mr Kurt Forrester
Ms Jenny Lau
Dr Ken Micklethwaite
Dr Philip Saunders
Familial Cancer
Clinical Director
A/Prof Judy Kirk
Research Group Leader
Dr Jenny Leary
Scientific Officer
Ms Barb Guild
Research Assistant
Ms Monique Dyson-Dalziel
Data Manager
Mrs Nishath Syed
Gene Expression
Research Group Leader
Dr Beric Henderson
Post-doctoral Fellow
Dr Mariana Brocardo
Dr Ying Lei
Dr Manisha Sharma
Dr Myth Tsz Shun Mok
Research Assistant
Miss Kirsty Brodie
PhD Student
Miss Wendy Au
Mrs Varsha Tembe
Honours Student
Mr Michael Johnson
Gynaecological Oncology
Research Group Leader
Dr Anna deFazio
Research Assistant
Ms Yoke-Eng Chiew
Ms Catherine Kennedy
PhD Student
Miss Natalie Gava
Miss Kylie Pryor
Miss Catherine Anne Emmanuel

52 53 > Research Report // AR 2006
Leukaemia Cell Biology
Research Group Leader
Dr Linda Bendall
Research Associate
Dr John Hewson
Research Officer
Ms Aileen dela Pena
Dr Roman Crazzolara
Research Assistant
Ms Rana Baraz
Mr Adam Cisterne
Miss Taoran Wang
PhD Student
Ms Shiva Gaundar
Mr Julius Juarez
Mr Naveed Khan
Honours Student
Miss Mandy Khoo
Miss Danielle Tyrrell
Melanoma and Genetic Epidemiology
Research Group Leader
A/Prof Graham Mann
Research Officer
Dr Gulietta Pupo
Biospecimen Manager
Miss Chantelle Agha-Hamilton
Project Co-ordinator
Ms Helen Schmid
Research Assistant
Ms Elizabeth Holland
Mr James Indsto
Mrs Gina Sherry
Ms CarolineWatts
PhD Student
Mrs Robyn Dalziell
Dr Sally de Zwaan
Ms Nadine Kasparian
Dr Angelo Sklavos
Translational Oncology
Research Group Leader
Dr Rosemary Balleine
Research Assistant
Miss Pamela Provan
PhD Student
Miss Lucy Webster
Dr Mark Wong
Liver and Metabolic
Storr Liver Unit
Acting Directors
Prof Jacob George
Prof Chris Liddle
Laboratory Manager
Ms Linda Frost
Clinical Hepatology
Director
Prof Jacob George
CCRE Project Co-ordinator
Dr Rosemary Carney
Staff Specialist
Dr Rita Lin
Research Fellow
Dr Dev Samarasinghe
PhD Students
Dr Hossein Poustchi
Ms Alexis St George
Clinical Research
Registered Nurse
Mrs Jasmin Canete
Research Nurse
Ms Seng Kee Teo
Dieticians
Miss Lauren McGrath
Technical Officer
Mrs Lee Russell
Ms Keshni Sharma
PhD Student
Ms Amanda Johnston
Molecular Pharmacology
Director
Prof Chris Liddle
Research Officer
Dr Kumar Subramanian
Research Assistant
Ms Sally Coulter
Technical Assistant
Ms Caroline Wilson
PhD Student
Miss Marina Kacevska
NASH studies
Research Officer
Dr Roslyn London
Dr Jianhua Wang
Research Assistant
Mrs Joanne Brymora
Mr James Hurrell
Neuroscience and Vision
Brain Dynamics Centre
Director
A/Prof Lea Williams
Deputy Director, Clinical Research
Dr Anthony Harris
Deputy Director, Basic Research
Dr Chris Rennie
Admin Officer
Ms Estelle de Neumann
Computer Systems Officer
Mr James Moey
Laboratory Manager
Dr Peter Boord
Project Officer
Ms Jan Ambrose
Attention Deficit Hyperactivity Disorder
ADHD Co-ordinator
Mr Daniel Hermens
Post-doc/Fellow
Dr Ilario Lazzaro (honorary)
PhD Student
Mr Nick Cooper
Brain Modelling
Head of Unit
Dr Chris Rennie
Prof Peter Robinson
Post-doc/Fellows
Dr Michael Breakspear (honorary)
Dr Jong-Won Kim
Dr Peter Loxley
Dr Donald Rowe (honorary)
Senior Research Officer
Dr Dmitri Melkonyan
Research Associate
Dr Peter Drysdale
PhD Students
Mr Matthew Barton
Mr Alan Chiang
Mr Jonathon Clearwater
Mr Richard Gray
Mr Hal Henke
Mr Sacha Van Albada
Ms Hui Ying Wu
Cognitive Neuroscience
Head of Unit
A/Prof Lea Williams
Research Associates
Ms Danielle Mathersul
Post-doc/Fellows
Dr Kerri Brown
Dr Justine Gatt
Dr Stacey Kuan
Dr Thomas Whitford
PhD Students
Ms Ainslie Hatch
Mr Kristan Kang
Ms Pamela Marsh
Ms Donna Palmer
Depression
Post-doc/Fellow
Dr Andrew Kemp
PhD Student
Mr Patrick Hopkinson
Honours Student
Ms Jane Tu
Post –traumatic stress disorder
Head of Unit
Prof Richard Bryant
Post-doc/Fellow
Dr Kim Felmingham
Clinical Psychologists
Ms Catherine Cahill
Ms Sally Hopwood
Ms Eva Kandris
Dr Lucy Kenny
Dr Julie Mastrodomenico
Dr Kathryn Taylor
PhD Students
Ms Leah Campbell
Ms Erin Falconer
Ms Fiona McCallum
Schizophrenia
Head of Unit
Dr Anthony Harris
Senior Research Officer
Dr Pritha Das
PhD Students
Dr Gary Flynn
Ms Daniella Toscana
Centre for Vision Research
Director
Prof Paul Mitchell
Deputy Director
Dr Jie Jin Wang
Administrative Manager
Ms Kirsten Jakobsen
Senior Hospital Scientist
Dr Xiao Yang Wang
Nutrional Epidemiologist
Dr Victoria Flood
Orthoptist
Mr Michael Cosstick
Data Entry
Ms Gail Leddin
Ms Anastasia Rochtchina
Senior Statistician
Ms Elena Rochtchina
Statistician
Mr George Burlutsky
Ms Annette Kifley
Photographic Grader,
Data and Computer Manager
Ms Ava Grace Tan
Photographic Grader
Ms Bronwen Taylor
Ms Victoria Cosatto
Ms Mireille Moffitt
Study Coordinator
Ms Melissa Mackay
Ms Tania de Loryn
Administrative Assistant
Ms Cora Li
Research Assistant
Mr Thomas Hong
PhD Students
Dr Ee-Munn Chia
Dr Sudha Cugati
Dr Reena Fotedar
Dr Paul Healey
Dr Jenny Ip
Dr Shweta Kaushik
Dr Anne Lee
Dr Gerald Liew
Dr Dana Robaei
Dr Jennifer Tan
Cardio-Respiratory
Centre for Heart Research
Director
Dr Pramesh Kovoor
Research Leaders
Prof David Ross
Dr Aravinda Thiagalingam
Dr Liza Thomas
Dr Stuart Thomas
Research Assistant
Mrs Anita Boyd
Miss Michelle Mikhail
Miss Valerie See
Mr Gary Wu
Technical Officer
Mr Tony Barry
PhD Student
Dr Toon Wei Lim
Mr Jim Pouliopoulos
Dr Gopal Sivagangabalan
Masters Student
Dr Suzanne Eshoo
Ludwig Engel Centre for
Respiratory Research
Director
A/Prof John Wheatley
Associate Director Research
Dr Terence Amis
Research Leaders
Dr Kristina Kairatis
A/Prof Peter Middleton
Dr Tracey Robinson
Research Fellow
Dr Jamie Lam
Research Officer
Dr Mervat Hallani
Research Assistant
Ms Manisha Verma
Research Study Co-ordinator
Mrs Sharon Lee
PhD Student
Mr Jason Amatoury
Miss Jyotishna Narayan
Masters Student
Miss Rita Perri
Executive
Director
Professor Tony Cunningham
Chief Operating Officer
Mr Mark Dado
Executive Assistant
Mrs Claire Wolczak
Operations and Support
Operations Manager
Mr Glenn Holden
