Dietary Inflammatory Index and Epithelial Ovarian Cancer in Southern Chinese Women: A Case-Control Study

The association between inflammatory properties of diet and ovarian cancer risk has been investigated in some Western populations. However, little evidence is available from Asian women whose ovarian cancer incidence rates are low and dietary and lifestyle patterns are very different from their Western counterparts. We aimed to examine whether more pro-inflammatory diets, as indicated by higher dietary inflammatory index (DII®) scores, are associated with increased odds of epithelial ovarian cancer in southern China. A case-control study was conducted during 2006-2008 in Guangzhou, Guangdong Province. Energy-adjusted DII (E-DII) scores were calculated based on dietary intake assessed by a validated food frequency questionnaire administered to 500 incident epithelial ovarian cancer patients and 500 hospital-based controls. Logistic regression models were used to assess the relationship between E-DII scores and odds of ovarian cancer. Positive associations were observed between higher E-DII scores and ovarian cancer odds, using both continuous DII scores (odds ratio (OR) 1.87; 95% confidence interval (CI) 1.65, 2.13) and by DII tertiles (ORtertile3vs1 7.04, 95% CI: 4.70, 10.54, p for trend < 0.001). Likewise, a more pro-inflammatory diet was associated with a higher chance of serous and mucinous ovarian tumors. Our results suggest that a pro-inflammatory diet was associated with increased odds of developing epithelial ovarian cancer in southern Chinese women. The findings add to epidemiological evidence for the role of dietary inflammatory potential in ovarian cancer development.

Association of polymorphisms in MALAT1 with the risk of endometriosis in Southern Chinese women

Endometriosis is a common estrogen-dependent inflammatory disease characterized by the presence of endometrial-like tissue outside the uterine cavity, which causes infertility and pelvic pain. Polymorphisms in MALAT1 have been demonstrated to play crucial roles in many diseases. However, the roles of MALAT1 polymorphisms in the etiology of endometriosis have not been well documented. We genotyped three MALAT1 polymorphisms in 555 endometriosis patients and 535 female control participants using quantitative polymerase chain reaction with TaqMan probes. To estimate the associations between MALAT1 polymorphisms and endometriosis risk, an unconditional logistic regression model was conducted to calculate an odds ratio (OR) and the 95% confidence interval (CI), adjusting for age, abortion history, number of deliveries, Body Mass Index (BMI), and The International Federation of Gynecology and Obstetrics (FIGO) stage. We found that the MALAT1 rs591291 C &gt; T polymorphism significantly enhanced endometriosis risk (heterogeneous: adjusted OR = 1.36, 95% CI = 1.00–1.85, P = 0.050; homogenous: adjusted OR = 1.55, 95% CI = 1.03–2.33, P = 0.037; dominant: adjusted OR = 1.41, 95% CI = 1.05–1.88, P = 0.021). In stratification analyses, these associations were more predominant in the patients younger than 35 years old, with a relatively high number of deliveries and with a BMI between 25 and 29.9. Compared with wild-type CCG haplotype carriers, individuals with TCC haplotypes had a higher risk of developing endometriosis. The MALAT1 rs591291 C &gt; T polymorphism was associated with a significant increase in endometriosis risk.