Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Pancreatic Neoplasms: HELP
Articles by Margaret T. Mandelson
Based on 10 articles published since 2010
(Why 10 articles?)
||||

Between 2010 and 2020, Margaret T. Mandelson wrote the following 10 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Clinical Trial Five-Year Actual Overall Survival in Resected Pancreatic Cancer: A Contemporary Single-Institution Experience from a Multidisciplinary Perspective. 2017

Picozzi, Vincent J / Oh, Stephen Y / Edwards, Alicia / Mandelson, Margaret T / Dorer, Russell / Rocha, Flavio G / Alseidi, Adnan / Biehl, Thomas / Traverso, L William / Helton, William S / Kozarek, Richard A. ·Digestive Disease Institute, Virginia Mason Medical Center, Seattle, WA, USA. hemvjp@vmmc.org. · Cancer Institute, Virginia Mason Medical Center, Seattle, WA, USA. hemvjp@vmmc.org. · Digestive Disease Institute, Virginia Mason Medical Center, Seattle, WA, USA. · Cancer Institute, Virginia Mason Medical Center, Seattle, WA, USA. · Department of Pathology, Virginia Mason Medical Center, Seattle, WA, USA. · Center for Pancreatic Disease and Mountain States Tumor Institute, Boise, ID, USA. ·Ann Surg Oncol · Pubmed #28054192.

ABSTRACT: BACKGROUND: Successful surgical resection combined with effective perioperative therapy is essential for maximizing long-term survival for pancreatic adenocarcinoma. PATIENTS AND METHODS: All patients with pancreatic adenocarcinoma who underwent curative resection at our institution from January 2003 to May 2010 were reviewed. Demographic and clinical details were retrospectively collected from medical records and cancer registry data. RESULTS: Overall, 176 patients were included in the analysis (148 with de novo resectable disease and 28 with borderline resectable disease at presentation). Among 106 patients who received all perioperative therapy at our institution, 94% received neoadjuvant and/or adjuvant treatment in addition to resection. Actual all-cause 5-year overall survival (OS) for all 176 patients was 30.7%, with a median OS of 33.9 months [95% confidence interval (CI) 28.1-39.6 months]. For patients who received all perioperative therapy at our institution, actual all-cause 5-year disease-free survival (DFS) was 32.1%, with a median DFS of 28.8 months (95% CI 20.1-43.6 months). Of these patients, 67/106 (63%) recurred: 8 (8%) locoregional only; 52 (49%) systemic only; and 7 (7%) combined recurrence. No difference in survival rates or recurrence patterns was seen between resectable and borderline resectable patients. In multivariate analysis, tumor differentiation (poor vs. non-poor) and lymph node ratio >20% produced a useful clinical model. CONCLUSION: The actual OS rates for resected pancreatic cancer shown in this study are reflective of those currently achievable at a tertiary medical center dedicated to this patient population. In considering these results, both frequency and type of adjuvant/neoadjuvant therapy administered in the context of the clinical experience/management techniques of providers administering these treatments will be discussed.

2 Article Gemcitabine and Taxane Adjuvant Therapy with Chemoradiation in Resected Pancreatic Cancer: A Novel Strategy for Improved Survival? 2018

Kanji, Zaheer S / Edwards, Alicia M / Mandelson, Margaret T / Sahar, Nadav / Lin, Bruce S / Badiozamani, Kasra / Song, Guobin / Alseidi, Adnan / Biehl, Thomas R / Kozarek, Richard A / Helton, William S / Picozzi, Vincent J / Rocha, Flavio G. ·Digestive Disease Institute, Virginia Mason Medical Center, Seattle, WA, USA. · Section of General Thoracic, and Vascular Surgery, Virginia Mason Medical Center, Seattle, WA, USA. · Cancer Institute, Virginia Mason Medical Center, Seattle, WA, USA. · Section of Radiation Oncology, Virginia Mason Medical Center, Seattle, WA, USA. · Digestive Disease Institute, Virginia Mason Medical Center, Seattle, WA, USA. flavio.rocha@virginiamason.org. · Cancer Institute, Virginia Mason Medical Center, Seattle, WA, USA. flavio.rocha@virginiamason.org. · Section of General Thoracic, and Vascular Surgery, Virginia Mason Medical Center, Seattle, WA, USA. flavio.rocha@virginiamason.org. ·Ann Surg Oncol · Pubmed #29344878.

