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94s Cancer Prevention/Epidemiology 1535 Poster Discussion Session (Board #24), Sun, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Genetic sequence variant (GSV) in TERT-CLPTM1L (5p15.33 locus) and survival in platinum-treated stage-IV non-small cell lung cancer (NSCLC). Presenting Author: Abul Kalam Azad, Ontario Cancer Institute, Princess Margaret Hospital, Toronto, ON, Canada Background: Lung cancer is a leading cause of cancer-related mortality in North America. Besides tobacco smoking, inherited genetic factors can also influence the development of lung cancer. These genetic factors may lead to biologically distinct subsets of cancers that have different outcomes. We evaluated whether GSVs associated with lung cancer risk are also associated with overall survival (OS) and progress free survival (PFS) in platinum-treated stage-IV NSCLC patients. We chose this subset of patients with lung cancer because they are uniformly treated and followed up at our institute (Princess Margaret Hospital). Methods: A total of 32 candidate GSVs in 21 genes previously reported to be associated with lung cancer risk were genotyped in 188 platinum-treated NSCLC stage-IV patients. Illumina Custom GoldenGate Genotyping Panel was used for the genotyping assay platform. Multivariate Cox proportional hazard models adjusted for the potential clinical prognostic factors were generated for OS and PFS. Results: Median age is 60 yr (range: 31-81); 73% with adenocarcinoma. Median follow-up time is 27 mo; median OS is 16 mo and PFS is 8 mo. The top significant GSV was rs4975616 (g.1315660G�A) in telomerase reverse transcriptase (TERT) and cleft lip and palate transmembrane 1-like (CLPTM1L) gene on chromosome 5p15.33. The adjusted hazard ratio (aHR) for OS was 0.76 (95% CI: 0.58-0.99; p�0.04) and for PFS aHR was 0.70 (95% CI: 0.55-0.90; p�0.005) for each protective allele, respectively. This GSV has previously been associated with lung cancer risk in genome-wide association study (PMID: 19654303). Conclusions: The TERT-CLPTM1L:rs4975616 GSV is not only a risk factor for lung cancer but also is associated with survival in patients with stage-IV NSCLC treated with platinum based chemotherapy. GSVs may be able to define subsets of patients with different risk and prognosis of NSCLC. Future studies should evaluate whether this GSV is predictive or prognostic. 1537 General Poster Session (Board #1A), Sat, 1:15 PM-5:15 PM Correlation of breast cancer risk in European BRCA2 mutation carriers with birth cohort. Presenting Author: Muy-Kheng Maria Tea, Medical University of Vienna, Department of OB/GYN, Division of Senology, Vienna, Austria Background: Mutations in the Breast Cancer Gene 1 (BRCA1) and Breast Cancer Gene 2 (BRCA2) lead to an elevated risk of developing breast (BC) and ovarian cancer (OC). However, risk estimates vary, depending on the study population. Furthermore, there are indications that birth cohort can influence the cancer risk. We investigated the risks for BC and OC associated with BRCA2 mutations in a cohort of female mutation carriers of a genetically heterogeneous central European population who were identified by molecular genetic testing in our institute. Methods: This study included 171 Caucasian women from Austria who underwent genetic counseling and where molecular genetic analysis identified a mutation in the BRCA2 gene at the Medical University of Vienna, Division of Senology, in Austria. A total of 57 healthy and 114 affected BRCA2-carriers were detected. The risk was estimated using the product limit method. The log rank test was used to compare different strata. Results: The risk of developing cancer to age 70 was found to be 85% for BC (95% CI 77–93%) and 31% for OC (95% CI 16–46%) in our BRCA2 study population. Female BRCA2-carriers born in 1958 or later were at a significantly higher risk of developing BC (p�0.001; 88% vs. 46% to age 40) but not of OC (p is not significant; 0% vs. 2% to age 40) compared to mutation carriers born earlier. Conclusions: We conclude that female BRCA2 mutation carriers should also be counseled about their cohortdependent cancer risk, especially for breast cancer. Further research about variables that may affect cancer risk like lifestyle-related factors should be considered. 