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90s Cancer Prevention/Epidemiology 1516 Poster Discussion Session (Board #5), Sun, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM PTEN germline mutations in patients first tested for other hereditary cancer syndromes: Would use of risk assessment tools have reduced health care costs? Presenting Author: Jessica Mester, Genomic Medicine Institute, Cleveland Clinic, Cleveland, OH Background: PTEN Hamartoma Tumor Syndrome (PHTS) includes patients with Cowden (CS) or Bannayan-Riley-Ruvalcaba syndrome (BRRS) with germline PTEN mutation. Breast, colon, endometrial cancer and GI polyposis are associated, creating overlap with Hereditary Breast and Ovarian Cancer (HBOC), Lynch (LS) and adenomatous polyposis syndromes (APS). We reviewed our PHTS patient series to find how often testing criteria for these syndromes were met or testing was pursued before PTEN. Methods: Patients were prospectively recruited by relaxed International Cowden Consortium criteria or presence of known germline PTEN mutation; mutations were identified by mutation scanning or MLPA analysis and confirmed by sequencing or quantitative PCR, respectively. Families were excluded if diagnosed with CS or BRRS before 1998, family history was unavailable, or proband was �18 yrs. Pedigree, genetic testing reports, and medical records were reviewed to determine if patients met HBOC testing criteria, Amsterdam II or Bethesda 2004 criteria, or had adenomatous polyps. Risk assessment was conducted for BRCA1/2 via the BRCAPRO, Myriad II, and Penn II models; for MLH1/MSH2/MSH6 via the PREMM1,2,6 and MMRPro models; and for PTEN via the Cleveland Clinic (CC) PTEN Risk Calculator. Results: 115 PTEN mutation-positive adult probands were identified among 3,405 patients. 53 (46.1%) met testing criteria for HBOC or LS and 34 (29.6%) underwent previous testing for HBOC, LS or APS. Average risk for BRCA1/2 and MLH1/MSH2/MSH6 mutations in tested patients were 7.5-16.9% and 33.1-41.4%, respectively; whereas PTEN mutation risks were 35.9% and 79.7%. No patient tested for APS (average PTEN mutation risk 73%) had �5 adenomas. An estimated $89,700 was spent on negative analyses for HBOC, LS and APS among patients ultimately found to have germline PTEN mutations. Conclusions: PHTS should be part of the differential diagnosis for patients referred for question of HBOC, LS or APS. Pathology review is key for patients with polyposis. Using the CC PTEN risk calculator enables clinicians to understand when PTEN mutation risk is high, allowing testing to proceed in a step-wise and cost-saving manner. 1519 Poster Discussion Session (Board #8), Sun, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Pathologic findings at risk-reducing salpingo-oophorectomy among women at increased ovarian cancer risk: Results from GOG-199. Presenting Author: Phuong L. Mai, National Cancer Institute, Rockville, MD Background: Although risk-reducing salpingo-oophorectomy (RRSO) is a standard management option for women with BRCA1/2 mutations, the lack of large, prospective cohort studies makes estimating the prevalence of cancer at RRSO problematic. Methods: GOG-199 is a large, nonrandomized multi-center trial which enrolled women at high-risk (due to BRCA mutations or strong family history) of ovarian cancer, comparing surgery at enrollment with serial transvaginal ultrasound and CA-125 screening. RRSO specimens were processed according to a standardized tissue processing protocol including 2-3mm sectioning of both ovaries and tubes. Results: 2,605 participants were accrued to GOG-199. Of the 1 030 enrolled in the baseline RRSO cohort, 28 were ineligible and 36 declined surgery after enrollment, resulting in 966 baseline RRSO. Pathology review demonstrated 4 tubal intraepithelial carcinoma and 20 serous pelvic cancers, of which 12 were identified only microscopically. Among the 20 serous cancers, the predominant or exclusive site of involvement was ovary in 10, fallopian tube in 5, and peritoneum in 5 cases. In addition, 6 endometrial cancers (among the 515 undergoing concomitant hysterectomy) and 3 adenocarcinomas suggestive of metastasis were identified. The serous pelvic cancer prevalence was: entire cohort�2.1% (20/966), all BRCA mutation carriers�3.2 (18/558), BRCA1 mutation carriers�3.7% (12/325), BRCA2 mutation carriers�2.6% (6/231), and mutationnegative�0.5% (2/402). Compared to those without cancer, women with serous pelvic cancer were older at surgery (p� .001), and more often menopausal (vs pre-menopausal, p� .002), nulliparous (vs parous, p�.04) and never users of tamoxifen (vs ever users, p� .04). Serous pelvic cancers were more frequent in BRCA mutation carriers (vs no mutation, p� .004), and among carriers, more common in those with BRCA1 mutations (vs BRCA2 mutation, p� .02). Conclusions: The prevalence of serous pelvic cancers in this cohort was 3.2% among carriers vs 0.5% among the mutation-negative but with a strong family history. Our data will be useful when counseling women at increased ovarian cancer risk who are contemplating risk-reducing surgery. 