ABSTRACT: BACKGROUND: Gemcitabine-taxane combination chemotherapy has demonstrated a survival benefit clinically in metastatic pancreatic cancer (PC). The authors present their experience with gemcitabine and docetaxel (gem/tax)-based adjuvant treatment (Rx) after surgery with curative intent. METHODS: Patients with de novo resectable PC from January 2010 to December 2015 were identified from the authors' institutional database and registry. The study included only patients who received gem/tax as their initial Rx administered exclusively at the authors' institution with or without chemoradiation (CRTx). Survival analysis was performed using Kaplan-Meier methods, and prognostic factors were investigated by Cox proportional hazard modeling. RESULTS: Of 102 patients identified, 58 met the study criteria. The median age at diagnosis was 65 years, with 55% of the patients undergoing an R1 resection (margin ≤ 1 mm). Tumor characteristics included a median tumor size of 28 mm, a poor differentiation rate of 54%, and a lymph node positivity of 67%. Most of the patients (90%, 52/58) completed 80% or more of the 24 week Rx. Of these patients, 71% received post-gem/tax CRTx Rx. Grade 3 or 4 toxicity was observed in 52% of the patients. The median follow-up period was 51.2 months, and the observed median overall survival (OS) was 52 months [95% confidence interval (CI) 27.4-not reached]. The actuarial 5-year OS was 49% (95% CI 33.7-63.4%). In the multivariate analysis, an R1 resection and American Joint Committee on Cancer (AJCC) stage 2 versus stage 1 disease were negatively associated with OS, whereas administration of CRTx was positively associated with OS. CONCLUSIONS: Adjuvant gem/tax with or without CRTx is feasible, with a favorable OS. Future prospective studies of gem/taxane-based adjuvant Rx for PC are warranted.

3 Article Localized pancreatic cancer with positive peritoneal cytology as a sole manifestation of metastatic disease: a single-institution experience. 2017

Oh, Stephen Y / Edwards, Alicia / Mandelson, Margaret T / Hahn, Hejin / Alseidi, Adnan / Biehl, Thomas / Kozarek, Richard A / Rocha, Flavio G / Helton, Scott / Picozzi, Vincent J. ·Digestive Disease Institute, Virginia Mason Medical Center, Seattle, WA, USA. · Cancer Institute, Virginia Mason Medical Center, Seattle, WA, USA. · Department of Pathology, Virginia Mason Medical Center, Seattle, WA, USA. · Department of General Surgery, Virginia Mason Medical Center, Seattle, WA, USA. · Department of Medical Oncology, Virginia Mason Medical Center, 1100 9th Avenue, MS: C2-HEM, Seattle, WA 98111, USA. Electronic address: Vincent.Picozzi@virginiamason.org. ·Am J Surg · Pubmed #27424044.

ABSTRACT: BACKGROUND: Pancreatic cancer patients with positive peritoneal cytology (PPC) as a sole metastatic site are poorly characterized. Whether they behave similarly to other stage IV patients is unknown. METHODS: Patients with stage IV disease at our institution between 2003 and 2013 were identified. Inclusion criteria for PPC cohort were PPC at laparoscopy and no laparoscopic and/or radiographic evidence of metastasis. Patients with gross metastasis had laparoscopic and/or radiographic evidence of metastasis. RESULTS: Among 308 patients, 43 patients had PPC and 265 had gross metastasis. PPC cohort: 3 (7%) resectable, 8 (19%) borderline resectable, and 32 (74%) unresectable tumor. Disease progression occurred in 37 (86%). Sixteen of 43 (37%) also received local therapy (1 surgery and 15 chemoradiation). PPC vs gross metastasis cohort differed as follows: baseline Ca 19-9 (440 vs 1,904 IU/mL, P < .0001); Eastern Cooperative Oncology Group (ECOG) score ≤1 (98 vs 88%, P = .04); median overall survival (13.9 vs 9.4 months, P = .0001). CONCLUSIONS: Patients with PPC failed to display long-term disease-free survival, although overall survival was superior compared with those with gross metastasis. Patients with PPC may need to be considered a specific subgroup for staging and survival analysis.

