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Circulating leptin and risk of pancreatic cancer: a pooled analysis of three cohorts (LB369)
Author(s) -
StolzenbergSolomon Rachael,
Newton Christina,
Silverman Debra,
Pollak Michael,
Nogueira Leticia,
Albanes Demetrius,
Männistö Satu,
Tao Yuzhen,
Jacobs Eric
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb369
Subject(s) - medicine , pancreatic cancer , adipokine , leptin , prostate cancer , odds ratio , overweight , obesity , cohort , nested case control study , oncology , incidence (geometry) , diabetes mellitus , confidence interval , cancer , endocrinology , physics , optics
Background: Diabetes, overweight and obesity are consistently associated with increased pancreatic cancer risk; however the underlying mechanism(s) is uncertain. Leptin is an adipokine important in metabolic regulation. Methods: We conducted a pooled nested case‐control study of participants from the Prostate, Lung, Colorectal, and Ovarian Cancer Trial (PLCO), Alpha‐Tocopherol, Beta‐Carotene Cancer Prevention Study (ATBC), and Cancer Prevention Study II Nutrition (CPS‐II) cohorts to investigate whether pre‐diagnostic circulating leptin concentrations were associated with pancreatic cancer. In total, 759 incident pancreatic adenocarcinoma cases were included in this analysis (average follow‐up 8.3 years, up to 20 years). Incidence density selected controls (n=1069) were matched to cases by cohort, age, sex, race, and date of blood draw. We used conditional logistic regression analysis to calculate adjusted odds ratios (OR) and 95% confidence intervals (CI) and sex‐specific quintiles (Q) based on the distribution of the controls. Results: Overall, we did not observe an association between leptin and pancreatic cancer (compared to Q1, Q5 OR=1.13, 95% CI 0.75‐1.70, p‐trend=0.39). There was a statistically significant interaction by follow‐up time (p‐interaction=0.003) such that significantly elevated risk was apparent only among cases occurring 10 or more years after blood draw (compared to Q1, Q4 OR=2.21, 95% CI 1.18‐4.13, Q5 OR=2.55, 95% CI 1.23‐5.27, p‐trend=0.004). There were no significant interactions by cohort, sex, smoking, age, baseline BMI or diabetes. Conclusion: The lack of association during early follow‐up might be explained by subclinical disease. Our results support the hypothesis that leptin plays a role in pancreatic carcinogenesis, however long follow‐up is necessary to observe the association.