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Pancreatic Neoplasms: HELP
Articles by Ruth M. Pfeiffer
Based on 2 articles published since 2010
(Why 2 articles?)

Between 2010 and 2020, Ruth M. Pfeiffer wrote the following 2 articles about Pancreatic Neoplasms.
+ Citations + Abstracts
1 Article Lack of germline PALB2 mutations in melanoma-prone families with CDKN2A mutations and pancreatic cancer. 2011

Yang, Xiaohong R / Jessop, Lea / Myers, Timothy / Amundadottir, Laufey / Pfeiffer, Ruth M / Wheeler, William / Pike, Kristen M / Yuenger, Jeff / Burdett, Laurie / Yeager, Meredith / Chanock, Stephen J / Tucker, Margaret A / Goldstein, Alisa M. ·Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, DHHS, Bethesda, MD, USA. ·Fam Cancer · Pubmed #21614589.

ABSTRACT: The presence of pancreatic cancer (PC) in melanoma-prone families has been consistently associated with an increased frequency of CDKN2A mutations, the major high-risk susceptibility gene identified for melanoma. However, the precise relationship between CDKN2A, melanoma and PC remains unknown. We evaluated a recently identified PC susceptibility gene PALB2 using both sequencing and tagging to determine whether PALB2 might explain part of the relationship between CDKN2A, melanoma, and PC. No disease-related mutations were identified from sequencing PALB2 in multiple pancreatic cancer patients or other mutation carrier relatives of PC patients from the eight melanoma-prone families with CDKN2A mutations and PC. In addition, no significant associations were observed between 11 PALB2 tagging SNPs and melanoma risk in 23 melanoma-prone families with CDKN2A mutations or the subset of 11 families with PC or PC-related CDKN2A mutations. The results suggested that PALB2 does not explain the relationship between CDKN2A, melanoma, and pancreatic cancer in these melanoma-prone families.

2 Article Body mass index, effect modifiers, and risk of pancreatic cancer: a pooled study of seven prospective cohorts. 2010

Jiao, Li / Berrington de Gonzalez, Amy / Hartge, Patricia / Pfeiffer, Ruth M / Park, Yikyung / Freedman, D Michal / Gail, Mitchell H / Alavanja, Michael C R / Albanes, Demetrius / Beane Freeman, Laura E / Chow, Wong-Ho / Huang, Wen-Yi / Hayes, Richard B / Hoppin, Jane A / Ji, Bu-Tian / Leitzmann, Michael F / Linet, Martha S / Meinhold, Cari L / Schairer, Catherine / Schatzkin, Arthur / Virtamo, Jarmo / Weinstein, Stephanie J / Zheng, Wei / Stolzenberg-Solomon, Rachael Z. ·Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. jiao@bcm.edu ·Cancer Causes Control · Pubmed #20383573.

ABSTRACT: OBJECTIVE: To investigate whether the positive association of body mass index (BMI, kg/m(2)) with risk of pancreatic cancer is modified by age, sex, smoking status, physical activity, and history of diabetes. METHODS: In a pooled analysis of primary data of seven prospective cohorts including 458,070 men and 485,689 women, we identified 2,454 patients with incident pancreatic cancer during an average 6.9 years of follow-up. Cox proportional hazard regression models were used in data analysis. RESULTS: In a random-effects meta-analysis, for every 5 kg/m(2) increment in BMI, the summary relative risk (RR) was 1.06 (95% confidence interval (CI) 0.99-1.13) for men and 1.12 (95% CI 1.05-1.19) for women. The aggregate analysis showed that compared with normal weight (BMI: 18.5 to <25), the adjusted RR was 1.13 (95% CI 1.03-1.23) for overweight (BMI: 25 to <30) and 1.19 (95% CI 1.05-1.35) for obesity class I (BMI: 30 to <35). Tests of interactions of BMI effects by other risk factors were not statistically significant. Every 5 kg/m(2) increment in BMI was associated with an increased risk of pancreatic cancer among never and former smokers, but not among current smokers (P-interaction = 0.08). CONCLUSION: The present evidence suggests that a high BMI is an independent risk factor of pancreatic cancer.