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96s Cancer Prevention/Epidemiology 1543 General Poster Session (Board #1G), Sat, 1:15 PM-5:15 PM Breast cancer in Irish families with Lynch syndrome. Presenting Author: Emmet Jordan, Mater Misericordiae University Hospital, Dublin, Ireland Background: Breast cancer is not among the recognised malignant manifestations of Lynch Syndrome which include colorectal, endometrial, gastric, ovarian and upper urinary tract tumours. In this study we report the prevalence of breast cancer in Irish Lynch Syndrome families and determine immunohistochemical (IHC) expression of mismatch repair proteins (MMR) in available breast cancer tissue. Methods: Breast cancer prevalence was determined among Lynch Syndrome kindreds from two institutions in Ireland. One kindred was omitted due to a biallelic MMR and BRCA1 mutation.The clinicopathological data that was collected on breast cancer cases included age of onset, morphology, and hormone receptor status, and a genotype phenotype correlation was investigated. Immunohistochemical staining was performed for MLH1, MSH2, MSH6, and PMS2 on all available breast cancer tissue from affected individuals. Results: The distribution of MMR mutations seen in sixteen pedigrees were as follows; MLH1 (n�5), MSH2 (7), MSH6 (3), PMS2 (1). Sixty cases of colorectal cancer and 14 cases of endometrial cancer were seen. Seven breast cancers (5 invasive ductal and 2 invasive lobular cancers) and 1 case of ductal carcinoma in situ were reported in 7 pedigrees. This compared with 4 cases of prostate cancer. Of the 7 LS kindreds containing breast cancer, 6 MSH2 mutations and 1 MSH6 mutations were identified. Median age of breast cancer diagnosis was 49 years (range 38-57). Hormone receptor status is available on 3 breast cancer cases at time of abstract submission; all were ER positive and HER 2 negative. All cases had grade 2 or 3 tumours. 5 samples were available for IHC evaluation. 3 out of 5 cases showed loss of MMR expression, all showed loss of MSH2 and MSH6 expression. One of the two cases with normal IHC expression in breast tissue belonged to a kindred where 3 siblings with colorectal cancer and documented deleterious mutations demonstrated no IHC loss. Conclusions: Breast cancer occurred at an early age and was more common than prostate cancer in Irish Lynch Syndrome pedigrees. All identified breast cancer were in kindreds with MSH2 or MSH6 mutations. Enhanced breast cancer screening may be warranted in certain Lynch Syndrome kindreds. 1545 General Poster Session (Board #2B), Sat, 1:15 PM-5:15 PM BRCA carrier status as an independent prognostic factor associated with earlier biochemical relapse in local prostate cancer. Presenting Author: Elena Castro, The Institute of Cancer Research and The Royal Marsden NHS Foundation Trust, London, United Kingdom Background: Biochemical relapse after local treatment for prostate cancer (PCa) indicates recurrent disease and is associated with shorter survival. Germline BRCA mutations are associated with worse PCa outcomes. BRCA carriers are currently treated with the same protocols used for non-carriers. We analyzed biochemical-progression free survival (bPFS) after conventional treatment for localized PCa in a cohort of BRCA patients (pts). Methods: In this retrospective case-control study, each BRCA carrier (9 BRCA1 and 34 BRCA2) treated with radical prostatectomy (RP) or external beam radiotherapy (RT) was matched with 3 non-carriers (NC) by age at diagnosis (�5 yrs), TNM stage, Gleason score, presenting PSA, local treatment , androgen-deprivation therapy (ADT) and year of treatment (�3 yrs). All NC were screened for BRCA1 and BRCA2 mutations. Biochemical failure was reviewed according to ASTRO and NCCN criteria. The Kaplan- Meier method and a multivariate Cox regression model adjusted by matching factors were employed. Results: 172 pts were included. Median follow-up was 76 months (ms). Median age at diagnosis was 58 yrs (43-75). Tumour stages were I 11%, IIA 19%, IIB 28%, III 28%, IV 14%. 80 pts received RT (18 BRCA2, 5BRCA1, 57NC) and 85% also received ADT (70% for �6 months). 92 pts underwent RP (16 BRCA2, 4 BRCA1 and 72 NC), and 9% of them received ADT (�6months). Overall, median bPFS was 71ms. For those treated with RT, median bPFS was 65ms in NC vs 39ms in BRCA carriers (p�0.023). bPFS was not affected by ADT duration. Median bPFS after RP was 65ms in BRCA carriers. No difference was observed in 3yrs-bPFS between BRCA carriers and NC (73% vs 76%). The adjusted MVA confirmed the independent prognostic value of tumour stage (p�0.004) and BRCA status (p�0.032) for bPFS. Among BRCA carriers, the risk was greater when the analysis was limited to BRCA2 pts (p�0.013, HR 2.1,.95%CI 1.2-3.7). Conclusions: Our results suggest that BRCA carriers with PCa have worse local disease control than NC when treated with RT, regardless of ADT duration. No differences in bPFS were observed in pts treated with RP after �6 yrs median follow-up. These results may have implications for tailoring clinical management for these patients. 