Issue 1 - San Antonio Breast Cancer Symposium

1 Issue 1
December 10, 2009
“An international scientific symposium for interaction and exchange among basic scientists and clinicians in breast cancer.”
ear Colleagues:
Welcome to the 32nd annual San Antonio Breast Cancer Symposium, and to our second year in
collaboration with the American Association for Cancer Research (AACR). This year’s program
will be bigger and more exciting than ever, with a combination of cutting-edge research, training
opportunities for young researchers, and a comprehensive review of the state of breast cancer
research today.
The plenary lecturers this year will offer up-to-the-minute assessments in the areas of epidemiology, tumor
immunotherapy, and molecular pathways associated with breast cancer. There will be 51 oral presentations in
the General Sessions and over 1100 posters, as well as daily mini-symposia covering nanotechnology, the role of
host-related factors, and the relationship between local control and long-term survival. Four major awards will
honor clinicians and scientists who have made special contributions to the field of breast cancer research.
Yesterday afternoon, continuing a highly successful program that was initiated last year, we featured a variety
of basic education programs, offering additional background in important aspects of breast cancer research,
including RNA interference, breast cancer prevention, and epigenetics, among others. Starting today, we will
also be bringing back the immensely popular lunchtime sessions, with basic science panel discussions in areas of
active controversy, as well as clinical case discussions.
We will be introducing a new feature this year on Sunday morning. Instead of the usual handful of research
presentations to close out the meeting, you are invited to attend a program called “The Year in Review.” This program
will feature expert summaries of the symposium and assessments of developments over the last year in basic research,
translational research, early breast cancer, and metastatic breast cancer.
It should be an exciting week for everyone. We welcome you to San Antonio, and hope that your time here will
be fruitful and enjoyable.
Charles A. Coltman Jr, MD
C. Kent Osborne, MD
32nd Annual
December 9-13, 2009
Henry B. Gonzalez Convention Center
San Antonio, Texas, USA
The 32nd Annual San Antonio Breast Cancer Symposium

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Your Health During the Symposium
For the safety of our symposium participants, vendors, and staff we have implemented several steps to help limit the spread
of influenza-like illnesses at the convention center:
• Anti-bacterial foam soap in all restrooms
• Hand sanitizing stations at all time clocks for employees to use before and after clocking in or out
• All staff to use disposable gloves and to change them often
• Containers of hand sanitizer in common areas
• Refreshing and spraying disinfectant in restroom areas
• Wiping all surfaces often, such as escalator hand rails, door knobs/handles, etc
If you feel unwell while attending the symposium, please visit one of our medical services locations. We have designated areas
where you can view the symposium sessions in a more comfortable setting while limiting contagion. All symposium hotels also
have programs in place to assist you.
Please take the following precautions recommended by the Centers for Disease Control and Prevention (CDC) to stay healthy:
• Cover your nose and mouth with a tissue when you cough or sneeze. Throw the tissue in the trash after you use it.
• Wash your hands often with soap and water, especially after you cough or sneeze. Alcohol-based hand cleaners are
also effective.
• Avoid touching your eyes, nose, or mouth. Germs spread that way.
• Stay home if you get sick. Limit contact with others to keep from infecting them.
• Try to avoid close contact with sick people.
When in San Antonio, if you will not be attending the symposium due to illness, please contact the “call out” number on the back
of your badge to enable us to track health-related issues for the protection of all symposium participants.
The CDC suggests you seek urgent medical care if you are experiencing any of the following symptoms:
• Difficulty breathing or shortness of breath
• Pain or pressure in the chest or abdomen
• Sudden dizziness
• Confusion
• Severe or persistent vomiting

Speaker & Schedule Changes
Thursday, December 10: 12:30–1:45 pm
Basic Science Panel Discussions: Controversies in Breast Cancer Models for Drug Development
Pre-clinical models for development of marker guided therapy in breast cancer
Laura J. van ‘t Veer, PhD
The Netherlands Cancer Institute, Amsterdam
Revised Schedule
Saturday afternoon 12/12/09
12:25–1:25 pm CASE DISCUSSION 2 – Ballroom A
12:25–1:25 pm BASIC SCIENCE FORUM – Ballroom B
1:30–3:00 pm MINI-SYMPOSIUM 3 – Exhibit Hall D
Local Control and Long-term Survival
