Although cancer is a major cause of morbidity and mortality in most nations, the spectrum of cancer occurrence varies substantially worldwide. Most previous epidemiologic studies investigating cancer etiology were conducted in North American and western European countries that are relatively homogenous in terms of cancer spectrums and many lifestyle exposures. These limitations may have hindered these studies from evaluating some important etiologic hypotheses. From 1996 to 2000, the Shanghai Women's Health Study recruited 74,942 adult Chinese women from selected urban communities, with a 92% response rate. All participants completed a detailed baseline survey and anthropometrics. Approximately 88% of cohort members donated a urine sample (n = 65,755) and a blood (n = 56,832) or exfoliated buccal cell (n = 8,934) sample. Noteworthy characteristics of this cohort include low consumption of alcohol (1.9%) and use of tobacco (2.4%); high intake of fish (mean, 50.8 g/day), soy foods (mean, 142.3 g/day), and certain vegetables; low prevalence of obesity (5.1%); and nearly 100% employment outside the home. Currently, this cohort of women is being followed via biennial in-person recontact and periodic linkage to cancer and vital statistics registries. The resources from the cohort will be valuable in future studies of environmental exposures and biomarkers for the risk of cancer and other chronic diseases.

To identify common genetic variants that contribute to lung cancer susceptibility, we conducted a multistage genome-wide association study of lung cancer in Asian women who never smoked. We scanned 5,510 never-smoking female lung cancer cases and 4,544 controls drawn from 14 studies from mainland China, South Korea, