Journal
JOURNAL OF GASTROENTEROLOGY
Volume 53, Issue 8, Pages 959-966Publisher
SPRINGER JAPAN KK
DOI: 10.1007/s00535-018-1430-x
Keywords
Chemoprevention; Cohort studies; Hydroxymethylglutaryl-CoA reductase inhibitors; Pancreatic neoplasms; Risk factors
Categories
Funding
- U.S. National Institutes of Health (NIH) Grants [UM1 CA186107, P01 CA87969, R01 CA49449]
- NIH [UM1 CA167552, R01 CA205406, R01 CA124908, P50 CA127003, R35 CA197735]
- Broman Fund for Pancreatic Cancer Research
- Robert T. and Judith B. Hale Fund for Pancreatic Cancer
- Perry S. Levy Fund for Gastrointestinal Cancer Research
- Pappas Family Research Fund for Pancreatic Cancer
- Hale Center for Pancreatic Cancer Research, NIH/National Cancer Institute (NCI) [U01 CA210171]
- Department of Defense [CA130288]
- Lustgarten Foundation
- Pancreatic Cancer Action Network
- Noble Effort Fund
- Peter R. Leavitt Family Fund
- Wexler Family Fund
- Promises for Purple
- Mitsukoshi Health and Welfare Foundation
- NATIONAL CANCER INSTITUTE [U01CA210171] Funding Source: NIH RePORTER
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Statins, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, are common lipid-lowering agents and may reduce the risk of several cancer types including pancreatic cancer. However, the association between statin use and pancreatic cancer risk has not been fully evaluated in prospective studies. We studied the association between statin use and incident pancreatic cancer in 113,059 participants from the prospective Nurses' Health Study and Health Professionals Follow-up Study. Statin use was self-reported via study questionnaires and updated biennially. Hazard ratios (HRs) and 95% confidence intervals (CIs) for incidence of pancreatic cancer were estimated using multivariable Cox proportional hazards models with adjustment for potential confounders. In total, 583 participants developed incident pancreatic cancer during 1.4 million person-years of follow-up. No difference was identified in pancreatic cancer risk for regular versus non-regular statin users (multivariable-adjusted HR 0.98; 95% CI 0.82-1.16). There was no significant heterogeneity in the association of statin use with pancreatic cancer risk between the cohorts. Similarly, longer duration of regular statin use was not associated with decreased risk of pancreatic cancer (P (trend) = 0.65). The results remained similar when we examined statin use status at baseline or accounting for 4-year latency period. We observed no statistically significant effect modification for the association of statin use with pancreatic cancer risk by body mass index, smoking status, or diabetes mellitus status (all P (interaction) > 0.21). Regular statin use was not associated with pancreatic cancer risk in two large prospective cohort studies in the U.S.
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