Facilities and Grants Administration
Manager
Mr Mark Smith
Finance Manager
Mr Mark Wissam
Marketing and Communications
Manager
Ms Gayle McNaught (to April 2006)
Laboratory Managers
Ms Linda Frost
Ms Rebecca Howard
Dr Greg Kaplan
Mr Gary Martinic
Mr Stephen Schibeci
HR Manager
Amanda Clout (to May 2006)
Shalini Singh
IT Manager
Mr Ian Magee
Computer Support Officers
Ms Chris Cannon
Mr Blair Lawton
Mr Bruno Marion
Mr Adrian Plummer
Admin Officer
Mrs Brenda Wilson
Safety and Training Officer
Mr Brian Horsfield
Stores Officer
Mr Cecil Nast
Reception
Mrs Gail Ladner
Biomedical Engineer
Dr Rob Wilkins
Research Facilities Co-ordinators
Mrs Christine Browne
Ms Caitlin van Holst Pellekaan
Wash Room Technicians
Ms Carol Devine
Mrs Hongya Liu
Core Technology Facilities
Confocal Microscopy
Imaging Officer
Ms Jacqui Mills
DNA Microarray
Microarray Technician
Ms Amanda Croft
Electron Microscope
E.M. Unit Co-ordinator
Mr Ross Boadle
Flow Cytometry
Flow Cytometry Technician
Ms Sandra Lum
Histology Services
Histology Technician
Ms Aysen Yuksel
Transgenics
Transgenic Animal Co-Ordinator
Ms Sandie Brown
Protein Production Facility
Proteomics Officer
Dr Eve Diefenbach
Westmead DNA
Manager
Mr Ilya Henner
Technical Officer
Miss Maryann Pincevic
Masters Student
Mr Mehdi Ramezani-Moghadam

54 55 > Research Report // AR 2006
Publications 2006
Alexander DM, Arns MW, Paul RH, Rowe DL,
Cooper N, Esser AH, Fallahpour K, Stephan
BCM, Heesen E, Breteler R, Williams LM
& Gordon E EEG Markers for Cognitive
Decline in Elderly Subjects with Subjective
Memory Complaints. Journal of Integrative
Neuroscience, 5, 49 - 74.
Alexander DM, Trengove C, Wright JJ, Boord
PR and Gordon E Measurement of phase
gradients in the EEG. Journal of Neuroscience
Methods, 156, 111 - 128.
Amatoury J, Howitt L, Wheatley JR, Avolio
AP, Amis TC. “Snoring-related energy
transmission to the carotid artery in rabbits.”
J Appl Physiol.
Amatoury, J., L. Howitt, et al. “Snoringrelated
energy transmission to the carotid
artery in rabbits.” J Appl Physiol.
Anaissie, E. J., Segal, B. H., Graybill, J. R.
& other authors Clinical research in the lay
press: irresponsible journalism raises a huge
dose of doubt. Clin Infect Dis 43, 1031-1039.
Anstey KJ, Lord SR, Hennessy M, Mitchell
P, Mill K, von Sanden C. The effect of
cataract surgery on neuropsychological
test performance: a randomized
controlled trial Journal of the International
Neuropsychological Society 12(5):632-9.
Antill, Y., Reynolds, J., Young, M. A., Kirk, J.,
Tucker, K., Bogtstra, T., Wong, S., Dudding, T.,
Di Iulio, J., and Phillips, K. A. Risk-reducing
surgery in women with familial susceptibility
for breast and/or ovarian cancer. European
Journal of Cancer, 42: 621-628.
Antill, Y. C., Reynolds, J., Young, M. A., Kirk,
J. A., Tucker, K. M., Bogtstra, T. L., Wong,
S. S., Dudding, T. E., Iulio, J. L., Phillips, K.
A., Antill, Y., Kirk, J., Tucker, K., Bogtstra,
T., Wong, S., Dudding, T., and Di Iulio, J.