4 Article Rare long-term survivors of pancreatic adenocarcinoma without curative resection. 2015

Oh, Stephen Y / Edwards, Alicia / Mandelson, Margaret T / Lin, Bruce / Dorer, Russell / Helton, W Scott / Kozarek, Richard A / Picozzi, Vincent J. ·Stephen Y Oh, Alicia Edwards, Richard A Kozarek, Digestive Disease Institute, Virginia Mason Medical Center, Seattle, WA 98101, United States. ·World J Gastroenterol · Pubmed #26730170.

ABSTRACT: Long-term outcome data in pancreatic adenocarcinoma are predominantly based on surgical series, as resection is currently considered essential for long-term survival. In contrast, five-year survival in non-resected patients has rarely been reported. In this report, we examined the incidence and natural history of ≥ 5-year survivors with non-resected pancreatic adenocarcinoma. All patients with pancreatic adenocarcinoma who received oncologic therapy alone without surgery at our institution between 1995 and 2009 were identified. Non-resected ≥ 5-year survivors represented 2% (11/544) of all non-resected patients undergoing treatment for pancreatic adenocarcinoma, and 11% (11/98) of ≥ 5-year survivors. Nine patients had localized tumor and 2 metastatic disease at initial diagnosis. Disease progression occurred in 6 patients, and the local tumor bed was the most common site of progression. Six patients suffered from significant morbidities including recurrent cholangitis, second malignancy, malnutrition and bowel perforation. A rare subset of patients with pancreatic cancer achieve long-term survival without resection. Despite prolonged survival, morbidities unrelated to the primary cancer were frequently encountered and a close follow-up is warranted in these patients. Factors such as tumor biology and host immunity may play a key role in disease progression and survival.

5 Article An absolute risk model to identify individuals at elevated risk for pancreatic cancer in the general population. 2013

Klein, Alison P / Lindström, Sara / Mendelsohn, Julie B / Steplowski, Emily / Arslan, Alan A / Bueno-de-Mesquita, H Bas / Fuchs, Charles S / Gallinger, Steven / Gross, Myron / Helzlsouer, Kathy / Holly, Elizabeth A / Jacobs, Eric J / Lacroix, Andrea / Li, Donghui / Mandelson, Margaret T / Olson, Sara H / Petersen, Gloria M / Risch, Harvey A / Stolzenberg-Solomon, Rachael Z / Zheng, Wei / Amundadottir, Laufey / Albanes, Demetrius / Allen, Naomi E / Bamlet, William R / Boutron-Ruault, Marie-Christine / Buring, Julie E / Bracci, Paige M / Canzian, Federico / Clipp, Sandra / Cotterchio, Michelle / Duell, Eric J / Elena, Joanne / Gaziano, J Michael / Giovannucci, Edward L / Goggins, Michael / Hallmans, Göran / Hassan, Manal / Hutchinson, Amy / Hunter, David J / Kooperberg, Charles / Kurtz, Robert C / Liu, Simin / Overvad, Kim / Palli, Domenico / Patel, Alpa V / Rabe, Kari G / Shu, Xiao-Ou / Slimani, Nadia / Tobias, Geoffrey S / Trichopoulos, Dimitrios / Van Den Eeden, Stephen K / Vineis, Paolo / Virtamo, Jarmo / Wactawski-Wende, Jean / Wolpin, Brian M / Yu, Herbert / Yu, Kai / Zeleniuch-Jacquotte, Anne / Chanock, Stephen J / Hoover, Robert N / Hartge, Patricia / Kraft, Peter. ·Department of Oncology, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland, United States of America ; Department of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins School of Medicine, Baltimore, Maryland, United States of America ; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America. ·PLoS One · Pubmed #24058443.