1544 General Poster Session (Board #2A), Sat, 1:15 PM-5:15 PM Cost sharing and hereditary cancer risk: Predictors of willingness-to-pay for genetic testing. Presenting Author: Jennifer Madeline Matro, Fox Chase Cancer Center, Philadelphia, PA Background: The increasing availability of genetic testing (GT) in cancer (CA) care has been paralleled by increasing cost-sharing practices by payors that are intended to reduce overuse of health care services. Patients referred for hereditary CA risk assessment may be subject to financial deterrents such as high out-of-pocket (OOP) costs. Little is known about what factors may influence high-risk patients’ willingness-to-pay (WTP) for GT. Methods: The Gastrointestinal (GI) Tumor Risk Assessment Registry includes individuals referred for evaluation of genetic CA risk based on personal and/or family hx. At enrollment, participants complete a survey collecting detailed demographic, CA hx, and psychosocial items related to CA risk. Baseline data on 406 participants were available; 21 who did not respond to WTP items were excluded. WTP items included intention for: GT only if paid by insurance; GT even if paid by self; and amount WTP (7 levels, $25 to $2000). Multivariable models examined predictors of WTP (self vs only if paid by insurance) (model 1, logistic), and predictors of amount WTP (model 2, ordinal logistic, 5 levels). All statistical tests are two-sided (��0.05). Results: Most participants were women (73%), white (92%) and aged 45-64 (58%). 51% had � 4 yr college degree; 22% had household income �$75,000; 42% had hx of GI CA; 56% had � 11st degree relative (FDR) with colorectal CA (CRC). Overall, 82 (21.3%) were willing to have GT only if paid by insurance, and 303 (78.7%) were WTP OOP. Of those WTP, 271 (89%) stated an amount. Independent predictors of WTP (model 1) were: 1) expectation of positive result, 2) confidence to control CA risk, 3) fewer perceived barriers to CRC screening and 4) benefit of guiding screening (all p�0.05). Subjects WTP a higher amount (model 2) were male, more educated, and had greater CA worry, fewer FDR with CRC (all p�0.05), and more positive attitudes toward GT (p�0.01). Conclusions: Patients who are WTP some OOP costs for GT anticipate benefits to control of CA risk afforded by GT. Women and less educated patients may face greater barriers from high co-pays. Identifying patient-level factors associated with WTP for genetic services is increasingly important as GT is integrated into routine CA care. 1546 General Poster Session (Board #2C), Sat, 1:15 PM-5:15 PM Comparison of BRCA1/2-positive and -negative women diagnosed with metachronous breast and ovarian cancers. Presenting Author: Amanda C. Brandt, University of Texas M. D. Anderson Cancer Center, Houston, TX Background: After a primary breast cancer (BC) or ovarian cancer (OC) diagnosis, women have a risk to develop a second primary cancer, significantly more so in women with a BRCA gene mutation. The objective was to evaluate characteristics of BRCA positive and negative women diagnosed with metachronous BC and OC. Methods: Women with metachronous BC and OC were identified at the University of Texas MD Anderson Cancer Center. BRCA test results, age at diagnosis of both BC and OC, first degree relatives (FDR) with BC and/or OC, total relatives affected, and histopathologic tumor features were obtained from a prospectively maintained research database. Univariate and logistical regression analyses were performed. Results: A total of 64 women with metachronous primary cancers underwent BRCA genetic testing. Of the 45 BRCA positive women, 36 (80%) were diagnosed with BC (mean 40 years) prior to OC and 9 (20%) were diagnosed with OC first (mean 47 years). Of the 19 BRCA negative women, 10 (53%) were diagnosed with BC first (mean 63 years), and 9 (47%) diagnosed with OC first (mean 48 years). Women diagnosed with BC first were more likely to be BRCA positive than women diagnosed with OC first (p�0.03). Patients with a FDR with BC were more likely BRCA positive than women without family history (p�0.0062). Patients with PR negative BR (p�0.0199) or triple negative (TN) BC (p�0.0139) were more likely to test BRCA positive. High grade ovarian carcinomas approached significance (p�0.053) in BRCA positive when compared to BRCA negative cohort. Ethnicity, total number of affected relatives with BC or OC, ER status, Her2 status, and nuclear grade were not statistically significant between the two groups. Conclusions: Women with OC preceding their BC with lack of family history of BC and OC are significantly less likely to test BRCA positive. BC is often the sentinel cancer in women with a BRCA mutation compared to BRCA negative women with metachronous BC and OC. This should be considered during the risk assessment to more accurately estimate the chance of identifying a BRCA mutation in women with metachronous BC and OC. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