1536 Poster Discussion Session (Board #25), Sun, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Second malignant neoplasms (SMN) among 18,627 testicular cancer survivors (TCS) after chemotherapy (CHEM) or surgery (SURG). Presenting Author: Chunkit Fung, James P. Wilmot Cancer Center, University of Rochester School of Medicine and Dentistry, Rochester, NY Background: Increased risks of SMN after radiotherapy (RT) for testicular cancer (TC) are well established. Few population-based studies, however, have focused on SMN risk among a contemporary group of TCS managed initially with non-RT approaches, including CHEM. Methods: Standardized incidence ratios (SIR) of SMN stratified by site and time since TC diagnosis were calculated for 18,627 TCS reported to the SEER program (1980- 2008) who initially had CHEM (n�8,058) or SURG (n�10,569) alone without RT, with each cohort accruing 65,398 and 92,681 person-years (PY) of follow-up respectively. Results: After CHEM, significantly increased risks of solid cancers (n�154; SIR 1.3; 95% CI 1.1-1.5; absolute excess risk (AER) 5.4 per 10,000 PY) and leukemias (n�18, SIR 3.9; 95% CI 2.3-6.1; AER 2.0) were observed. Solid cancer risk remained elevated for � 20 yrs, whereas excess leukemias were concentrated within 10 years after diagnosis. SIRs for solid cancers during the �1, 1-4, 5-9, 10-14, 15-19, and 20� yr periods were 2.0 (95% CI 1.03-3.5), 1.4 (95% CI 0.97-2.0), 0.8 (95% CI 0.5-1.2), 1.3 (95% CI 0.9-1.8), 1.6 (95% CI 1.05-2.2), and 1.5 (95% CI 0.95-2.2) respectively (P-trend 0.5) whereas SIRs for leukemia were 3.2, 9.9 (P�0.05), 2.6, and 2.3 respectively, with no cases reported in the latter 2 intervals. Median latencies to the development of solid cancers and leukemia were 12.5 yr (0.1-28) and 2.5 yr (0.1-14) respectively. Increased site-specific risks were apparent for cancers of liver (SIR 1.9; 95% CI 0.6-4.4); pancreas (SIR 2.1; 95% CI 0.8-4.6); soft tissue (SIR 4.9; 95% CI 2.1-9.7); bladder (SIR 1.9; 95% CI 1.02-3.3); kidney (SIR 2.6; 95% CI 1.4-4.3); brain/CNS (SIR 1.8; 95% CI 0.7-3.7), and thyroid (SIR 3.9; 95% CI 2.1-6.6). Secondary leukemias included 16 non-lymphocytic and 2 lymphocytic leukemias. In contrast, among TCS managed initially with SURG alone, no excess solid cancers were observed (n�198; SIR 1.0; 95% CI 0.8-1.1), albeit an increased risk of leukemia (n�15; SIR 1.9; 95% CI 1.1-3.2, AER 0.8) was seen. Conclusions: Future analytic studies should further evaluate the sitespecific risks of SMN after modern CHEM for TC and the baseline risk among patients managed with non-cytotoxic approaches. 1538 General Poster Session (Board #1B), Sat, 1:15 PM-5:15 PM Identification of new susceptibility genes in familial breast cancer by exome sequencing. Presenting Author: Henry T. Lynch, Creighton University, Omaha, NE Background: Familial breast cancer was described in the early 1970s with its syndromy confirmed by the discovery of BRCA germline mutations in the 1990s. BRCA mutations account for less than 10% of affected families. Efforts made in the past two decades have resulted in limited results in identifying additional susceptibility genes for familial breast cancer. Methods: Using exome sequencing, we analyzed eight members in a BRCA1-, BRCA2-, p53- and PTEN-negative breast cancer family; five with breast cancer and three unaffected. Mutation candidates were idenified by bioinformatics analysis, experimentally validated by Sanger sequencing and their damaging effect was predicted by the SIFT program. Validated mutations were also tested in 42 additional breast cancer samples from BRCA-negative breast cancer families. Results: We identified 55 nonsynonymous germline mutations affecting 49 genes in multiple members of this family, 20 of 22 selected mutations predicted to cause damaging effects were validated. As an exemplar, two mutations in the MYST4 gene were detected at the C terminal (p.D1516Y and p.R1577C), validated, and predicted to cause damaging consequences. MYST4 is a histone acetyltransferase (Champagne, N. et al. JBC. 274, 28528-28536,1999). It contains a C2HC-type finger and a PHD-type zinc finger. Its N-terminal is involved in transcriptional repression while its C-terminal is involved in transcriptional activation and interacts with important transcriptional regulators RUNX1 and RUNX2. MYST4 is involved in DNA replication, transcriptional regulation, and epigenetic modification of chromatin structure. A translocation t(10;16)(q22;p13) between CREBBP and MYST4 was identified in acute myeloid leukemia. The 20 validated germline mutations were tested by Sanger sequencing in 42 additional breast cancer cases from 26 BRCAnegative families. None of the 20 mutations were detected. Conclusions: Results show that remaining unknown susceptibility genes are likely family-specific and can be detected in each affected family using genome sequencing approaches. These results may be the first reported in an exome sequencing study of BRCA-negative breast cancer families. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