Moderators: Jay Harris, MD, Dana-Farber Cancer Institute, Boston, MA and Monica Morrow, MD, FACS,
Memorial Sloan-Kettering Cancer Center, New York, NY
1:30 pm Overview of the randomized trials of radiotherapy in early breast cancer
Sarah Darby, PhD
CTSU Oxford University, Oxford
2:00 pm How the ‘4:1 ratio’ will likely change with increasingly effective systemic therapy
Jay Harris, MD
Dana-Farber Cancer Institute, Boston, MA
2:30 pm Minimizing local recurrence: what’s proven, what’s not
Monica Morrow, MD, FACS
Memorial Sloan-Kettering Cancer Center, New York, NY
3:00–5:30 pm GENERAL SESSION 6 – Exhibit Hall D
3:00 pm 80. Results of chemotherapy alone, with sequential or concurrent addition of trastuzumab in the NCCTG
N9831 HER2-positive adjuvant breast cancer trial
Perez EA, Suman VJ, Davidson NE, Gralow J, Kaufman PA, Ingle JN, Dakhil SR, Pisansky TM, Jenkins
RB. Mayo Clinic, Jacksonville, FL; Mayo Clinic, Rochester, MN; University of Pittsburgh, Pittsburgh,
PA; Seattle Cancer Center Alliance, Seattle, WA; Dartmouth Hitchcock Medical Center, Hanover,
MD; Cancer Center of Kansas, Wichita, KS; National Cancer Institute, Bethesda, MD
Posters Rescheduled
The following posters will be presented outside of their originally scheduled times:
4028 Thursday 12/10/09 5:30–7:30 pm
5077 Thursday 12/10/09 5:30–7:30 pm
5109 Thursday 12/10/09 5:30–7:30 pm
6033 Friday 12/11/09 5:30–7:30 pm
6091 Friday 12/11/09 5:30–7:30 pm
6125 Friday 12/11/09 5:30–7:30 pm
Poster 5090 has been renumbered and rescheduled as:
710 Saturday 12/12/09 7:00–9:00 am Poster Discussion Session 7
Posters Withdrawn
702, 810, 1003, 1029, 1073, 3018, 3169, 4028, 4030, 4069, 6059, 6060, 6121
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Late-Breaking Abstracts
The following abstracts were received and accepted too late for inclusion in the SABCS abstract book. They will be published
in the January issue of Cancer Research.
Abstract 80
Results of chemotherapy alone, with sequential or concurrent addition of 52 weeks of trastuzumab in the NCCTG N9831
HER2-positive adjuvant breast cancer trial
Perez EA, Suman VJ Davidson NE, Gralow J, Kaufman PA, Ingle JN, Dakhil SR, Zujewski JA, Pisansky TM, Jenkins RB. Mayo
Clinic, Jacksonville, FL; Mayo Clinic, Rochester, MN; University of Pittsburg, Pittsburg, PA; Seattle Cancer Center Alliance, Seattle,
WA; Dartmouth Hitchcock Medical Center, Hanover, MD; Cancer Center of Kansas, Wichita, KS; National Cancer Institute,
Bethesda, MD
Background: N9831 is the only randomized phase 3 trial comparing safety and efficacy of the addition of trastuzumab (H) to
doxorubicin and cyclophosphamide then paclitaxel (Arm A: AC T) either following (Arm B: AC T H) or starting concurrently
with paclitaxel (Arm C: AC T+H H) for women with resected Stage I-III invasive HER2+ breast cancer. The 3-y cumulative
incidence of NYHA class III or IV congestive heart failure or sudden cardiac death was previously reported: 3.3% in Arm C, 2.8% in
Arm B (Perez EA et al, JCO 2008). The comparison of AC T to AC T+H H was reported in a joint analysis of N9831 and NSABP
B-31 in 2005 and updated in 2007, demonstrating a 52% reduction in risk of a disease event (Romond E et al, NEJM 2005; Perez
EA et al, ASCO 2007).
Materials and Methods: Primary endpoint is disease-free survival (DFS). At the second planned interim analysis of Arm A vs
Arm B, the O’Brien-Fleming boundary (OFB) was crossed. NCCTG Independent Data Safety Monitoring Committee approved
the release of these data, as well as the data pertaining to Arm B vs Arm C, due to slow pace of events [expected 647 events in
4-y follow-up period (f/u) vs actual 334 events in 4.5-y f/u]. Shortly thereafter, there were sufficient events to perform the first
planned interim analysis of B vs C. We present the results of each of these pairwise comparisons taking into account the potential
for crossover to Arm C after the release of the joint analysis findings in 2005.
Results: From 5/2000 to 4/2005, 2448 eligible women were enrolled for the Arm A (n=1087) vs Arm B (n=1097) comparison.
Median f/u is 5.5 y, with 386 events. The addition of trastuzumab sequentially to AC T significantly improved DFS univariately
[HR(Arm B/Arm A)=0.70; 95% CI, 57-86, logrank P=0.0005] and after adjusting for age, tumor size, number of positive nodes, and
ER [PPH: HR adj =0.67; 95% CI, 0.55-0.82]. 5-y DFS was increased from 72% with AC T to 80% with AC T H.
From 5/2000 to 4/2005, 1903 eligible women were enrolled for the Arm B (n=954) vs Arm C (n=949) comparison. Median f/u is
5.3 y, with 312 events. The log-rank P value testing whether DFS differs with respect to starting time of trastuzumab was 0.019
(not crossing pre-specified OFB for statistical significance). After adjusting for tumor size, number of positive nodes, and ER,
[HR adj (Arm C/Arm B)=0.75; 95% CI, 0.60-0.94]. 5-y DFS was increased from 80% with AC T H to 84% for AC T+H H.