ABSTRACT: PURPOSE: We developed an absolute risk model to identify individuals in the general population at elevated risk of pancreatic cancer. PATIENTS AND METHODS: Using data on 3,349 cases and 3,654 controls from the PanScan Consortium, we developed a relative risk model for men and women of European ancestry based on non-genetic and genetic risk factors for pancreatic cancer. We estimated absolute risks based on these relative risks and population incidence rates. RESULTS: Our risk model included current smoking (multivariable adjusted odds ratio (OR) and 95% confidence interval: 2.20 [1.84-2.62]), heavy alcohol use (>3 drinks/day) (OR: 1.45 [1.19-1.76]), obesity (body mass index >30 kg/m(2)) (OR: 1.26 [1.09-1.45]), diabetes >3 years (nested case-control OR: 1.57 [1.13-2.18], case-control OR: 1.80 [1.40-2.32]), family history of pancreatic cancer (OR: 1.60 [1.20-2.12]), non-O ABO genotype (AO vs. OO genotype) (OR: 1.23 [1.10-1.37]) to (BB vs. OO genotype) (OR 1.58 [0.97-2.59]), rs3790844(chr1q32.1) (OR: 1.29 [1.19-1.40]), rs401681(5p15.33) (OR: 1.18 [1.10-1.26]) and rs9543325(13q22.1) (OR: 1.27 [1.18-1.36]). The areas under the ROC curve for risk models including only non-genetic factors, only genetic factors, and both non-genetic and genetic factors were 58%, 57% and 61%, respectively. We estimate that fewer than 3/1,000 U.S. non-Hispanic whites have more than a 5% predicted lifetime absolute risk. CONCLUSION: Although absolute risk modeling using established risk factors may help to identify a group of individuals at higher than average risk of pancreatic cancer, the immediate clinical utility of our model is limited. However, a risk model can increase awareness of the various risk factors for pancreatic cancer, including modifiable behaviors.

6 Article Family history of diabetes and pancreatic cancer as risk factors for pancreatic cancer: the PACIFIC study. 2013

Austin, Melissa A / Kuo, Elena / Van Den Eeden, Stephen K / Mandelson, Margaret T / Brentnall, Teresa A / Kamineni, Aruna / Potter, John D. ·Authors' Affiliations: Departments of Epidemiology and Gastroenterology, University of Washington; Group Health Research Institute and Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington; Division of Research, Kaiser Permanente Northern California, Oakland, California; and Centre for Public Health Research, Massey University, Wellington, New Zealand. ·Cancer Epidemiol Biomarkers Prev · Pubmed #23966578.

ABSTRACT: Genetic association studies have identified more than a dozen genes associated with risk of pancreatic cancer. Given this genetic heterogeneity, family history can be useful for identifying individuals at high risk for this disease. The goal of this analysis was to evaluate associations of family history of diabetes and family history of pancreatic cancer with risk of pancreatic cancer. PACIFIC is a case-control study based on two large health plans. Cases were diagnosed with pancreatic ductal adenocarcinoma (PDA) and controls were selected from the health plan enrollment databases and frequency matched to cases. Family history data were collected using an interviewer-administered questionnaire and were available on 654 cases and 697 controls. Logistic regression was used for the association analyses. First-degree relative history of diabetes was statistically significantly associated with increased risk of PDA [OR, 1.37; 95% confidence interval (CI), 1.10-1.71]. The highest risk of PDA was observed for an offspring with diabetes (OR, 1.95; 95% CI, 1.23-3.09). In addition, history of pancreatic cancer increased risk for PDA with an OR of 2.79 (95% CI, 1.44-4.08) for any first-degree relative history of pancreatic cancer. This population-based analysis showed that family history of diabetes was associated with increased risk of PDA and confirmed previous studies showing that first-degree family history of pancreatic cancer is associated with PDA. These results support the need for ongoing studies of genetic influences on pancreatic cancer in large samples and investigations of possible pleiotropic genetic effects on diabetes and pancreatic cancer.

