Joint Annual Research Report 2004 - The Royal Marsden

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The new Genetic Epidemiology Building, which will open in the autumn of 2005. Research Highlights The most important event so far in our Genetic Epidemiology Programme occurred in September with the launch of the Breakthrough Generations Study. This exciting new partnership with Breakthrough Breast Cancer seeks to understand the environmental, lifestyle and genetic factors that cause breast cancer. Led by Professor Tony Swerdlow, Chairman of the Section of Epidemiology, and Professor Alan Ashworth, Director of the Breakthrough Toby Robins Breast Cancer Research Centre, the study will recruit over 100,000 women and follow them for forty years. It will collect data on their genetics, their reproductive history, their hormonal status and their lifestyle, and from such information we hope to deduce the factors that cause the disease. Such knowledge is essential if there are ever to be effective prevention programmes. This study, and others of a similar nature, will be greatly facilitated by the new Genetic Epidemiology Building, which will open in the autumn of 2005, and has been made possible by a £9.2M grant from the Higher Education Funding Council for England’s Science Research Investment Fund. As well as providing state of the art accommodation for the scientists involved, the building will provide us with the capacity to store the vast number of samples, and paper questionnaire records, that will be collected from the participants. Our understanding of the genetic basis of cancer advances rapidly. Professor Mike Stratton, with colleagues in the Cancer Genome Project, showed that a subset of lung cancer patients carry mutations in the ErbB2 gene. This encodes a tyrosine kinase and is thus a highly promising target for therapeutic intervention, given that we know that mutations in the related ErbB1 gene confer sensitivity to the drug Iressa. Professor Nazneen Rahman, team leader in the Section of Cancer Genetics and Honorary Consultant in Medical Genetics, studied a very rare condition called Multiple Variegated Aneupoloidy. Aneuploidy, a feature of many tumour cells, means that they have the wrong number of chromosomes, and it has long been argued whether it is a cause or a consequence of cancer. Children with the condition have an elevated risk of cancer. She showed that it results from mutations in the Bub1B gene, which we knew from studies in yeast is involved in the process by which the daughter chromosomes are separated at each cell division. Her data show clearly that aneuploidy is a cause, it significantly increases the risk of cancer. Dr Arthur Zelent, a member of the new joint Section of Haemato-oncology, was part of an international collaboration that showed that a transcriptional repressor called Pokemon is a critical factor in tumour formation. In the absence of this protein, cells are completely refractory to oncogeneinduced transformation while its over-expression causes
REVIEW OF 2004 tumours. It is highly expressed in human cancers in a fashion related to clinical outcome and is thus an attractive target for therapeutic intervention. In Molecular Pathology one of our main objectives is to find ways of telling whether prostate cancer, diagnosed following a PSA test, is aggressive and requires immediate clinical intervention, or whether it is indolent, ie it will grow slowly and the patient can be spared treatment, needing only careful monitoring. It was thus of great significance when Colin Cooper, the Grand Charity of the Freemasons Professor of Molecular Biology, and his colleagues showed that the E2F-3 gene is over-expressed in prostate cancer, and that the levels of expression correlate very well with the aggressiveness of the tumour. It will now be important to see if this observation can be developed into a routine test. Moreover, because we know that the E2F-3 protein functions in the control of the cell cycle, we may also have identified a therapeutic target. To complement this, the hospital has a major clinical research programme in early prostate cancer called Active Surveillance, in which suitable patients are monitored closely rather than treated immediately, and it seems that the majority of these patients will completely avoid the need for radical treatments. This was a year of much progress in the development and validation of new treatment modalities. For a considerable number of years Professor Paul Workman, Director of the Cancer Research UK Centre for Cancer Therapeutics, and his colleagues have been studying inhibitors of the molecular chaperone HSP90, which is involved in the proper folding of a number of proteins known to play key roles in oncogenesis. Together with the team of Professor Laurence Pearl, Co-Chairman of the Section of Structural Biology, they have developed novel small molecule inhibitors of the chaperone, in a highly Expression of E2F-3 protein (brown) detected by immunohistochemistry in primary prostate cancer 7
Page 1 and 2: ANNUAL RESEARCH REPORT 2004 The Roy
Page 3 and 4: CONTENTS Review of 2004 - from the
Page 5: Cancer genes Scientific Strategy: f
Page 9 and 10: REVIEW OF 2004 While there have bee
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Page 13 and 14: Academic Dean’s Report 2004 Our a
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Page 17 and 18: Technology Transfer Report 2004 The
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Page 21 and 22: differentiated lactating lobules ar
Page 23 and 24: CANCER BIOLOGY SMAC ’em dead It i
Page 25 and 26: Extracellular environment Signal Re
Page 27 and 28: CANCER THERAPEUTICS/CANCER BIOLOGY
Page 29 and 30: Examples of current projects A vari
Page 31 and 32: CANCER THERAPEUTICS No. of patients
Page 33 and 34: CANCER THERAPEUTICS molecular diagn
Page 35 and 36: e very useful. Examples include tha
Page 37 and 38: CANCER THERAPEUTICS Integrating new
Page 39 and 40: The duration of adjuvant chemothera
Page 41 and 42: CANCER THERAPEUTICS Future directio
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Page 45 and 46: CANCER THERAPEUTICS Four randomised
Page 47 and 48: Lung cancer In collaboration with D
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HEALTH RESEARCH The Breakthrough Ge
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elative risk of developing breast c
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HEALTH RESEARCH Accordingly, in our
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In addition to browsing lists of re
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MOLECULAR PATHOLOGY Section of Haem
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ACADEMIC BOARD The Institute and th
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SENIOR STAFF & COMMITTEES 2004 MEDI
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Joint Annual Research Report 2004 - The Royal Marsden

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