PurposeThe objective of this study is to investigate and analyze the epidemiologic characteristics and time trends of ovarian cancer incidence and mortality in Jiangsu Province of China during 2003–2012.MethodData were collected from eligible cancer registries in Jiangsu Province. Crude rates, age-specific rates, truncated age-standardized rate, and proportions of ovarian cancer were calculated. The Segi’s World Population was used to calculate age-standardized rates for world (ASW). Poisson distribution was used to analyze the differences between urban and rural areas. Joinpoint regression was performed to estimate the annual percent change (APC) of ovarian cancer incidence/mortality.ResultsA total number of 4,401 new cases and 1,918 deaths were identified during period 2003–2012. The incidence and mortality ASW was 3.64/100,000 and 1.52/100,000, respectively. ASW of incidence was 4.48/100,000 in urban areas, while 3.04/100,000 in rural areas. The mortality of ASW was slight higher in urban areas than in rural areas. Age-specific incidence showed a peak at the age group of 60–64 years, whereas mortality peaked at age group of 65–69 years. A significant increase of incidence was observed from 2003 to 2006, with an APC of 34.0% (95% CI: 9.7, 63.7), the increasing rate declined since 2006 (APC = 3.3%, 95% CI: −3.5, 10.5). The mortality showed a gentle upward trend as compared with incidence, with an APC of 9.9% (95% CI: 7.7, 12.2) per year, continuously from 2003 to 2012. It is apparent that both incidence and mortality presented a rising trend in all areas, but urban were higher than that in rural areas.ConclusionOvarian cancer is a highly lethal disease which is becoming a significant public health problem in Chinese women. It is vital to improve the understanding of current status of ovarian cancer. Moreover, prevention and control policies should be formulated to reduce the disease burden of ovarian cancer in China.

Genome-wide association studies (GWAS) have indicated that gene polymorphisms in alleles of RAS p21 protein activator 2 (RASA2), cell adhesion molecule 1 (CADM1) and hypoxia inducible factor 1 alpha subunit inhibitor (HIF1AN) are associated with the risk of obesity. In this study, we explored the interactions between candidate SNPs of RASA2 (rs16851483), CADM1 (rs12286929) and HIF1AN (rs17094222) and body fatness for breast cancer risk. Unconditional logistic regression models were applied to measure the associations of related factors with breast cancer by odds ratios (ORs) and 95% confidence intervals (CIs). It was observed that cases had a statistically higher body mass index (BMI ≥ 28 kg/m2, OR = 1.77), waist circumference (WC ≥ 90cm, OR = 2.89) and waist-to-hip ratio (WHR ≥ 0.9, OR = 3.41) as compared to controls. Significant differences were also found in the genotype distributions of RASA2 rs16851483 T/T homozygote and CADM1 rs12286929 G/A heterozygote between cases and controls, with an OR of 1.68 (95% CI: 1.10–2.56) and 0.80 (95% CI: 0.64–0.99), respectively. Furthermore, significant interactions were observed between polymorphisms of three genes and body fatness for the risk of breast cancer based on both additive and multiplicative scales. These results of our study suggest that body fatness possibly plays an important role in the development of breast cancer and this risk might be modified by specific genotypes of some potential genes, especially for obese women in China.

Observational studies have demonstrated an association between elevated homocysteine (Hcy) level and risk of multiple myeloma (MM). However, it remains unclear whether this relationship is causal. We conducted a Mendelian randomization (MR) study to evaluate whether genetically increased Hcy level influences the risk of MM. We used the methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism as an instrumental variable, which affects the plasma Hcy levels. Estimate of its effect on plasma Hcy level was based on a recent genome-wide meta-analysis of 44,147 individuals, while estimate of its effect on MM risk was obtained through meta-analysis of case-control studies with 2,092 cases and 4,954 controls. By combining these two estimates, we found that per one standard-deviation (SD) increase in natural log-transformed plasma Hcy levels conferred a 2.67-fold increase in risk for MM (95% confidence interval (CI): 1.12–6.38; P = 2.7 × 10−2). Our study suggests that elevated Hcy levels are causally associated with an increased risk of developing MM. Whether Hcy-lowering therapy can prevent MM merits further investigation in long-term randomized controlled trials (RCTs).