1539 General Poster Session (Board #1C), Sat, 1:15 PM-5:15 PM Evaluation of genes associated with undescended testes as predictors of TGCT susceptibility. Presenting Author: Ariela Marshall, Hospital of the University of Pennsylvania, Philadelphia, PA Background: Testicular germ cell tumors (TGCTs) are highly heritable. Cryptorchidism (undescended testes; UDT) is a strong risk factor for TGCT, with increased risk to both the ipsilateral and contralateral testes. However, recent genome-wide association studies (GWAS) identifying genetic variants associated with TGCT susceptibility have not found differences in genotype carriage between TGCT patients with and without UDT. We investigated the role of potential risk variants for UDT as risk factors for TGCT. Methods: 1300 SNPs in and around 25 gene regions with published associations with UDT were evaluated in 474 TGCT cases (45 with UDT) and 919 controls. Genotype information was available from the Affymetrix Genome-Wide Human SNP Array 6.0. Statistical analysis was performed using PLINK, and statistical significance was assessed by Fisher’s Exact test. Results: Comparing TGCT cases with and without UDT, variants in the region of four genes (EPHB2, ESR1, SEMA3C, TGFBR3) were suggestively associated with UDT. When TGCT cases with UDT were compared with unaffected controls, the associations all met the required level of significance (p � 4x10-5 ). Only variation at ESR1 approached significance (P�0.0004) when TGCT cases and unaffected controls were compared. Conclusions: We identified variants at three genetic loci - SEMA3C, TGFBR3 and EPHB2 - that were significantly associated with UDT, but not with TGCT. The association of variation in EPHB2 and SEMA3C with UDT are novel findings. While associated with UDT, variation at ESR1 is also potentially associated with TGCT risk. These data continue to suggest that genetic risk factors for UDT are largely independent of those for TGCT. Thus, screening for TGCT could be targeted in a UDT population to those with genetic risk factors. Further studies should be done to investigate the genetic link between UDT and TGCT. 1541 General Poster Session (Board #1E), Sat, 1:15 PM-5:15 PM Clinical characteristics of patients with malignant pleural mesothelioma (MPM) harboring somatic BAP1 mutations. Presenting Author: Marjorie Glass Zauderer, Memorial Sloan-Kettering Cancer Center, New York, NY Background: Efforts to elucidate tumorigenic mutations in MPM are essential to advance therapy. We reported a 23% incidence of somatic mutations in BRCA1-associated protein-1 (BAP1) in 53 patients with MPM (Bott et al. Nat Genet 2011). Germline BAP1 mutations were also reported in two families with a predisposition to mesothelioma and uveal melanoma (Testa et al. Nat Genet 2011). While BAP1 somatic mutations are more common in poor prognosis uveal melanoma (84% class 2, 4% class 1; Harbour et al. Science 2010), the significance of these mutations in MPM is unknown. Therefore, we analyzed the clinical characteristics of patients with somatic BAP1 mutations in order to describe this newly identified subpopulation. Methods: We reviewed the charts of 121 patients with tumors tested for somatic BAP1 mutations. Results: Patient characteristics are in the Table. Twenty percent harbored somatic BAP1 mutations. Other than the percent of current or former smokers (75% BAP1 mutations, 42% BAP1 wild-type, p�0.006), no other clinical feature was significantly different among those with and without BAP1 mutations. Among 53 samples analyzed for NF2 mutation and p16 deletion, no correlation was seen with BAP1 mutation. Conclusions: Somatic BAP1 mutations occur in about 20% of MPM tumors. Aside from smoking history, no other differences in clinical characteristics or outcomes were noted in the BAP1 mutated cases. Similar efforts are needed to describe the features of germline mutations in order to define this new cancer predisposition syndrome. We are planning a prospective trial to further evaluate the prevalence of germline BAP1 mutations, and we are also exploring the therapeutic implications. BAP1 mutants (N�24) BAP1 wild-type (N�97) p value Gender (M � male) M: 79% M: 68% 0.33 Median age at diagnosis 65 63 0.31 Histology E: 71% E: 77% 0.28 E � epithelial M: 25% M: 12% M � mixed S � sarcomatoid S: 4% S: 10% Stage I: 13% I: 5% 0.43 II: 25% II: 27% III: 33% III: 45% IV: 29% IV: 22% Known asbestos exposure 54% 46% 1 Smoking (former or current) 75% 42% 0.006 Surgery EPP: 54% EPP: 55% 1 EPP � extrapleural pneumonectomy Other: 38% Other: 35% None: 8% None: 10% Median overall survival from diagnosis (months) 14.8 15.3 0.78 Cancer Prevention/Epidemiology 95s 1540 General Poster Session (Board #1D), Sat, 1:15 PM-5:15 PM MEN1 gene mutations with different phenotypic presentations in two families: Is it a time to grade MEN1 mutations as high-risk and low-risk? Presenting Author: Alexander L. Shifrin, Jersey Shore University Medical Center, Neptune, NJ Background: MEN1 syndrome results from MEN1 gene mutations and is characterized by primary hyperparathyroidism (PHPT), pancreatic endocrine tumors (PET), pituitary adenomas, thymic and other tumors. About 600 different mutations have been reported on Human Gene Mutation Database and 30 of them presented as Familial Isolated Hyperparathyroidism (FIHP); however, no genotype-phenotype correlations have been identified. Methods: We characterized 2 independent families with newly diagnosed MEN1. Mutation analyses were performed in Dept of Genetics Yale University. Diagnostic tests, surgical treatment were implemented. Results: Family 1 has 21 members. 