7 Article Polymorphisms in genes related to one-carbon metabolism are not related to pancreatic cancer in PanScan and PanC4. 2013

Leenders, Max / Bhattacharjee, Samsiddhi / Vineis, Paolo / Stevens, Victoria / Bueno-de-Mesquita, H Bas / Shu, Xiao-Ou / Amundadottir, Laufey / Gross, Myron / Tobias, Geoffrey S / Wactawski-Wende, Jean / Arslan, Alan A / Duell, Eric J / Fuchs, Charles S / Gallinger, Steven / Hartge, Patricia / Hoover, Robert N / Holly, Elizabeth A / Jacobs, Eric J / Klein, Alison P / Kooperberg, Charles / LaCroix, Andrea / Li, Donghui / Mandelson, Margaret T / Olson, Sara H / Petersen, Gloria / Risch, Harvey A / Yu, Kai / Wolpin, Brian M / Zheng, Wei / Agalliu, Ilir / Albanes, Demetrius / Boutron-Ruault, Marie-Christine / Bracci, Paige M / Buring, Julie E / Canzian, Federico / Chang, Kenneth / Chanock, Stephen J / Cotterchio, Michelle / Gaziano, J Michael / Giovanucci, Edward L / Goggins, Michael / Hallmans, Göran / Hankinson, Susan E / Hoffman-Bolton, Judith A / Hunter, David J / Hutchinson, Amy / Jacobs, Kevin B / Jenab, Mazda / Khaw, Kay-Tee / Kraft, Peter / Krogh, Vittorio / Kurtz, Robert C / McWilliams, Robert R / Mendelsohn, Julie B / Patel, Alpa V / Rabe, Kari G / Riboli, Elio / Tjønneland, Anne / Trichopoulos, Dimitrios / Virtamo, Jarmo / Visvanathan, Kala / Elena, Joanne W / Yu, Herbert / Zeleniuch-Jacquotte, Anne / Stolzenberg-Solomon, Rachael Z. ·Department of Epidemiology and Biostatistics, School of Public Health, Imperial College, London, UK. M.Leenders-6@umcutrecht.nl ·Cancer Causes Control · Pubmed #23334854.

ABSTRACT: PURPOSE: The evidence of a relation between folate intake and one-carbon metabolism (OCM) with pancreatic cancer (PanCa) is inconsistent. In this study, the association between genes and single-nucleotide polymorphisms (SNPs) related to OCM and PanCa was assessed. METHODS: Using biochemical knowledge of the OCM pathway, we identified thirty-seven genes and 834 SNPs to examine in association with PanCa. Our study included 1,408 cases and 1,463 controls nested within twelve cohorts (PanScan). The ten SNPs and five genes with lowest p values (<0.02) were followed up in 2,323 cases and 2,340 controls from eight case-control studies (PanC4) that participated in PanScan2. The correlation of SNPs with metabolite levels was assessed for 649 controls from the European Prospective Investigation into Cancer and Nutrition. RESULTS: When both stages were combined, we observed suggestive associations with PanCa for rs10887710 (MAT1A) (OR 1.13, 95 %CI 1.04-1.23), rs1552462 (SYT9) (OR 1.27, 95 %CI 1.02-1.59), and rs7074891 (CUBN) (OR 1.91, 95 %CI 1.12-3.26). After correcting for multiple comparisons, no significant associations were observed in either the first or second stage. The three suggested SNPs showed no correlations with one-carbon biomarkers. CONCLUSIONS: This is the largest genetic study to date to examine the relation between germline variations in OCM-related genes polymorphisms and the risk of PanCa. Suggestive evidence for an association between polymorphisms and PanCa was observed among the cohort-nested studies, but this did not replicate in the case-control studies. Our results do not strongly support the hypothesis that genes related to OCM play a role in pancreatic carcinogenesis.

8 Article Pathway analysis of genome-wide association study data highlights pancreatic development genes as susceptibility factors for pancreatic cancer. 2012

