Vitamin D-binding protein and pancreatic cancer: a nested case-control study.

Authors

Piper MR, Freedman DM, Robien K, Kopp W, Rager H, Horst RL, Stolzenberg-Solomon RZ

Affiliations

• From the Nutritional Epidemiology Branch (MRP and RZS-S) and the Radiation Epidemiology Branch (DMF), Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD; the Departments of Epidemiology and Biostatistics and Exercise Science, Milken Institute School of Public Health, George Washington University, Washington, DC (KR); the Clinical Support Laboratory, Leidos Biomedical Research Inc./Frederick National Laboratory for Cancer Research, Frederick, MD (WK and HR); and Heartland Assays Inc., Iowa State University, Ames, IA (RLH).
• From the Nutritional Epidemiology Branch (MRP and RZS-S) and the Radiation Epidemiology Branch (DMF), Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD; the Departments of Epidemiology and Biostatistics and Exercise Science, Milken Institute School of Public Health, George Washington University, Washington, DC (KR); the Clinical Support Laboratory, Leidos Biomedical Research Inc./Frederick National Laboratory for Cancer Research, Frederick, MD (WK and HR); and Heartland Assays Inc., Iowa State University, Ames, IA (RLH). rs221z@nih.gov.

Abstract

BACKGROUND: Vitamin D-binding protein (DBP) is the primary carrier of 25-hydroxyvitamin D [25(OH)D] in the circulation. One prospective study in male smokers found a protective association between DBP and pancreatic cancer, particularly among men with higher 25(OH)D concentrations.

OBJECTIVE: The objective was to examine the association between DBP and pancreatic cancer risk in an American population.

DESIGN: We conducted a nested case-control study in the Prostate, Lung, Colorectal, and Ovarian Cancer screening trial cohort of men and women aged 55-74 y at baseline. Between 1993 and 2010, 295 incident pancreatic adenocarcinoma cases were reported (follow-up to 15.1 y). Two controls (n = 590) were matched to each case by age, race, sex, and month of blood draw. We calculated smoking- and diabetes-adjusted ORs and 95% CIs with the use of conditional logistic regression.

RESULTS: DBP concentration was not significantly associated with pancreatic cancer overall [highest (≥7149.4 nmol/L) vs. lowest (<3670.4 nmol/L) quintile; OR: 1.75; 95% CI: 0.91, 3.37; P-trend = 0.25]. For serum 25(OH)D compared with the referent (50 to <75 nmol/L), individuals in the highest group had a significantly higher risk (≥100 nmol/L; OR: 3.23; 95% CI: 1.24, 8.44), whereas those in the lowest group had no significant association (<25 nmol/L; OR: 2.50; 95% CI: 0.92, 6.81). Further adjustment for DBP did not alter this association.

CONCLUSION: Our results do not support the hypothesis that serum DBP or 25(OH)D plays a protective role in pancreatic cancer. This trial was registered at clinicaltrials.gov as NCT00339495.