Screening behavior in women at increased
familial risk for breast cancer. Fam Cancer,
42: 621-628, 2006
Risk-reducing surgery in women with familial
susceptibility for breast and/or ovarian
cancer. Fam Cancer, 42: 621-628.
Antonenas, V., Garvin, F., Webb, M., Sartor,
M., Bradstock, K. F., and Gottlieb, D.
Fresh PBSC harvests, but not BM, show
temperature-related loss of CD34 viability
during storage and transport. Cytotherapy,
8: 158-165.
Backhouse, J. L., Gidding, H. F., McIntyre,
P. B. & Gilbert, G. L. Evaluation of two
enzyme immunoassays for detection of
immunoglobulin G antibodies to mumps
virus. Clin Vaccine Immunol 13, 764-767.
Baguley IJ Cooper J, Felmingham
KL Aggressive behaviour following
Traumatic Brain Injury: How common
is commonJournal of Head Trauma
Rehabilitation, 21, 45 - 57.
Balleine, R. L., Murali, R., Bilous, A. M.,
Farshid, G., Waring, P., Provan, P., Byth, K.,
Thorne, H., Kirk, J. A., and Investigators,
K. Histopathological features of breast
cancer in carriers of ATM gene variants.
Histopathology, 49: 523-532.
Barclay AW, Brand-Miller JC, Mitchell P.
Macronutrient intake, glycaemic index and
glycaemic load of older Australian subjects
with and without diabetes: baseline data
from the Blue Mountains Eye Study. British
Journal of Nutrition 96(1):117-123
Beard, F., McIntyre, P., Gidding, H. & Watson,
M. Influenza related hospitalisations in
Sydney, New South Wales, Australia. Arch
Dis Child 91, 20-25
Belov, L., Mulligan, S. P., Barber, N., Woolfson,
A., Scott, M., Stoner, K., Chrisp, J. S., Sewell,
W. A., Bradstock, K. F., Bendall, L., Pascovici,
D. S., Thomas, M., Erber, W., Huang, P.,
Sartor, M., Young, G. A., Wiley, J. S., Juneja,
S., Wierda, W. G., Green, A. R., Keating, M. J.,
and Christopherson, R. I. Analysis of human
leukaemias and lymphomas using extensive
immunophenotypes from an antibody
microarray. Br J Haematol, 135: 184-197.
Bendall, L. and Bradstock, K. New therapies
targeting chemokine receptors: can changing
the way cells traffic be used to treat human
disease Current Topics in Membanes, 55:
331-365.0
Berglund LJ, Jones GJ, Murali R, Fulcher
DA. TACI mutation with invasive polyclonal
CD8+ T-cell lymphoproliferation in a patient
with common variable immunodeficiency. J
Allergy Clin Immunol. ;117:870-877
Bose S, Morgan LJ, Booth DR, Goudie DR,
Ferguson-Smith MA, Richards FM. The
elusive multiple self-healing squamous
epithelioma (MSSE) gene: further mapping,
analysis of candidates, and loss of
heterozygosity. Oncogene. ;25:806-812.
Bradstock, K. Chemotherapy for patients with
acute myeloid leukemia in first remission.
Current Hematologic Malignancy Reports,
1: 108-113.
Bradstock, K. F., Hertzberg, M. S., Kerridge,
I. H., Svennilson, J., McGurgan, M., Huang,
G., Antonenas, V., and Gottlieb, D. J. Unrelated
umbilical cord blood transplantation for
adults with haematological malignancies:
results from a single Australian centre. Intern
Med J, 36: 355-361.
Breakspear M, Bullmore ET, Aquino K, Das
P and Williams LM The Multiscale character
of evoked cortical activity Breakspear M,
Roberts JA, Terry JR, Rodrigues, Mahant
N and Robinson PA A Unifying explanation
of primary generalized seizures through
nonlinear brain modeling and bifurcation
analysis. Cerebral Cortex, 16, 1296-1313.
Brickman AM, Zimmerman ME, Paul RH,
Grieve SM, Tate DF, Cohen RA, Williams LM,
Clark CR & Gordon E Regional white matter
volume and neuropsychological functioning
across the adult lifespan. Biological
Psychiatry, 60, 444 - 453.