Li, Donghui / Duell, Eric J / Yu, Kai / Risch, Harvey A / Olson, Sara H / Kooperberg, Charles / Wolpin, Brian M / Jiao, Li / Dong, Xiaoqun / Wheeler, Bill / Arslan, Alan A / Bueno-de-Mesquita, H Bas / Fuchs, Charles S / Gallinger, Steven / Gross, Myron / Hartge, Patricia / Hoover, Robert N / Holly, Elizabeth A / Jacobs, Eric J / Klein, Alison P / LaCroix, Andrea / Mandelson, Margaret T / Petersen, Gloria / Zheng, Wei / Agalliu, Ilir / Albanes, Demetrius / Boutron-Ruault, Marie-Christine / Bracci, Paige M / Buring, Julie E / Canzian, Federico / Chang, Kenneth / Chanock, Stephen J / Cotterchio, Michelle / Gaziano, J Michael / Giovannucci, Edward L / Goggins, Michael / Hallmans, Göran / Hankinson, Susan E / Hoffman Bolton, Judith A / Hunter, David J / Hutchinson, Amy / Jacobs, Kevin B / Jenab, Mazda / Khaw, Kay-Tee / Kraft, Peter / Krogh, Vittorio / Kurtz, Robert C / McWilliams, Robert R / Mendelsohn, Julie B / Patel, Alpa V / Rabe, Kari G / Riboli, Elio / Shu, Xiao-Ou / Tjønneland, Anne / Tobias, Geoffrey S / Trichopoulos, Dimitrios / Virtamo, Jarmo / Visvanathan, Kala / Watters, Joanne / Yu, Herbert / Zeleniuch-Jacquotte, Anne / Amundadottir, Laufey / Stolzenberg-Solomon, Rachael Z. ·Department of Gastrointestinal Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA. ·Carcinogenesis · Pubmed #22523087.

ABSTRACT: Four loci have been associated with pancreatic cancer through genome-wide association studies (GWAS). Pathway-based analysis of GWAS data is a complementary approach to identify groups of genes or biological pathways enriched with disease-associated single-nucleotide polymorphisms (SNPs) whose individual effect sizes may be too small to be detected by standard single-locus methods. We used the adaptive rank truncated product method in a pathway-based analysis of GWAS data from 3851 pancreatic cancer cases and 3934 control participants pooled from 12 cohort studies and 8 case-control studies (PanScan). We compiled 23 biological pathways hypothesized to be relevant to pancreatic cancer and observed a nominal association between pancreatic cancer and five pathways (P < 0.05), i.e. pancreatic development, Helicobacter pylori lacto/neolacto, hedgehog, Th1/Th2 immune response and apoptosis (P = 2.0 × 10(-6), 1.6 × 10(-5), 0.0019, 0.019 and 0.023, respectively). After excluding previously identified genes from the original GWAS in three pathways (NR5A2, ABO and SHH), the pancreatic development pathway remained significant (P = 8.3 × 10(-5)), whereas the others did not. The most significant genes (P < 0.01) in the five pathways were NR5A2, HNF1A, HNF4G and PDX1 for pancreatic development; ABO for H.pylori lacto/neolacto; SHH for hedgehog; TGFBR2 and CCL18 for Th1/Th2 immune response and MAPK8 and BCL2L11 for apoptosis. Our results provide a link between inherited variation in genes important for pancreatic development and cancer and show that pathway-based approaches to analysis of GWAS data can yield important insights into the collective role of genetic risk variants in cancer.

9 Article Association of diabetes susceptibility gene calpain-10 with pancreatic cancer among smokers. 2010

Fong, Pui-yee / Fesinmeyer, Megan D / White, Emily / Farin, Federico M / Srinouanprachanh, Sengkeo / Afsharinejad, Zahra / Mandelson, Margaret T / Brentnall, Teresa A / Barnett, Matt J / Goodman, Gary E / Austin, Melissa A. ·Institute for Public Health Genetics, University of Washington, Box 357236, Seattle, WA 98195, USA. ·J Gastrointest Cancer · Pubmed #20178008.

ABSTRACT: OBJECTIVE: The objective of this study was to test the association between calpain-10 (CAPN10), a diabetes susceptibility gene, with risk of pancreatic cancer (PC). METHODS: DNA samples from 83 incident exocrine PC cases and 166 controls, all of whom were smokers, were genotyped for four markers of CAPN10 in a nested case-control study based on the Beta-Carotene and Retinol Efficacy Trial (CARET), a randomized chemoprevention trial of subjects at high risk of lung cancer. Controls were matched on sex, race, age, CARET intervention arm, duration of exposure to asbestos, and smoking history. Conditional logistic regression was used for statistical analyses. RESULTS: The minor allele of SNP-43 (rs3792267) in intron 3 was associated with increased risk of PC with an odds ratio of 1.57 (95%CI 1.03-2.38, p = 0.035) per allele. The three markers of the highest risk haplotype had an odds ratio of 1.98 (95%CI 1.12-3.49, p = 0.019) for risk of PC compared to the most common haplotype. There was no evidence of interaction between either of these associations by diabetes status. CONCLUSION: These results suggest that variation in CAPN10 may be associated with increased risk of PC among smokers. Thus, studies of genes associated with diabetes risk in PC are warranted in a larger population.