Conclusions: DFS is significantly improved with the addition of 52 weeks of H (sequentially or concurrently) to AC T. There
is a statistically significant 33% reduction in the risk of an event with the sequential addition of H following AC T. There is
a strong trend for a 25% reduction in the risk of an event with starting H concurrently with T relative to sequentially after T.
Therefore, based on a positive risk/benefit ratio, we recommend that trastuzumab be incorporated in a concurrent fashion with
T chemotherapy.
Acknowledgements: NIH CA25224, Breast Cancer Research Foundation, Genentech

Abstract 112
Prediction of 10-year chemotherapy benefit and breast cancer-specific survival by the 21-gene Recurrence Score (RS) assay in
node-positive, ER-positive breast cancer—An update of SWOG-8814 (INT0100)
Albain KS, Barlow WE, Shak S, Hortobagyi GN, Livingston RB, Yeh I-T, Ravdin P, Bugarini R, Baehner FL, Davidson NE, Sledge
GW, Winer EP, Hudis C, Ingle JN, Perez EA, Pritchard KI, Shepherd L, Gralow JR, Yoshizawa C, Allred DC, Osborne CK, and
Hayes DF for The Breast Cancer Intergroup of North America. Loyola University Chicago Cardinal Bernardin Cancer Center,
Maywood, IL.
Background: A low 21-gene RS identifies patients with ER-positive breast cancer who do not appear to benefit from anthracyclinebased
chemotherapy (CAF) added to tamoxifen (T) despite positive axillary lymph nodes (Albain KS et al, Lancet Oncology, in
press). However, in the low RS group, the lack of improvement by CAF in the 64% disease-free survival (DFS) at 10 years is not
considered definitive evidence against the use of chemotherapy for conventionally identified high-risk patients. We conducted
new DFS prediction analyses within nodal categories by RS over 10 years and assessed whether the assay has predictive utility for
breast cancer specific survival (BCSS).
Methods: RT-PCR analyses for the 21 gene RS assay were feasible in 148 patients on T from the parent trial and 219 on CAF
followed by T, as previously described. In this update, we conducted 10-year DFS analyses within nodal categories 1-3+ and 4+
by the linear RS. For the exploratory analysis of BCSS, only deaths due to breast cancer were counted as events, censoring deaths
due to other causes (such as late cardiovascular events), as well as patients alive at the last follow-up visit. The clinically utilized
(trichotomized) RS categories of low (

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Revised Abstracts
Revisions of the following abstracts were received and accepted too late for inclusion in the SABCS abstract book. They will
be published in the January issue of Cancer Research.
Abstract 41
Final overall survival (OS) results from the randomized, double-blind, placebo-controlled, phase 3 AvADO study of
bevacizumab (Bv) plus docetaxel (D) compared with placebo (PL) plus D for the first-line treatment of locally recurrent
(LR) or metastatic breast cancer (mBC)
Miles DW, Chan A, Romieu G, Dirix LY, Cortés J, Pivot X, Tomczak P, Juozaityte E, Harbeck N, Steger GG, the BO17708 study
group. Mount Vernon Cancer Centre, Middlesex, United Kingdom; Mount Hospital, Mount Breast Group, Perth, Australia; CRLCC Val
d’Aurelle, P. Lamarque Service Chimioimmunotherapie, Montpellier, France; Algemeen Ziekenhuis St. Augustinus, Wilrijk, Belgium;
University Hospital Vall d’Hebron Oncology, Barcelona, Spain; University Hospital of Besancon, France; Klinika Onkologii Oddzial
Chemioterapii, Poznań, Poland; Kaunas Medical University Hospital, Oncology Clinic, Kaunas, Lithuania; Breast Centre, University of
Cologne, Cologne, Germany; Medical University of Vienna, Department of Internal Medicine I-Oncology, Vienna, Austria
Background: Anti-VEGF monoclonal antibody BV significantly improves efficacy in combination with standard therapies in
multiple tumor types, with limited impact on toxicity. Three randomized phase 3 trials (E2100, AVADO, and RIBBON-1) in mBC
have demonstrated that BV + 1st-line chemotherapy (CTx) significantly improves progression-free survival (PFS) and overall
response rates (ORR). We present mature OS data from AVADO.
Methods: Patients (pts) with HER2-negative LR/mBC were randomized to D 100 mg/m 2 + PL, D + BV 7.5 mg/kg or D + BV 15 mg/kg.
D was given q3w for ≤9 cycles. BV or PL was given q3w until disease progression/unacceptable toxicity. After progression, pts were
offered BV with 2nd-line anticancer therapy in a post-study treatment phase. The primary endpoint was PFS; secondary endpoints
included OS, time to treatment failure, ORR, duration of response and safety. An exploratory analysis conducted in pts receiving
post-progression CTx compared OS in pts receiving 2nd-line BV with those who did not.
Results: 736 pts were enrolled March 2006–April 2007. The primary analysis (data cut-off October 2007; median follow-up 10.2
months) showed significant improvements in PFS and ORR for both BV-containing arms compared with PL + D. Mature OS data
(data cut-off April 2009; median follow-up 25 months) are shown (Table). There was no difference in median OS between the
study arms (range 30–32 months). Recognizing the limitations of the non-randomized comparison in exploratory analyses, results
suggest that use of BV with 2nd-line therapy is a possible reason for lack of OS difference. Updated PFS and ORR were superior for
the 15 mg/kg BV arm compared with PL + D. Results for the 7.5 mg/kg BV arm also indicated a less pronounced treatment benefit.
