Abstract
BackgroundAssociations of obesity and obesity-related metabolic factors (adiposity factors) with uterine corpus cancer (UCC) and ovarian cancer (OVC) risk have been described. Still, a cause-effect relationship and the underlying mediators remain unclear, particularly for low-incidence populations. We aimed to prospectively determine whether adiposity factors could predict the development of UCC and OVC in Taiwanese women. To explore the biological mediators linking adiposity factors to cancer risk, we examined the association of two adipokines, leptin and adiponectin, with the gynecological cancers.MethodsTotally, 11,258 women, aged 30–65, were recruited into the Community-Based Cancer Screening Program (CBCSP) study during 1991–1993, and were followed for UCC and OVC cases until December 31, 2011. Cox proportional hazard models were used to estimate hazard ratios (HRs). Adiposity factors and risk covariates were assessed at recruitment. Newly-developed cancer cases were determined from data in the government’s National Cancer Registry and Death Certification System. For adipokienes study, a nested case-control study was conducted within the cohort. Baseline plasma samples of 40 incident gynecological cancer cases and 240 age-menopause-matched controls were assayed for adipokines levels.FindingsThere were 38 and 30 incident cases of UCC and OVC, respectively, diagnosed during a median 19.9 years of follow-up. Multivariate analysis showed that alcohol intake (HR = 16.00, 95% = 4.83–53.00), high triglyceride levels (HR = 2.58, 95% = 1.28–5.17), and years of endogenous estrogen exposure per 5-year increment (HR = 1.91, 95% = 1.08–3.38) were associated with increased UCC risk. High body mass index (BMI≥27 kg/m2, HR = 2.90, 95% = 1.30–6.46) was associated with increased OVC risk. Analysis further showed an independent effect of adipokines on UCC and OVC risk after adjustment of the risk covariates.ConclusionWe provided evidence that alcohol intake, high triglyceride levels and long endogenous estrogen exposure increase UCC risk, whereas obesity positively predicts OVC risk. Circulating adipokines may mediate the link of adiposity factors to gynecological cancer risk.
Highlights
Compared to Western countries, the incidences of non-viral gynecological cancers are relatively low in Asian countries [1,2]
To further investigate the molecules mediating the relationship of adiposity factors to the cancer risk, we examined the associations of two adipokines, leptin and adiponectin, with the development of gynecological cancers
Years of endogenous estrogen exposure was significantly higher in the uterine corpus cancer (UCC) group, but not in the ovarian cancer (OVC) group, as compared with without the cancers group after accounting for age
Summary
Compared to Western countries, the incidences of non-viral gynecological cancers are relatively low in Asian countries [1,2]. The low incidences may reflect the differences in etiological factors and/or the prevalence of related factors among Asian women In westernized countries, both reproductive factors and obesity/overweight were suggested to have a close association with the gynecological cancers (‘‘gynecological cancers’’ or ‘‘UCC and OVC’’) [4]. A body mass index (BMI) greater than 25 kg/m2 is a significant risk factor for UCC, increasing the risk by 2.89-fold per 10-unit increment of BMI [6]. This association has been related to a mechanism of hormonal disturbance, including elevated estrogen level [7]. Associations of obesity and obesity-related metabolic factors (adiposity factors) with uterine corpus cancer (UCC) and ovarian cancer (OVC) risk have been described. To explore the biological mediators linking adiposity factors to cancer risk, we examined the association of two adipokines, leptin and adiponectin, with the gynecological cancers
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