1547 General Poster Session (Board #2D), Sat, 1:15 PM-5:15 PM Features of familiality in a cohort of patients (pts) with sarcoma. Presenting Author: Georgios Lypas, Dana-Farber Cancer Institute, Boston, MA Background: Sarcomas occur in a number of cancer predisposition syndromes, yet genetic evaluation is rarely recommended for sarcoma pts. We broadly reviewed the family cancer histories of unselected pts in a tertiary center sarcoma clinic to explore the potential relevance of genetic assessment. Methods: Between 2005 and 2008, 397 pts (median age 52 years) with documented sarcoma who consented to research use of medical records and tissues also completed a family history questionnaire. Patient and family histories were reviewed for features suggesting hereditary risk (e.g. early age at diagnosis or familial clustering of certain associated diagnoses). Results: A family history of malignancy was noted in 301 of 397 pts (76%). Seventy-six pts (19%) were diagnosed with 99 additional malignancies, most frequently breast cancer (n�23), prostate cancer (12), melanoma (12), thyroid cancer (6) or a second sarcoma (10). Sarcoma was diagnosed prior to or synchronously (within 6 months) with another malignancy in 20 pts and metachronously in 56 pts. In 18 pts, sarcoma arose within a prior radiation field. Thirty-seven pts (9%) had a sarcoma subtype associated with a recognized syndrome: desmoid fibromatosis (n�16), malignant peripheral nerve sheath tumor (11), PEComa/ angiomyolipoma (6), retinoblastoma (3), and GIST with paraganglioma (1). Based on additional features, the associated syndromes were confirmed in 6 of them (1.5% of the cohort): familial adenomatous polyposis (n�1), neurofibromatosis type 1 (2), familial retinoblastoma (2), and Carney- Stratakis dyad (1). Thirty-three pts (8% of the cohort, or 16% of pts age �50) fulfilled TP53 testing criteria (Chompret, Birch or classical Li- Fraumeni Syndrome [LFS] criteria). Another 147 pts (37% of the entire cohort) did not fulfill LFS testing criteria, but were diagnosed with sarcoma before age 50 and had at least one first or second degree relative with a diagnosis of malignancy before age 50. Conclusions: Sarcomas are rare and diverse cancers. Given the potential association with cancer predisposition syndromes, genetic evaluation should be strongly considered in sarcoma pts based on age at diagnosis, histology, and family cancer history. 1549 General Poster Session (Board #2F), Sat, 1:15 PM-5:15 PM Predictors of contralateral prophylactic mastectomy among patients with ductal carcinoma in situ (DCIS) who underwent evaluation for BRCA genetic testing. Presenting Author: Nisreen Elsayegh, University of Texas M. D. Anderson Cancer Center, Houston, TX Background: Patients with DCIS are at increased risk for developing contralateral breast cancer (CBC). Therefore, an increasing number of women with DCIS are electing for contralateral prophylactic mastectomy (CPM). In a previous study involving 2072 women with DCIS, 13.5% chose CPM. In this study, we aimed to evaluate factors associated with CPM in patients with DCIS who underwent genetic counseling for BRCA. Methods: 165 women with pure DCIS, who underwent genetic counseling, were included in the study. Patients’ characteristics were obtained from a prospectively maintained research database at UT M.D. Anderson Cancer Center. Univariate and multivaraite logistic regression analysis were used to determine predictive factors associated with CPM. Patients’ characteristics included age, marital and educational status, tumor markers, nuclear grade, family history with breast (BC) and ovarian cancer (OC), race, Ashkenazi Jewish ancestry, and BRCA genetic test results. Results: Out of 165 patients, 17(10.3%) were found to have a BRCA deleterious mutation. 44(26.7%) underwent CPM. Younger patients (median � 45 yr) were more likely to elect for CPM than older patients (p� 0.0098). Patients who tested positive for a BRCA mutation were more likely to elect for CPM than those who tested negative or were not tested (p� 0.0001). Patients who had a family history of OC (15 (57.7%) were more likely to choose CPM than those who did not (p� 0.0004). These three factors remained significant in the multivariate model (p �0.008). Marital and educational status, tumor markers, nuclear grade, and family history of breast cancer were not significant predictors of CPM. Conclusions: The rate of CPM in patients with DCIS is high. Factors associated with increased likelihood of undergoing CPM include family history of OC, age, and BRCA positivity. Further studies are needed to evaluate patients perception of CBC risk, and if this may play a role in the high number of CPM. Cancer Prevention/Epidemiology 97s 1548 General Poster Session (Board #2E), Sat, 1:15 PM-5:15 PM Analysis of mutations in formalin-fixed paraffin-embedded (FFPE) tumor samples from two phase II clinical trials using a Sequenom-based approach. Presenting Author: Maria Orr, AstraZeneca, Macclesfield, United Kingdom Background: Analysis of tumour samples for biomarker discovery, personalised health care and disease stratification is becoming increasingly important. Methods to detect somatic mutations are often limited by the requirement for a significant amount of input DNA, low sensitivity or low sample throughput. The aim of this work was to obtain a comprehensive mutation profile of tumour samples taken from patients enrolled on two Phase II clinical trials. A Sequenom based approach was used to determine mutation profiles for the samples so that these could be correlated with response at some future date. Methods: After successfully piloting the Sequenom MassArray 4 platform on formalin fixed paraffin embedded (FFPE) tumour samples and tumour cell line admixes, we ran an exploratory analysis of 177 melanoma and 230 non small cell lung cancer (NSCLC) FFPE samples collected from two phase II clinical trials. DNA was extracted from the FFPE samples using the QIAmp DNA FFPE Tissue Kit (Qiagen). We designed a panel of 86 assays in 14 genes covering approximately 160� mutations. Mutations were chosen based on mutation frequency and biological significance in these tumour types. Results: Using this approach we were able to detect concomitant mutation profiles in a significant percentage of samples using only approximately 20uL of FFPE DNA (500 copies/�L average). Mutation status concordance was over 97% in BRAF and KRAS when compared to data generated via other approaches (sequencing, ARMS). Conclusions: Using Sequenom to screen tumour material, collected during clinical trials, is a feasible, rapid and comprehensive approach. Such an approach can be used to identify mutation profiles which correlate with patient response, potentially identify further patient stratification and help generate new hypotheses for further exploration. 1550 General Poster Session (Board #2G), Sat, 1:15 PM-5:15 PM Profiling uptake of single site testing (SST) for familial cancer (CA) risk in an administrative genetic testing database. Presenting Author: Michael J. Hall, Fox Chase Cancer Center, Philadelphia, PA Background: Among the anticipated social and cost-saving benefits to identifying a mutation in a CA predisposition gene in an individual is the subsequent opportunity to perform SST in close relatives to confirm risk status and to guide risk-reducing interventions. Despite ample research into uptake of primary genetic testing for Lynch syndrome (LS) and hereditary breast ovarian syndrome (HBOS) among moderate- and high-risk individuals, few studies have focused on the resultant cascade of SST that is predicted to follow in families. Methods: Administrative data on 2,631 consecutive single-site mutation tests performed over a 3-month interval (12/1/10-2/28/11) were obtained from a commercial genetic testing database maintained by Myriad Genetic Laboratories. 14 subjects (29 tests) were excluded due to multiple entries. Demographic, personal/family history (hx), and provider data are collected on a Test Requisition Form included in kits. All statistical tests are 2-sided (��0.05). Results: Women had SST more often than men (HBOS 82.8%; LS 65.5%). Mean age at time of SST was 42.7 yrs, and was higher for HBOS than LS (p�0.01). Among subjects with hx of CA, mean age at CA diagnosis (dx) was similar (HBOS 48.6; LS 48.7 yrs). Subjects reported CA in �1 relatives (range 1-16) with a mean age at dx 40.1 yrs. Compared to HBOS, those tested for LS were more likely to report CA in a 1st degree relative (81.3 vs 74.4%, p�0.001) and a lower age of youngest CA dx in the family (p�0.001). Non-European ancestry was more common for HBOS SST than LS (30.0 vs 24.8%) (p�0.05). SST positive test rate was no different by syndrome or ancestry, but was higher for men (47.5 vs 42.0%, p�0.02). Conclusions: Uptake of commercial SST in high-risk families is uneven by age, sex, ancestry and CA syndrome. While between-syndrome variability in CA risks may explain some differences, more research is needed to understand barriers to uptake of SST among at-risk individuals if CA prevention goals are to be realized. Characteristics of 2,602 subjects undergoing SST for familial CA risk. % Sex F 79.5 M 20.5 Cancer Hx Y 19.9 N 71.6 Unreported 8.5 Ancestry European 70.5 Other 29.5 Syndrome (genes) HBOS (BRCA1/2) 82.7 LS (MLH1/MSH2/MSH6) 13.1 Other 4.2 Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
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Volume 30, Issue 15S, Part I of II
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Editor: Michael A. Carducci, MD Man
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Volume 30, Issue 15S Supplement to
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Letter from the Editor The 2012 ASC
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JOURNAL of CLINICAL ONCOLOGY ......