BV had limited impact on the safety profile of docetaxel. Increased SAEs in the 15 mg/kg BV arm may be due to more pts receiving
9 cycles of D than in the PL arm (51% vs 42%).
Conclusions: There was no difference in OS between study arms. Exploratory analyses suggest that use of 2nd-line BV with CTx
may influence OS. These mature data confirm the improvement in PFS and ORR with BV 15 mg/kg combined with D compared
with PL + D.

Abstract 41
PL + D
(n=241)
BV 7.5 mg/kg + D
(n=248)
BV 15 mg/kg + D
(n=247)
Deaths, % 44.8 47.6 47.0
OS
HR 1.05 1.03
95% CI 0.81–1.36 0.79–1.33
P value
P value
P value
0.7198 0.8528
Median 31.9 30.8 30.2
Stratified PFS*
HR 0.80 0.67
95% CI 0.65–1.00 0.54–0.83
P value † 0.0450 0.0002
Median 8.1 9.0 10.0
ORR ‡ , % 46.4 55.2 64.1
0.0739 0.0003
1-y survival, % 76 81 84
PL + D
(n=231)
0.198 0.02
BV 7.5 mg/kg + D
(n=252)
BV 15 mg/kg + D
(n=247)
SAEs, % 32.5 37.3 42.9
Pts discontinuing
treatment due to
AE, %
BV/PL 11.7 8.7 13.8
D 24.7 20.6 24.3
AEs leading to
death, %
2.6 1.6 1.6
*Pts were censored if they had started non-protocol therapy before disease progression.
† Exploratory.
‡ Pts with measurable disease at baseline.
NR, not reached.

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Abstract 44
A double-blind, randomized, placebo-controlled, phase 2b study evaluating the efficacy and safety of sorafenib (SOR) in combination
with paclitaxel (PAC) as a first-line therapy in patients (pts) with locally recurrent or metastatic breast cancer (BC)
William J. Gradishar, Feinberg School of Medicine, Northwestern University, Chicago, IL; Virginia Kaklamani, Northwestern
University, Chicago, IL; Tarini Prasad Sahoo, Jawaharlal Nehru Cancer Hospital, Bhopal-1, M.P, India; D. Lokanatha, Kidwai Institute
of Oncology, Bangalore, India; Vinod Raina, Institute Rotary Cancer Hospital, New Delhi, India; Shailesh Bondarde, Shatabadi
Hospital, Nashik, India; Minish Jain, Ruby Hall Clinic, Pune, India; Lee Schwartzberg, West Clinic, Memphis, TN
Introduction: SOR is a targeted therapeutic agent indicated for advanced renal cell carcinoma and hepatocellular carcinoma.
SOR targets multiple kinases involved in tumor growth and angiogenesis. The TIES (Trials to Investigate the Effects of Sorafenib
in BC) program includes 4 phase 2b randomized, double-blind, placebo-controlled screening trials in HER2-negative BC. Recently,
the first of these trials, SOR+capecitabine (CAP) vs placebo (PL)+CAP demonstrated a significant progression-free survival (PFS)
benefit in pts with advanced BC. Here we present initial results from the second of the 4 trials. This study evaluated the efficacy
and safety of SOR in combination with PAC as a first-line regimen for pts with advanced BC.
Methods: Pts with HER2-negative, locally recurrent or metastatic BC were eligible for first-line treatment for advanced BC.
Previous cytotoxic (non-metastatic), endocrine, or radiation therapy was allowed. Pts were randomized 1:1 (stratified by visceral
vs non-visceral metastatic disease) to SOR (400 mg, orally, twice daily, continuously) or PL in combination with PAC (90 mg/m 2
weekly, IV, 3 weeks on/1 week off). The primary endpoint was PFS. Secondary endpoints included overall survival (OS), time to
progression (TTP), overall response rate (ORR), and safety. A sample size of 220 pts was planned to detect a targeted HR of 0.65
(90% power and 1-sided a=0.14). The study is registered at ClinicalTrials.gov (NCT00499525).
Results: From January 2008 to January 2009, 237 pts were randomized to SOR+PAC (n=119) vs PL+PAC (n=118), with 170
pts in India (74% vs 69%), 52 pts in the United States (21% vs 23%), and 15 pts in Brazil (5% vs 8%). Treatment groups were
balanced for age (mean, 51.9 y), ECOG performance 0 (45%) and 1 (53%), stage IV disease (85%), visceral metastatic disease
(75%), and previous non-metastatic chemo (58%). Results of the study were as follows for SOR+PAC vs PL+PAC: median
PFS 6.9 vs 5.6 mos (HR 0.788; 95% CI, 0.558-1.112; 1-sided log rank P=0.0857), median TTP 8.1 vs 5.6 mo (HR 0.674; 95% CI,
0.465-0.975; 1-sided log rank P=0.0171), and ORR of 67% vs 54% (1-sided Cochran-Mantel-Haenszel P=0.0234). OS data
are pending. Discontinuation of study treatment due to adverse events occurred in 23 pts (19%) in the SOR+PAC vs 5 pts
(4%) in the PL+PAC. Grade 3/4 toxicities (SOR+PAC vs PL+PAC) included hand-foot skin reaction (30% vs 3%), asthenia
(7% vs 3%), peripheral neuropathy (6% vs 7%), neutropenia (13% vs 7%), and anemia (11% vs 6%). Treatment-related deaths
occurred in 2 pts (malaria and liver dysfunction), both in the SOR+PAC arm.