1518 Poster Discussion Session (Board #7), Sun, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Risk-reducing salpingo-oophorectomy and prophylactic mastectomy among BRCA mutation “previvors.” Presenting Author: Laura L. Holman, University of Texas M. D. Anderson Cancer Center, Houston, TX Background: We prospectively evaluated the timing and uptake of riskreducing surgery in a cohort of female BRCA mutation carriers that have no personal cancer history (“previvors”). Methods: Patients at high risk of breast and ovarian cancer were enrolled between 2007 and 2011 and followed in a high-risk ovarian cancer screening clinic. Women were offered risk-reducing salpingo-oophorectomy (RRSO) and/or prophylactic mastectomy (PM) per guidelines. Their clinical data were recorded and analyzed using descriptive statistics. Results: Of 260 BRCA mutation carriers enrolled, 73 have no personal history of cancer and are “previvors.” Patients have been followed for a median of 26.5 months (1-50 months). The median age is 38 years, 81.1% are white, 16.2% are Ashkenazi Jewish, and 79.7% are premenopausal. BRCA1 carriers account for 43.2% of participants and 55.4% have a BRCA2 mutation. The majority of patients (77.6%) presented for ovarian cancer screening �1 year after their BRCA testing. In all, 60.8% of women underwent prophylactic surgery: 28.4% chose RRSO, 18.9% chose PM, and 13.5% chose both procedures. Postmenopausal women were more likely to choose RRSO, while uptake for both procedures was common for premenopausal women (Table, p�0.04). RRSO was also more likely in parous than nulliparous premenopausal women (35.2% vs 9% p�0.001). PM was not associated with parity (p�0.79). Of women that had both surgeries, 20% had them concurrently and 20% had PM first. Of the 60% that underwent RRSO first, all had their second surgery within 14 months. Conclusions: BRCA mutation “previvors” have a high overall uptake of prophylactic surgery. Premenopausal women are more likely to choose PM than postmenopausal women; reasons for this are unclear. “Previvors” that choose RRSO and PM typically have both surgeries within a fairly short timeframe. With the growing population of “previvors” in the US, further study of patient preferences regarding preventative surgery and long-term consequences is needed. Surgery choices of pre- versus postmenopausal women. None RRSO PM RRSO�PM Premenopausal 35.6% 23.7% 22% 16.9% Postmenopausal 20% 46.7% 0% 6.7% 1520 Poster Discussion Session (Board #9), Sun, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM A multi-institution study of the accuracy of BRCAPRO in predicting BRCA1/BRCA2 mutations in women with ovarian cancer. Presenting Author: Molly S. Daniels, University of Texas M. D. Anderson Cancer Center, Houston, TX Background: 10-15% of ovarian cancer patients have a germline BRCA1 or BRCA2 mutation, with significant management implications for both patients and relatives. Genetic testing decisions are guided in part by the estimated likelihood of identifying a mutation. The BRCAPRO model uses personal and family history of breast and ovarian cancer to calculate the likelihood of a BRCA1/2 mutation. This study’s purpose was to assess the ability of BRCAPRO to accurately determine this likelihood. Methods: BRCAPRO scores were calculated using CancerGene v5.1 for 589 ovarian cancer patients referred for genetic counseling at three institutions. The study population was divided into quintiles by BRCAPRO score, with cutpoints chosen such that each quintile represented 20% of the sample. Chi-square goodness-of-fit test was used to compare observed BRCA1/2 mutations to the number predicted. ANOVA models were used to assess factors impacting BRCAPRO accuracy. Results: 180/589 (31%) ovarian cancer patients tested positive for a BRCA1/2 mutation. At BRCAPRO scores under 40%, more mutations were observed than expected (93 observed vs. 34.1 expected, p�0.001). If patients with BRCAPRO scores �10% had not been offered genetic testing, almost one-third of mutations (51/180, 28%) would have been missed. Multivariate analysis demonstrated that BRCAPRO underestimated risk for high grade serous ovarian cancers but overestimated risk for other histologies (p�0.0001), underestimation increased as age at diagnosis decreased (p�0.02), and model performance varied by institution (p�0.02). Conclusions: Ovarian cancer patients classified as low risk by BRCAPRO are more likely to test positive than predicted, therefore the BRCAPRO prediction could falsely reassure patients considering genetic testing. BRCAPRO performance could be improved by incorporating factors such as ovarian cancer histology. Alternatively, given the high prevalence of BRCA1/2 mutations in high grade serous ovarian cancer and the apparent limitations of using family history to predict mutation probability, BRCA1/2 genetic testing could be offered to high grade serous ovarian cancer patients regardless of family history. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