5 presented with early onset of PHPT and no other tumors. 3 ½ parathyroidectomies were performed. A proband had direct sequencing that showed a mutation in Exon 7, consisting of single base insertion in codon 319 (TAC to TTAC)(c1065_1066insT). There were no deaths in the family. Family 2 has 20 members. 7 were tested and showed a mutation in Exon 2, consisting of single base deletion in codon 103 (CTG to _TG)(c417delC). One 1st generation member died from PET at age 79, three 3rd generation members had multifocal metatstatic malignant gastrinomas (ages 32, 39, 41). The proband had total pancreatectomy at age 32. Five members had PHPT, angiofibromas. Three 2nd generation members had thymic carcinomas (ages 20, 54, 60). Conclusions: Phenotypic presentation of MEN1 syndrome may vary with the same mutation suggesting a lack of genotype-phenotype correlation and the effect of modifying factors. On the other hand, these two families—one with a mutation predicted to truncate the menin protein close to its terminus and the other with a truncating mutation early in the coding sequence—have dramatically different severity of the syndrome. Our findings suggest that the exon 7 mutation has a milder effect on protein function resulting in FIHP. The management may be heavily influenced by the predicted clinical phenotype, we are proposing the development of a grading system for MEN1 gene mutations as low-risk and high-risk and to attempt to identify other modifying genetic and environmental factors to improve screening and timing for surgery. 1542 General Poster Session (Board #1F), Sat, 1:15 PM-5:15 PM Genetic testing referral, uptake, and results in a program for women age 40 or younger with breast cancer. Presenting Author: Asma Ali, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, ON, Canada Background: PYNK: Breast Cancer Program for Young Woman is a novel program started in 2008 at our center to optimize management and promote research for women � age 40 newly diagnosed with breast cancer. Clinical and epidemiological data including cancer family history (FH) is prospectively collected on each consenting patient. As Toronto’s population is uniquely multiethnic we sought to determine BRCA testing eligibility, uptake and results for PYNK patients. Methods: Of the 145 consecutive patients, data were available for 109, of whom 2 had testing prior to diagnosis. Our provincial BRCA testing criteria are age � 35 at diagnosis; suspicious FH; or Ashkenazi Jewish (AJ) and age � 50 at diagnosis. Results: Of the 107 previously untested patients, 40 were � 35 at diagnosis. In 5 of the other 67 testing eligibility could not be assessed. 66 of the 102 (65%) were eligible and of those 65 (98%) were offered referral for counseling. One declined counseling, 9 were not yet seen, 2 declined testing, and 53 were tested. Test results are available for 47 as follows: 30 (64%) no mutation, 4 (8%) variant of uncertain significance (VUS), 7(15%) BRCA1 mutations and 6 (13%) BRCA2 mutations including 1 of the 4 AJ women. Ethnicity of the other 12 mutation carriers was: 1 Hispanic, 2 European, 2 African, 4 Asians, 1 mix, 1 unknown and 1 not recorded. Two (15%) of the mutation carriers had no FH of breast or ovarian cancer. Four additional women opted for counseling and testing despite ineligibility and none had mutations. Conclusions: A specialized program for young women facilitates appropriate referral for genetic testing and encourages high testing uptake, which is important given the high prevalence of mutations (28% of tested women). Further research is necessary to assess the psychological and management impact of having a VUS on young women compared to their older counterparts. 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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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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Oguri, Senri 5556 Oh, Do Youn 1003
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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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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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Wischnewsky, Manfred 1078 Wischnik,
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Yasuda, Hiromi e14029 Yasuda, Hiroy
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Zhang, Xinmin e16022 Zhang, Xu Dong
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