Bridgewater FH, Zeitz K, Katelaris C, Field
J. Latex allergy in the prehospital setting.
Prehospital Disaster Med. ;21:322-328.
Bryant RA Moulds M, Nixon RDV,
Mastrodomenico J, Felmingham KL,
Hopwood S Hypnotherapy and cognitive
behaviour therapy of acute stress disorder: A
three-year follow up.Behaviour Research and
Therapy, 44, 1331 - 1335.
Bryant, R.A. and F.G. Njenga Cultural
sensitivity: making trauma assessment and
treatment plans culturally relevant. J Clin
Psychiatry, 67 Suppl 2: p. 74-9.
Bryant, R.A., Longitudinal psychophysiological
studies of heart rate: mediating
effects and implications for treatment Ann N
Y Acad Sci, 1071: p. 19-26.
Bryant, R.A., Recovery after the tsunami:
timeline for rehabilitation. () J Clin
Psychiatry, 67 Suppl 2: p. 50-5.
Bugeja MJ, Booth D, Bennetts B, Heard
R, Rubio J, Stewart G. An investigation
of polymorphisms in the 17q11.2-12 CC
chemokine gene cluster for association with
multiple sclerosis in Australians. BMC Med
Genet. ;7:64.
Bugeja MJ, Booth DR, Bennetts BH,
Heard RN, Stewart GJ. An investigation of
polymorphisms in the 4q1 3.3-21.1 CXC
chemokine gene cluster for association with
multiple sclerosis in Australians. Mult Scler.
;12:710-722.
Bugianesi E, Marchesini G, Gentilcore
E, Cua IH, Vanni E, Rizzetto M, George J.
Fibrosis in genotype 3 chronic hepatitis C
and nonalcoholic fatty liver disease: Role
of insulin resistance and hepatic steatosis.
Hepatology. 44(6):1648-55.
Chadli, A., Graham, J. D., Abel, M. G.,
Jackson, T. A., Gordon, D. F., Wood, W.
M., Felts, S. J., Horwitz, K. B., and Toft,
D. GCUNC-45 is a novel regulator for the
progesterone receptor/hsp90 chaperoning
pathway. Molecular and Cellular Biology, 26:
1722-1730.
Chandrasekaran S, Cumming RG, Rochtchina
E, Mitchell P. Associations between elevated
intraocular pressure and glaucoma, use of
glaucoma medications and 5-year incident
cataract: the Blue Mountains Eye Study.
Ophthalmology 113(3):417-24
Chapman, J. R. “Not all donors are equal.”
Transplantation 81(7): 976-7.
Chapman, J. R. and B. J. Nankivell
“Nephrotoxicity of ciclosporin A: shortterm
gain, long-term pain” Nephrol Dial
Transplant 21(8): 2060-3.
Chapman, J., A. Bock, et al. “Follow-up
after renal transplantation with organs from
donors after cardiac death.” Transpl Int
19(9): 715-9.
Charles KA, Rivory LP, Brown SL, Liddle C,
Clarke SJ, Robertson GR. Transcriptional
repression of hepatic cytochrome P450 3A4
gene in the presence of cancer. Clin Cancer
Res. 12:7492-7497.
Chen, S., Slavin, M., Nguyen, Q., Marriott, D.,
Playford, E. G., Ellis, D. & Sorrell, T. Active
surveillance for candidemia, Australia.
Emerg Infect Dis 12, 1508-1516.
Cherepanoff S, Mitchell P, Wang JJ, Gillies
MC. Retinal autoantibody profile in early
age-related macular degeneration: results
from the Blue Mountains Eye Study. Clinical
& Experimental Ophthalmology 34(6):590-5
Chia E-M, Wang JJ, Rochtchina E, Mitchell P.