Conclusions: Results of the primary endpoint, PFS, demonstrated a trend favoring SOR+PAC over PL+PAC in the treatment of
advanced BC (HR 0.788; P=0.0857). In addition, significant improvements in TTP and ORR were observed. OS data are pending.
There were no new toxicities observed with the combination and AEs were manageable. These data indicate that SOR provides
added benefit when combined with PAC compared with single-agent PAC in the first-line treatment of advanced BC.

Abstract 710
A phase 2 study of trastuzumab-DM1 (T-DM1), a novel HER2 antibody–drug conjugate, in HER2+ metastatic breast cancer (MBC)
patients previously treated with conventional chemotherapy, lapatinib and trastuzumab
Ian Krop, Dana Farber Cancer Institute, Boston, MA; Patricia LoRusso, Karmanos Cancer Institute, Detroit, MI; Kathy D. Miller,
Indiana University Melvin-Bren Simon Cancer Center, Indianapolis, IN; Shanu Modi, Memorial Sloan-Kettering Cancer Center, New
York, NY; Denise Yardley, Sarah Cannon Research Institute, Nashville, TN; George Rodriguez, South Texas Oncology/Hematology,
San Antonio, TX; Sam Agresta, BioOncology, Genentech, South San Francisco, CA; Maoxia Zheng, BioOncology, Genentech, South
San Francisco, CA; Lukas Amler, BioOncology, Genentech, South San Francisco, CA; Hope Rugo, UCSF Comprehensive Cancer
Center, San Francisco, CA
Background: T-DM1 combines the HER2-inhibiting properties of trastuzumab with targeted delivery of the anti-microtubule
agent DM1. In a prior phase 2 study, single agent T-DM1 was well tolerated and had significant activity (objective response rate
[ORR] of 26% by independent review [IRF]) in 112 patients (pts) with pre-treated HER2+ MBC (Vogel CL et al, J Clin Oncol, 27:15s,
2009 [suppl; abstr 1017]). To confirm and extend these findings, we conducted a phase 2 study that enrolled a more homogenous
population of HER2+ MBC pts who had all received prior anthracycline, taxane, capecitabine, trastuzumab, and lapatinib therapy
and progressed on the last regimen received (at least 2 HER2-directed regimens had to be given for metastatic disease).
Methods: This is an open-label, single-arm study of T-DM1 given at 3.6 mg/kg IV q3w. Primary objectives are to assess ORR by
IRF and evaluate the safety of T-DM1. Key secondary objectives assess the clinical benefit rate (CBR = ORR + stable disease [SD]
at 6 months), duration of response (DoR) and progression-free survival (PFS). Pts remain on study until disease progression
or unmanageable toxicity. Key exploratory objectives were the assessment of ORR and clinical benefit rate (CBR) by IRF in
retrospectively tested, centrally confirmed HER2+ patients.
Results: The study completed enrollment of 110 patients. This analysis has a median follow-up of 8.3 months (range 0.7-13.1).
Median age was 52.5 y (range 34–77). Pts received a median of 7 agents for metastatic disease (range 1–15). Median
durations of prior trastuzumab and lapatinib treatment in metastatic setting were 19.4 and 6.9 months respectively. The
ORR was 32.7% and the CBR was 44.5% by IRF. Median DoR and PFS have not reached maturity. In retrospectively tested,
centrally confirmed HER2+ patients, the ORR was 39.5% and the CBR was 52.6% by IRF. T-DM1 was well tolerated, with no
dose-limiting cardiotoxicity. One pt with pre-existing non-alcoholic fatty liver disease died with hepatic dysfunction. The
most common adverse events were fatigue (59.1% of pts), nausea (37.3%), and thrombocytopenia (29.1%); 41.8% of pts
experienced at least one grade 3 or above adverse event.
Conclusions: In this study, single agent T-DM1 demonstrates a 32.7% ORR with an acceptable safety profile in a well defined,
homogeneous, and extensively pretreated population that has not been previously studied. Centrally confirmed HER2 positivity
strongly correlated with objective response. These results confirm the activity of T-DM1 in treatment resistant HER2+ MBC. An
ongoing global randomized phase 23 study is evaluating T-DM1 compared with lapatinib plus capecitabine in pts with advanced
HER2+ who have been previously treated with a taxane and trastuzumab.