1521 Poster Discussion Session (Board #10), Sun, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Alcohol and breast cancer risk in postmenopausal women: The PLCO experience. Presenting Author: Roni Falk, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD Background: Moderate alcohol consumption is an established breast cancer (BC) risk factor. Invasive BC is a heterogeneous disease comprised of several histological subtypes with distinct biological features that suggest etiologic differences. Several studies show the alcohol link may be stronger for estrogen receptor-positive tumors (ER�/PR� and ER�/PR-) and for lobular BC. Few have evaluated the role of alcohol consumption by BC histology and hormone receptor status combined. Methods: We evaluated the risk of BC by baseline alcohol consumption in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial cohort (54649 participants, 1786 incident invasive breast cancers) by histology and hormone receptor status. Histologic subtype-specific associations were evaluated using a recently developed Cox proportional hazards model to calculate multivariate hazards ratios (HR) and 95% confidence intervals (CI). Results: 1444 ductal (81%), 233 lobular (13%) and 109 mixed ductal lobular (6%) cases were identified. The majority were ER�/PR� (ductal: 959 ER�/PR�, 136 ER�/PR-, 229 ER-/PR-; lobular: 179 ER�/PR�,37ER�/PR-, 6 ER-/PR-; mixed ductal/lobular: 88 ER�/PR�, 6ER�/PR-, 5 ER-/PR-). For ductal and lobular BC, risks for alcohol consumption were modestly elevated; compared to never drinkers, women consuming 7-14 drinks/week had a 40% increase in HR in both histologic subtypes. Risks for mixed ductal lobular cancer were significantly higher, particularly for women consuming 7-14 drinks per week (HR�3.0; 95% CI�1.5, 6.1). For all histologies combined, alcohol risks were confined to ER�/PR� cancers with HR�1. 6 (95% CI�1.3, 2.1) for women consuming 7-14 drinks/ week; p trend�0.0005. Similarly, for each histologic subtype, the risk for alcohol consumption was limited to ER�/PR� tumors, and notably, very few cases with pure lobular or mixed ductal lobular cancer were either ER�/PR- or ER-/PR-. Conclusions: Moderate alcohol consumption is associated with risk of ER�/PR� BC in each of the predominant histologic subtypes, but not with hormone receptor-negative cancer. Unlike other studies, we did not find a link between alcohol consumption and ER�/PR- BC. 1523 Poster Discussion Session (Board #12), Sun, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Genetic polymorphisms of the OPG gene associated with breast cancer. Presenting Author: Gunter Assmann, University Medical School of Saarland and Jose Carreras Research Center, Homburg, Germany Background: The receptor activator of NfkappaB (RANK) and osteoprotegerin (OPG) cascade system have been reported to play a role in the pathogenesis of breast cancer (BC). Genetic variations in the genes coding for RANK, RANK ligand (RANKL), and OPG are supposed to play a role in the susceptibility of breast cancer. Methods: In the present case-control study genomic DNA was obtained from 307 BC patients (age: median 56) and 396 healthy female controls (healthy blood donors, HC; age median: 45). We studied six single nucleotide polymorphisms (SNPs) in the genes coding for RANK (2 SNPs, rs1805034, rs35211496), OPG (2 SNPs, rs3102735, rs2073618), and RANKL (2 SNPs, rs9533156, rs2277438) using TaqMan assay-guided PCR for the respective SNPs. The genotype and allelic frequencies comparing BC with HC were analyzed with �2 test for 2x3 and 2x2 tables, respectively. Results: The genotype distributions as well as the allelic frequencies of the SNP rs3102735 in the OPG gene differed significantly (p�0.006 and p�0.019, respectively) between BC patients and HC; the genotypes containing the minor allele were more frequent in BC patients (table). In the OPG SNP rs2073618 the minor allele C was significantly less frequent in BC patients compared to HC (43.8 vs. 49.7%; OR: 0.788; p�0.031). In addition, BC patients carried less frequently the homozygous genotype of the minor allele compared to major allele (18.6 vs. 23.9%, p�0.083). No significant risk was detected for the other SNPs investigated in this study. Conclusions: This is the first study reporting a significant association of the SNP rs3102735 in the OPG gene with the susceptibility to develop BC in the Caucasian population. The minor allele C of OPG SNP rs2073618, however, seems to be protective against BC disease. The impact of the OPG SNP rs3102735 (location: 5�near region, chromosome 8q24) and of the OPG SNP rs2073618 (a missense SNP, leading to amino acid exchanges Leu3Asn) on the pathogenesis of BC are unclear. SNP Allele / genotypes Breast cancer Healthy females OR (95% CI) p value OPG rs3102735 n�614 (%) n�784 (%) Allele minor C 113 (18.4%) 102 (13.0%) 1.508 0.006 Major T 501 (81.6%) 682 (87.0%) (1.127-2.018) n�307 (%) n�392 (%) Genotype CC 10 (3.3%) 5 (1.3%) 0.019 CT 93 (30.3%) 92 (23.5%) TT 204 (66.4%) 295 (75.3%) Cancer Prevention/Epidemiology 91s 1522 Poster Discussion Session (Board #11), Sun, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Contribution of TP53 p.R337H mutation to breast cancer prevalence in Brazil. Presenting Author: Patricia Ashton-Prolla, UFRGS/HCPA, Porto Alegre, Brazil Background: The exact contribution of TP53 germline mutations, associated with Li Fraumeni Syndrome, to the overall burden of cancer is still only partially known. Studies in Southern and Southeastern Brazil have shown that a specific germline mutation at codon 337 (c.1010G�A; p.R337H), has incomplete penetrance and may be present in a significant number of subjects (estimated frequency at the populational level of 1:300 individuals). In an exploratory approach, the aim of the study is to assess the frequency of the p.R337H mutation in women from different Brazilian regions, diagnosed with breast cancer (BC) before 46 and after 55 years of age, and unselected for family history of cancer. Methods: Formalin-fixed paraffin-embedded (FFPE) non-tumoral tissue (lymph nodes or normal breast) of women diagnosed with BC between 2000 and 2010 in 3 pathology laboratories from the Brazilian cities of Porto Alegre, São Paulo and Barretos were obtained retrospectively and analyzed after anonimization. Genomic DNA was isolated with standard methods and genotyping performed in duplicates by qPCR (TaqMan assay). Confirmation of all mutation-positive and a sample of mutation-negative cases were done by TP53 exon 10 sequencing or by a second independent qPCR analysis. Results: Analysis of 515 BC-affected women identified the p.R337H mutation in the germline of 70 (8,6%) cases: 49/403 (12,1%) diagnosed before 46 years and 21/412 (5,1%) diagnosed after 55 years. BC occurred earlier in p.R337H mutation carriers than in non-carriers (p�0.001). Conclusions: Preliminary analysis in a sample of women with BC indicates that p.R337H founder mutation is present in a high proportion of cases, especially those diagnosed at a young age. Regional genetic background and recruitment strategies may account for the different mutation frequencies observed in the centers of study. The occurrence of this mutation at such a high frequency in a particular geographic region has important implications for disease management and cancer risk counseling for these patients and families. This mutation likely contributes to a significant proportion of the health burden associated with BC in Brazil. Financial support: FIPE-HCPA, CAPES, FAPERGS and Glaxo Smith Kline. 1524 Poster Discussion Session (Board #13), Sun, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Breast cancer intrinsic subtypes by PAM50 in older women. Presenting Author: Emily Oldham Jenkins, University of North Carolina Lineberger Comprehensive Cancer Center, Chapel Hill, NC Background: Breast cancer (BC) incidence dramatically increases with age and the number of older BC patients (pts) in the U.S. is rising. Although immunohistochemical (IHC) data confirm that the incidence of luminal BC increases with age while the incidence of triple negative (TN) BC decreases, age-specific data on the frequency of BC subtypes defined by gene expression is limited. We characterized the incidence of BC intrinsic subtypes using gene microarrays according to age. Methods: Data from 2,150 pts were pooled from publicly available microarray datasets to determine the incidence of PAM50 breast cancer intrinsic subtypes (Luminal A [LumA], Luminal B [LumB], HER2-enriched [Her2E], Basallike [Basal] and Normal-like [Norm]) by age. Adjuvant treatment data (none, chemotherapy, endocrine therapy or both) were available for 1,741 samples. Relapse-free (RFS) and overall survival (OS) differences were determined using the Kaplan-Meier method. Results: PAM50 intrinsic subtypes by age are tabulated below. The incidence of luminal (A, B, A�B) tumors increased with age (p�0.01, p�0.0001, p�0.0001, respectively), while the percentage of basal tumors decreased (p�0.0001). Basal tumors represented 13% of pts aged � 70 years (yrs); of the 70% with available IHC data, 74% were TNBC. Age as a continuous variable was not associated with RFS (p � 0.37). Subtype alone (n�2031), and after controlling for treatment (n�1645), was significantly associated with RFS (both p�0.0001). The addition of age to a multivariate analysis added no prognostic information. Conclusions: Though more favorable subtypes increase with age, older BC pts still have a substantial percentage of high-risk subtypes. Age alone was not a significant factor in outcome. Tumor biology as defined by intrinsic subtype is an important clinical predictor. PAM50 intrinsic subtypes by age. Age (total n�2150)
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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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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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Yasuda, Hiromi e14029 Yasuda, Hiroy
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Zhang, Xinmin e16022 Zhang, Xu Dong
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