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Pancreatic Neoplasms: HELP
Articles by Jennifer A. Simon
Based on 4 articles published since 2010
(Why 4 articles?)

Between 2010 and 2020, Jennifer Simon wrote the following 4 articles about Pancreatic Neoplasms.
+ Citations + Abstracts
1 Article Including additional controls from public databases improves the power of a genome-wide association study. 2011

Mukherjee, Semanti / Simon, Jennifer / Bayuga, Sharon / Ludwig, Emmy / Yoo, Sarah / Orlow, Irene / Viale, Agnes / Offit, Kenneth / Kurtz, Robert C / Olson, Sara H / Klein, Robert J. ·Gerstner Sloan-Kettering Graduate School of Biomedical Sciences, Memorial Sloan-Kettering Cancer Center, New York, USA. ·Hum Hered · Pubmed #21849791.

ABSTRACT: Though genome-wide association studies (GWAS) have identified numerous susceptibility loci for common diseases, their use is limited due to the expense of genotyping large cohorts of individuals. One potential solution is to use 'additional controls', or genotype data from control individuals deposited in public repositories. While this approach has been used by several groups, the genetically heterogeneous nature of the population of the United States makes this approach potentially problematic. We empirically investigated the utility of this approach in a US-based GWAS. In a small GWAS of pancreatic cancer in New York, we observed clear population structure differences relative to controls from the database of Genotypes and Phenotypes (dbGaP). When we conduct the GWAS using these additional controls, we find large inflation of the test statistic that is properly corrected by using eigenvectors from principal components analysis as covariates. To deal with errors introduced due to different sources, we propose simultaneously genotyping a small number of controls along with cases and then comparing this group to the additional controls. We show that removing SNPs that show differences between these control groups reduces false-positive findings. Thus, through an empirical approach, this report provides practical guidance for using additional controls from publicly available datasets.

2 Article Feasibility and yield of screening in relatives from familial pancreatic cancer families. 2011

Ludwig, Emmy / Olson, Sara H / Bayuga, Sharon / Simon, Jennifer / Schattner, Mark A / Gerdes, Hans / Allen, Peter J / Jarnagin, William R / Kurtz, Robert C. ·Gastroenterology and Nutrition Service, Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA. ludwige@mskcc.org ·Am J Gastroenterol · Pubmed #21468009.

ABSTRACT: OBJECTIVES: Pancreatic adenocarcinoma is a lethal disease. Over 80% of patients are found to have metastatic disease at the time of diagnosis. Strategies to improve disease-specific outcome include identification and early detection of precursor lesions or early cancers in high-risk groups. In this study, we investigate whether screening at-risk relatives of familial pancreatic cancer (FPC) patients is safe and has significant yield. METHODS: We enrolled 309 asymptomatic at-risk relatives into our Familial Pancreatic Tumor Registry (FPTR) and offered them screening with magnetic resonance cholangiopancreaticogram (MRCP) followed by endoscopic ultrasound (EUS) with fine needle aspiration if indicated. Relatives with findings were referred for surgical evaluation. RESULTS: As of 1 August 2009, 109 relatives had completed at least one cycle of screening. Abnormal radiographic findings were present on initial screening in 18/109 patients (16.5%), 15 of whom underwent EUS. A significant abnormality was confirmed in 9 of 15 patients, 6 of whom ultimately had surgery for an overall diagnostic yield of 8.3% (9/109). Yield was greatest in relatives >65 years old (35%, 6/17) when compared with relatives 55-65 years (3%, 1/31) and relatives <55 years (3%, 2/61). CONCLUSIONS: Screening at-risk relatives from FPC families has a significant diagnostic yield, particularly in relatives >65 years of age, confirming prior studies. MRCP as initial screening modality is safe and effective.

3 Article Germline PALB2 mutation analysis in breast-pancreas cancer families. 2011

Stadler, Zsofia K / Salo-Mullen, Erin / Sabbaghian, Nelly / Simon, Jennifer A / Zhang, Liying / Olson, Sara H / Kurtz, Robert / Offit, Kenneth / Foulkes, William D / Robson, Mark E / Tischkowitz, Marc. ·Clinical Genetics and Gastroenterology Services, Department of Medicine, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA. stadlerz@mskcc.org ·J Med Genet · Pubmed #21415078.

ABSTRACT: BACKGROUND: Germline mutations in the PALB2 gene have been implicated in both breast cancer and pancreatic cancer susceptibility. The extent to which PALB2 mutations account for cancer susceptibility in breast-pancreas cancer families is unknown. METHODS: High Resolution Melting analysis and Multiplex Ligation-dependent Probe Amplification were performed to investigate the prevalence of PALB2 mutations in patients with either a personal history of both breast and pancreatic cancer or a personal history of breast cancer and a family history of a first degree relative with pancreatic cancer. RESULTS: No PALB2 mutations were identified in 77 breast-pancreas cancer families, which included 22 probands with a personal history of both breast and pancreatic cancer. CONCLUSION: Mutations within the PALB2 gene are rare events that do not account for a substantial proportion of cancer susceptibility in breast-pancreas cancer families. Routine screening of breast-pancreas cancer families for the presence of PALB2 mutations appears to be low yield.

4 Article Allergies, obesity, other risk factors and survival from pancreatic cancer. 2010

Olson, Sara H / Chou, Joanne F / Ludwig, Emmy / O'Reilly, Eileen / Allen, Peter J / Jarnagin, William R / Bayuga, Sharon / Simon, Jennifer / Gonen, Mithat / Reisacher, William R / Kurtz, Robert C. ·Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA. olsons@mskcc.org ·Int J Cancer · Pubmed #20143395.

ABSTRACT: Survival from pancreatic adenocarcinoma remains extremely poor, approximately 5% at 5 years. Risk factors include smoking, high body mass index (BMI), family history of pancreatic cancer, and long-standing diabetes; in contrast, allergies are associated with reduced risk. Little is known about associations between these factors and survival. We analyzed overall survival in relation to risk factors for 475 incident cases who took part in a hospital based case-control study. Analyses were conducted separately for those who did (160) and did not (315) undergo tumor resection. Kaplan-Meier methods were used to describe survival according to smoking, BMI, family history, diabetes, and presence of allergies. Cox proportional hazards models were used to adjust for covariates. There was no association with survival based on smoking, family history, or history of diabetes in either group. Among patients with resection, those with allergies showed nonstatistically significant longer survival, a median of 33.1 months (95% CI: 19.0-52.5) vs. 21.8 months (95% CI: 18.0-33.1), p = 0.25. The adjusted hazard ratio (HR) was 0.72 (95% CI: 0.43-1.23), p = 0.23. Among patients without resection, those with self-reported allergies survived significantly longer than those without allergies: 13.3 months (95% CI: 10.6-16.9) compared to 10.4 months (95% CI: 8.8-11.0), p = 0.04, with an adjusted HR of 0.68 (95% CI: 0.49-0.95), p = 0.02. Obesity was nonsignificantly associated with poorer survival, particularly in the resected group (HR = 1.62, 95% CI: 0.76-3.44). The mechanisms underlying the association between history of allergies and improved survival are unknown. These novel results need to be confirmed in other studies.