9

10
Revised Author Credits
2132
validated 3 gene signature predicts response to neo-adjuvant chemotherapy in luminal breast cancer—results from
GeparTrio and Geparquattro
von Minckwitz G, Budczies J, Loibl S, Darb-Esfahani S, Kaufmann M, Huober J, Engels K, Denkert C, Kronenwett R, von
Toerne C. German Breast Group, Neu-Isenburg, Germany; University of Frankfurt, Frankfurt/Main, Germany; University of
Tuebingen, Tuebingen, Germany; Charité, Berlin, Germany
6139
Gene transcripts in the tumor suppressor region of chromosome 3 (3p21)
Reefy S, Al Sarakbi W, Sasi W, Jiang WG, Roberts T, Newbold RF, Mokbel K. St George’s University of London, London, United
Kingdom; University, Wales College of Medicine, Cardiff University, Cardiff, United Kingdom; Institute of Cancer Genetics and
Pharmacogenomics, Brunel University, Middlesex, Uxbridge, United Kingdom

SABCS Scholarship Recipients
This year, 5 programs provided scholarships designed to promote the education and professional development of earlycareer
scientists who are actively pursuing research in breast cancer by facilitating their attendance at SABCS. Scholarships
were awarded to graduate students, medical students, residents, and clinical and postdoctoral fellows whose abstracts were
accepted for presentation, based on the quality of the abstracts. This year’s awardees, by program, are:
SABCS Clinical Scholars: For clinical scientists-in-training who are actively pursuing clinical or clinical/translational
research in breast cancer.
Young Kwang Chae Helen Heneghan Derek McHaffie
Elizabeth Comen Catherine Kelly Erin Cobain
Ghada Farhat Laura Kenny Huaying Liu
Luca Fumagalli
SABCS Basic Science Scholars: For laboratory-based investigators-in-training whose work focuses on the biology of
breast cancer and preclinical models of its development and progression.
Rachel Atkinson David Gyorki Cornelia Liedtke
Kyle Covington Cameron Johnstone Beate Litzenburger
Joan Garrett Alexandra Leary Ryan Hartmaier
Ritwik Ghosh
Avon Foundation-AACR International Scholars: For abstract presenters traveling from countries with emerging
economies.
Soo Ahn Mikiya Ishihara Yuri Urata
Pablo Arrieta-Joffe Osvaldo Pontiggia Benlong Yang
Mateus Barros Filho Mika Shirasu Jae Kyo Yi
Pradeep Chaluvally-Raghavan A. Marcell Szasz Guochen Zhang
Hirokuni Ikeda Satoru Tanaka
AACR Translational Research Scholars, funded by Susan G. Komen for the Cure®: For presenters of highly related
abstracts focused on translational breast cancer research.
Phillipe Bedard Melanie Seal Dipika Misra
Hui Gao Adel Tabchy Sarah Andres
Michail Ignatiadis Rinat Yerushalmi Michal Mego
Chann Lagadec Brent Rexer Amir Eitan
Todd Miller Xing Li Mi-Ran Choi
Ciara O’Brien Christina Yau Zhi Hu
Esther Reijm Tracey Martin Karsten Pilones
Dave Bhuvanesh Oleg Gluz Beatrix Elsberger
AACR Minority Scholars, funded by Susan G. Komen for the Cure®: For abstract presenters working within
the United States and within minority groups defined by the National Cancer Institute as being traditionally
underrepresented in cancer and biomedical research.
Mariana Chavez-MacGregor Kavitha Raj
Laura Gonzalez-Malerva Cesar Sanchez
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AACR Outstanding Investigator Award
The AACR Outstanding Investigator Award for Breast Cancer Research is presented to an investigator no more than 50 years
of age whose novel and significant work has had, or may have, a far-reaching impact on the etiology, detection, diagnosis,
treatment, or prevention of breast cancer. This award, now in its second year, is funded by Susan G. Komen for the Cure®.
Therapeutic Implications of the Molecular Portraits of Breast Cancer
Thursday, December 10, 11:30 am
Charles Perou, PhD
Lineberger Cancer Center, Chapel Hill, NC
Charles Perou, PhD, is an Associate Professor of Genetics and Pathology & Laboratory Medicine at the University
of North Carolina at Chapel Hill. Dr Perou is a member of the Lineberger Comprehensive Cancer Center, the
Carolina Center for Genome Sciences, and the Scientific Director of the UNC Genomics and Bioinformatics
Core Facility. He received his PhD in Cellular and Molecular Biology from the Department of Pathology at the
University of Utah (1996) where he cloned and characterized the human Chediak-Higashi syndrome gene. He
next performed his postdoctoral training in the laboratory of David Botstein at Stanford University (1997-2000)
where he began his genomic studies of human tumors using DNA microarrays. These genomic analyses resulted
in the identification of novel subtypes of human breast tumors that predict patient survival times and response
to therapy. Dr Perou’s laboratory at UNC is focused on using genomics, genetics, and animal models to decipher
the underlying biology of the molecular subtypes of breast cancer, and then using this biological information
to develop therapies that are specifically targeted against each of these distinct subtypes of breast cancer. He has identified at least
5 biologically distinct subtypes of breast tumor that are predictive of relapse, overall survival, and responsiveness to chemotherapy.