10 Article A genome-wide association study identifies pancreatic cancer susceptibility loci on chromosomes 13q22.1, 1q32.1 and 5p15.33. 2010

Petersen, Gloria M / Amundadottir, Laufey / Fuchs, Charles S / Kraft, Peter / Stolzenberg-Solomon, Rachael Z / Jacobs, Kevin B / Arslan, Alan A / Bueno-de-Mesquita, H Bas / Gallinger, Steven / Gross, Myron / Helzlsouer, Kathy / Holly, Elizabeth A / Jacobs, Eric J / Klein, Alison P / LaCroix, Andrea / Li, Donghui / Mandelson, Margaret T / Olson, Sara H / Risch, Harvey A / Zheng, Wei / Albanes, Demetrius / Bamlet, William R / Berg, Christine D / Boutron-Ruault, Marie-Christine / Buring, Julie E / Bracci, Paige M / Canzian, Federico / Clipp, Sandra / Cotterchio, Michelle / de Andrade, Mariza / Duell, Eric J / Gaziano, J Michael / Giovannucci, Edward L / Goggins, Michael / Hallmans, Göran / Hankinson, Susan E / Hassan, Manal / Howard, Barbara / Hunter, David J / Hutchinson, Amy / Jenab, Mazda / Kaaks, Rudolf / Kooperberg, Charles / Krogh, Vittorio / Kurtz, Robert C / Lynch, Shannon M / McWilliams, Robert R / Mendelsohn, Julie B / Michaud, Dominique S / Parikh, Hemang / Patel, Alpa V / Peeters, Petra H M / Rajkovic, Aleksandar / Riboli, Elio / Rodriguez, Laudina / Seminara, Daniela / Shu, Xiao-Ou / Thomas, Gilles / Tjønneland, Anne / Tobias, Geoffrey S / Trichopoulos, Dimitrios / Van Den Eeden, Stephen K / Virtamo, Jarmo / Wactawski-Wende, Jean / Wang, Zhaoming / Wolpin, Brian M / Yu, Herbert / Yu, Kai / Zeleniuch-Jacquotte, Anne / Fraumeni, Joseph F / Hoover, Robert N / Hartge, Patricia / Chanock, Stephen J. ·Department of Health Sciences Research, College of Medicine, Mayo Clinic, Rochester, Minnesota, USA. ·Nat Genet · Pubmed #20101243.

ABSTRACT: We conducted a genome-wide association study of pancreatic cancer in 3,851 affected individuals (cases) and 3,934 unaffected controls drawn from 12 prospective cohort studies and 8 case-control studies. Based on a logistic regression model for genotype trend effect that was adjusted for study, age, sex, self-described ancestry and five principal components, we identified eight SNPs that map to three loci on chromosomes 13q22.1, 1q32.1 and 5p15.33. Two correlated SNPs, rs9543325 (P = 3.27 x 10(-11), per-allele odds ratio (OR) 1.26, 95% CI 1.18-1.35) and rs9564966 (P = 5.86 x 10(-8), per-allele OR 1.21, 95% CI 1.13-1.30), map to a nongenic region on chromosome 13q22.1. Five SNPs on 1q32.1 map to NR5A2, and the strongest signal was at rs3790844 (P = 2.45 x 10(-10), per-allele OR 0.77, 95% CI 0.71-0.84). A single SNP, rs401681 (P = 3.66 x 10(-7), per-allele OR 1.19, 95% CI 1.11-1.27), maps to the CLPTM1L-TERT locus on 5p15.33, which is associated with multiple cancers. Our study has identified common susceptibility loci for pancreatic cancer that warrant follow-up studies.