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Prospective study of urinary prostaglandin E2 metabolite and pancreatic cancer risk
Author(s) -
Cui Yong,
Shu XiaoOu,
Li HongLan,
Yang Gong,
Wen Wanqing,
Gao YuTang,
Cai Qiuyin,
Rothman Nathaniel,
Yin HuiYong,
Lan Qing,
Xiang YongBing,
Zheng Wei
Publication year - 2017
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.31007
Subject(s) - medicine , odds ratio , prospective cohort study , urine , quartile , pancreatic cancer , urinary system , nested case control study , confidence interval , cancer , confounding , cohort study , endocrinology , european prospective investigation into cancer and nutrition , case control study , gastroenterology
The cyclooxygenase 2 (COX‐2) pathway is upregulated in many pancreatic cancer cells, and it is believed that carcinogenetic effects of COX‐2 upregulation are largely through prostaglandin E2 (PGE2) overproduction. We tested this hypothesis by evaluating the association between urinary PGE2 metabolites (PGE‐M), a biomarker of in vivo PGE2 overproduction, and pancreatic cancer risk. We conducted a case–control study with 722 subjects (239 cases and 483 controls) nested within two prospective cohort studies, the Shanghai Women's Health Study (SWHS) and Shanghai Men's Health Study (SMHS). Pre‐diagnosis urine samples were measured for PGE‐M using a liquid chromatography/tandem mass spectrometric method. Conditional logistic regression was used to estimate odds ratio (OR) and 95% confidence intervals (95%CI), with adjustment for potential confounders. Compared to those with the lowest urine level of PGE‐M (the first quartile), individuals with higher urine levels of PGE‐M had an increased risk of developing pancreatic cancer, with adjusted ORs (95%CI) of 1.63 (0.98–2.73), 1.55 (0.90–2.69) and 1.94 (1.07–3.51), for the second to the fourth quartile groups, respectively ( p for trend = 0.054). This dose–response positive association was more evident among those who had BMI <25 kg/m 2 than overweight individuals ( p for interaction = 0.058). After excluding cases diagnosed in the first year of follow‐up and their matched controls, this positive association persisted ( p for trend = 0.037) and the interaction became statistically significant ( p for interaction = 0.017). Our study adds additional evidence that the COX‐2 pathway is involved in pancreatic carcinogenesis and suggests that urinary PGE‐M may serve as a biomarker for predicting pancreatic cancer risk.