Impact of multiple impairments on quality
of life, hospitalisations and use of aged
care services. Medical Journal of Australia
184(9):478-9
Chia E-M, Chia E-M, Rochtchina E, Wang
JJ, Mitchell P. Utility and validity of the selfadministered
SF-36: Findings from an older
population. Annals, Academy of Medicine,
Singapore 35(7):461-7
Chia E-M, Mitchell P, Foran S, Rochtchina
E, Golding M, Wang JJ. Association between
vision and hearing impairments and their
combined effects on quality of life. Archives
of Ophthalmology 124:1465-70
Chia E-M, Mitchell P, Ojaimi E, Rochtchina
E, Chia E-M, Wang JJ. Assessment of visionrelated
quality of life in an older population
subsample: the Blue Mountains Eye Study.
Ophthalmic Epidemiology 13(6):371-7
Chiu C, Booy R, Dwyer DE. Antivirals for
the treatment and prevention of human
seasonal influenza. Australian Microbiology;
27:163-165.
Chitturi S, George J. Hepatitis C and overweight.
Hot topics in Viral Hepatitis.2:15-21.
Chong JJ, Kumar S, Thomas L, Thomas S.
Supraventricular ectopy and recurrence
of atrial fibrillation after electrical
cardioversion. Europace;8(5):341-344.
Christopherson, R. I., Stoner, K., Barber, N.,
Belov, L., Woolfson, A., Scott, M., Bendall,
L., and Mulligan, S. P. Classification of AML
using a monoclonal antibody microarray.
Methods Mol Med, 125: 241-251.
Crowther, H., Collins, D., Antonenas, V.,
McGurgan, M., Kerridge, I., Gottlieb, D.,
and Bradstock, K. Successful autologous
peripheral blood stem cell harvest and
transplant in a patient with cold agglutinins.
Bone Marrow Transplantion, 37: 329-330.
Chua B, Flood V, Rochtchina E, Wang JJ,
Smith W, Mitchell P. Dietary fatty acids
and the 5-year incidence of age-related
maculopathy. Archives of Ophthalmology
124(7):981-6
Chua B, Kifley A, Wong TY, Mitchell P.
Homocysteine and retinal emboli: the Blue
Mountains Eye Study. American Journal of
Ophthalmology 142(2):322-4
Clark CP, Brown GG, Frank L, Thomas L,
Sutherland AN, Gillin JC. Improved anatomic
delineation of the antidepressant response
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60
Westmead Millennium Institute at a glance
Research Divisions
Collaborative Research Centres
Trp 211(A)
Infection and Immunity
Centre for Infectious Diseases and Microbiology
Centre for Transplant and Renal Research
Centre for Virus Research
Institute for Dental Research
Institute for Immunology and Allergy
Cancer
Westmead Institute for Cancer Research
Liver and Metabolic
Storr Liver Unit
Neuroscience and Vision
Brain Dynamics Centre
Centre for Vision Research
Cardio-respiratory
Ludwig Engel Centre for Respiratory Medicine
Centre for Heart Research
NHMRC Centre of Clinical Research Excellence to Improve
Outcomes in Chronic Liver Disease
NHMRC Centre of Clinical Research Excellence in Renal Medicine
NHMRC Centre of Clinical Research Excellence to Improve
Outcomes in Immunosuppressed Haematology Patients
Australian Centre for HIV and Hepatitis Virology Research
NSW Breast Cancer Tissue Bank
International Melanoma Consortium
Kathleen Cuningham Foundation Consortium for Research into
Familial Breast Cancer
Genes Associated with Multiple Sclerosis in Europeans (GAME)
Swedish and Australian Collaboration for Research into Atopic
Dermatitis
National Pancreas Transplantation Centre
The Millennium Foundation
Medical research relies on the support of individuals,
business, community and service groups. The Millennium
Foundation is the main fundraising body supporting Westmead
Millennium Institute.
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The Millennium Foundation is grateful for any support, as
every donation is valuable.
Donations over $2.00 are tax deductible. Donations can be
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to the following address (please indicate if you have a specific
interest in a particular research area).
The Millennium Foundation, PO Box 74, Westmead NSW 2145,
or contact us on our toll free number: 1800 639 037.
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Founding donors include: Australian Cancer Research Foundation, The Millennium Foundation, Robert W Storr Estate,
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We wish to thank the staff and the families that assisted
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