Tsuyoshi Hamada1, Natalia Khalaf2, Chen Yuan3,4, Ana Babic3, Vicente Morales-Oyarvide3, Zhi Rong Qian1, Jonathan Andrew Nowak5, Kimmie Ng3, Peter Kraft4,6, Douglas Adam Rubinson3, Meir Jonathan Stampfer4,7,8, Edward Luciano Giovannucci4,7,8, Charles Stewart Fuchs9,10,11, Shuji Ogino1,4,5, Brian Matthew Wolpin12. 1. Department of Oncologic Pathology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA. 2. Division of Gastroenterology, Hepatology, and Endoscopy, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. 3. Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, 450 Brookline Avenue, Boston, MA, 02215, USA. 4. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 5. Program in MPE Molecular Pathological Epidemiology, Department of Patholog, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. 6. Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 7. Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. 8. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 9. Yale Cancer Center, New Haven, CT, USA. 10. Department of Medicine, Yale School of Medicine, New Haven, CT, USA. 11. Smilow Cancer Hospital, New Haven, CT, USA. 12. Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, 450 Brookline Avenue, Boston, MA, 02215, USA. bwolpin@partners.org.
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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 (Ptrend = 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 Pinteraction > 0.21). CONCLUSIONS: Regular statin use was not associated with pancreatic cancer risk in two large prospective cohort studies in the U.S.
BACKGROUND: 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. METHODS: 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. RESULTS: 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 (Ptrend = 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 Pinteraction > 0.21). CONCLUSIONS: Regular statin use was not associated with pancreatic cancer risk in two large prospective cohort studies in the U.S.
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