Dr Perou will receive his award and present a lecture entitled Therapeutic Implications of the Molecular Portraits of Breast Cancer
this morning at 11:30 am.
Brinker Awards Go to Researchers in Endocrine Therapy
Susan G. Komen for the Cure® Brinker Awards for Scientific Distinction
The Susan G. Komen for the Cure® Brinker Awards for Scientific Distinction are presented to basic and clinical researchers who
have made seminal advances in the fight against breast cancer. This year, the Brinker Awards will be presented to 1 clinical
researcher and 2 basic science researchers who have made significant contributions in the area of endocrine therapy.
Understanding SERM Actions in Breast Cancer
Thursday, December 10, 4:30 pm
Geoffrey L. Greene, PhD
The University of Chicago, Chicago, IL
Dr Green will receive an award for basic science research. Geoffrey L. Greene earned a PhD in chemistry
from Northwestern University in 1974, and came to the University of Chicago the same year as a
postdoctoral trainee in the Ben May Laboratory for Cancer Research. He joined the faculty as an assistant
professor in 1980 and became a professor in 1991. Currently, Dr Greene is the Virginia and D.K. Ludwig
Professor and associate director of the Ben May Department for Cancer Research, chair of the Committee
on Cancer Biology, associate director of the Cancer Research Center, and co-director of the Ludwig Center
for Metastasis Research at the University of Chicago. The overall goal of his research is to determine the
molecular mechanisms by which female steroid hormones regulate development, differentiation, cellular
proliferation, and survival in hormone-responsive tissues and cancers. Dr Greene has received a number
of prestigious awards for his research contributions, and serves on several national committees, as well as
journal editorial boards.

Issue 1, December 10, 2009
Brinker Awards Go to Researchers in Endocrine Therapy
Susan G. Komen for the Cure® Brinker Awards for Scientific Distinction (continued)
Genomics of Estrogen Receptor Signaling in Breast Cancer and Endocrine Resistance
Thursday, December 10, 4:45 pm
Benita katzenellenbogen, PhD
University of Illinois-Urbana Champaign, Urbana, IL
Benita S. Katzenellenbogen, PhD, will also receive an award for basic science research.
Dr Katzenellenbogen, PhD, is the Swanlund Professor of Molecular and Integrative Physiology,
Cell and Developmental Biology at the University of Illinois Urbana-Champaign. She is a world expert
on nuclear hormone receptors, especially on estrogen receptors and their actions in breast cancer.
Her work has elucidated fundamental aspects of structure-function relationships and mechanisms of
action of the estrogen receptors, and has provided a framework for the development of anti-hormonal
treatments that are used in breast cancer treatment and prevention. Dr Katzenellenbogen has trained
many young investigators who have gone on to successful careers, and she has served on many important
committees and review panels and as President of the Endocrine Society from 2000-2001. Her research
contributions have been recognized by multiple prestigious awards and honors from professional
societies and foundations.
Getting the Best Out of Neoadjuvant Therapy
Thursday, December 10, 5:00 pm
Professor Ian Smith
Royal Marsden Hospital, London, United Kingdom
Professor Ian Smith is Professor of Cancer Medicine at the Institute of Cancer Research and the Royal
Marsden Hospital, London, where he is also the Head of the Breast Unit. His principal research interests
have been in the biology and treatment of breast cancer and lung cancer, and in new drug development. He
was involved in the early clinical development of several successful anti-cancer drugs, including letrozole
and carboplatin. One of his main interests is in neoadjuvant and short-term preoperative treatments
and in the molecular changes associated with these therapies. He is Chief Investigator of 2 international
neoadjuvant endocrine therapy trials, IMPACT and IRESSA 223, and the UK Principal Investigator for
several international multicenter adjuvant trials, including HERA (trastuzumab), BIG1-98 (letrozole), and
ALTTO (lapatinib). He is the first chairman of the recently formed UK Breast Trials Intergroup and recent
past chairman of the British Breast Group. He has also been Chairman of several national professional
bodies, including the Association of the Cancer Physicians, the Royal College of Physicians Specialist Advisory Committee for
Medical Oncology, and the NCRI Lung Cancer Clinical Studies Group. He is a member of numerous international cancer societies
and has over 300 peer-reviewed publications.
13

14
Plenary Lectures to Address Epidemiology,
Molecular Biology, Immunology
Each day of the SABCS traditionally begins with a plenary lecture featuring a world-renowned researcher presenting a
definitive update on his or her field of interest. This year is no exception, with invited speakers who offer a very good reason
to get up early each morning.
On Thursday morning at 8:45 am, Valerie Beral, MD, will speak on An Epidemiological Perspective on the Causes and Prevention
of Breast Cancer. Dr Beral is the director of the Cancer Epidemiology Unit and a professor of epidemiology at the University
of Oxford. Her research has focused on the role of reproductive, hormonal, and infectious agents in cancer. She is principal
investigator for the Million Women Study, the largest study in the world investigating how a woman’s reproductive history can
affect her health.