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ASCO Conflict of Interest Policy an
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2012 ASCO Annual Meeting Proceeding
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Author Index Note: Numerals refer t
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Alexanian, Raymond 8093 Alexeev, Bo
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Arkenau, Hendrik-Tobias 2540, 3000,
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Ballen, Karen K. 6606, 6617, 6618,
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Ben-Aharon, Irit 548, 2556, e13080
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Blancas, Isabel e11535, e11545, e21
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Brandes, Johann Christoph 7048, 106
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Cakir, Betul 9567 Calabek, Bernadet
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Ceraulo, Domenica 4017 Cerbone, Lin
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Chinen, Ludmilla T.D. e16046 Chinen
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Come, Steven E. 9071, 9100 Comis, S
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Dahlheimer, Tambra 2546 Dahmane, El
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DeLacure, Mark D. e16052 Delage, Ju
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Domingo, Gelenis 6568, 6575, 6588 D
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El Sherbeiny, Esam e15129 El-Deiry,
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Fayad, Luis 6501, 8067 Fayette, Jer
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Foroni, Chiara e11546 Foroni, Letiz
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Gang, Wu 7091, e14511 Gangaram, Anj
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Gimenez Capitan, Ana 4068, 10596, e
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Granowetter, Linda 9537 Grant, Barb
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Hainsworth, John D. 618, 1018, 1086
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Heerschap, Arend e13111 Heersink, M
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Hong, Seung-Mo 3568 Hong, Sook Hee
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Im, Young-Hyuck 598^, 644, TPS649,
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Ji, Yongling e17527 Jia, Jingquan e
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Kaparelou, Maria 583 Kapaun, Christ
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Kim, Chan Kyu e14688 Kim, Chang Won
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Komatsu, Yoshihiro e14689 Komatsu,
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Laack, Nadia N. 2032, e14507 Laadem
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Lee, Ji-Hyun TPS3114, 6100 Lee, Jih
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Lim, Kian-Huat e14584 Lim, Kiat Hon
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Loupakis, Fotios 3518, 3540, 3546,
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Man, Shan e11061, e15177^ Manaloor,
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Mathieu-Nicot, Florence e19623 Math
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Mergenthaler, Hans-Guenther e15026
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Molero, Xavier e21035 Moles-Moreau,
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Munoz-Sanchez, MM e19590 Munsell, M
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Ng, Daniel e15050 Ng, Dawn Marie e1
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Oguri, Senri 5556 Oh, Do Youn 1003
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Palassini, Elena 10026, 10053, 1006
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Peisker, Uwe 10600 Peker, Deniz e18
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Piwnica-Worms, Helen 3047 Pizzo, Fa
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Rabinowits, Guilherme 5501, 5582, 9
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Reyes-Rivera, Irmarie CRA3503 Reyna
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Rose, Steven C. 3590 Rosell, Rafael
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Schenkein, David P. 6606 Schepp, Wo
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Sha, Dan 3564 Sha, Huifang e13528 S
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Silva, Jose D. 5567 Silva, Milton J
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Sousa, Carlos Eduardo Pires 643 Sou
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Tan, Chee Seng 1064, e19523 Tan, Ch
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Uchiyama, Tomotaka e21108 Udovitsa,
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Wang, Yuan e15124 Wang, Yunfei 547
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Wischnewsky, Manfred 1078 Wischnik,
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Zhang, Xinmin e16022 Zhang, Xu Dong
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