On Friday at 9:00 am, William Sellers, MD, will discuss the role of the PI3K/Akt/mTOR pathway in cancer. Dr Sellers is currently
the vice president and global head of oncology for the Novartis Institute of BioMedical Research in Cambridge, Massachusetts.
mTOR is a cytoplasmic protein kinase that acts as a central regulator in cell proliferation, angiogenesis, and cell metabolism. It
represents an exciting potential therapeutic target because it is a key intracellular point of convergence for many important
signaling pathways located upstream from it. These pathways can be activated by various signaling proteins, including cell surface
growth factor receptors such as VEGFR, a number of which are abnormally activated in cancer.
Tyler Curiel, MD, will speak on Saturday at 9:00 am, assessing new paradigms in cancer immunology. Dr Curiel is the former
executive director of the Cancer Therapy & Research Center at the University of Texas Health Science Center at San Antonio.
In a landmark paper published in Nature Medicine in 2004, Dr Curiel and his team made the first definitive identification
of an “off switch” in human cancer, the specific recruitment of regulatory T cells to mediate the suppression of tumorassociated
antigen-reactive lymphocytes. He is considered one of the leading researchers in the study of immunopathological
mechanisms in human cancer.

Issue 1, December 10, 2009
Supporters
We are proud to acknowledge the following for their contributions to and generous support of
our program (at press time).
ANGEL PLUS
Abraxis Bioscience
Genentech BioOncology
GlaxoSmithKline
Lilly USA, LLC
Novartis Oncology
sanofi-aventis
ANGEL
Genomic Health, Inc.
Pfizer
PATRON PLUS
Amgen
AstraZeneca
Bristol-Myers Squibb
Merck Oncology
MAJOR SUPPORTER PLUS
Wyeth Pharmaceuticals
MAJOR SUPPORTER
Monogram Biosciences
Onyx
CONTRIBUTOR
bioTheranostics, Inc.
Carl Zeiss Meditec, Inc.
Eisai, Inc.
EMD Serono
Halo Breast Pap Test (Neomatrix)
HistoRx
Imclone Systems
IOS Press
CONTRIBUTOR (continued)
Ipsogen
Myriad Genetic Laboratories, Inc.
Research To Practice
SenoRx
Ventana Medical Systems, Inc.
A Member of the Roche Group
DONOR
Agendia, Inc.
American Express OPEN
AmeriPath, Inc.
Amoena USA Corporation
Aurora Imaging Technology, Inc.
Biocare Medical
Biopsy Sciences
Caris Diagnostics
Clarient, Inc.
Clinical Care Options
Clinical Oncology News
Combimatrix Molecular Diagnostics
CuraScript
CVS Caremark/CarePlus
Cytori Therapeutics, Inc.
Dako North America, Inc.
deCODE genetics
Diplomat Specialty Pharmacy
DXS Ltd
Endomagnetics Ltd
Faxitron X-Ray LLC
Gamma Medica-Ideas
Hologic
ImpediMed, Inc
Informed Medical Decisions, Inc.
SABCS gratefully acknowledges Susan G. Komen for the Cure® for generous support of AACR Outstanding Investigator Award for
Breast Cancer Research , CTCR-AACR San Antonio Breast Cancer Symposium Educational Sessions, AACR Translational Research
Scholars, and Minority Scholar Awards for Breast Cancer Research.
SABCS wishes to thank Avon Foundation for support of the Avon Foundation-AACR International
Scholar-In-Training Grants.
DONOR (continued)
IntraOp Medical Corporation
Leica Microsystems
Lippincott Williams & Wilkins
Medtronic
Milestone
Onco Inc.
Patient Advocate Foundation
PhenoPath Laboratories, PLLC
Physicians’ Education Resource
PRIME Oncology
R&D Systems, Inc.
RadPharm, Inc.
Siemens Healthcare Diagnostics
Springer
Sysmex America, Inc.
US Labs
US Oncology
Varian Medical Systems
Xceed Molecular
CONFERENCE GRANTS
American Cancer Society, Texas Division
National Cancer Institute
SERvICE IN kIND
Adjuvant, Inc.
AlphaMed Press/The Oncologist
Elsevier
Inter-American Breast Cancer Conference
The Oncology Group
15

Contributing Faculty Editor:
Gary C. Chamness, PhD
This newsletter is made possible with support from
Abraxis BioScience
The 2009 San Antonio Breast Cancer Symposium
(SABCS) is presented by the CTRC, AACR, and the
Baylor College of Medicine. The driving force behind
this collaboration is the shared mission of the organizations
to advance progress against breast cancer.
By combining their respective strengths, the San
Antonio Breast Cancer Symposium encompasses
the full spectrum of breast cancer research and facilitates
the rapid transition of new knowledge into
improved care for breast cancer patients.
Issue 1, December 10, 2009
Exhibitors
The following information was received too late for inclusion in the SABCS
Pocket Program.
Exhibitors Added
Clinical Oncology News .................................259
IOS Press .................................................................456
Patient Advocate Foundation ....................442
Exhibitor Correction
Lilly Oncology ............................................300/308
Lilly .............................................................................309
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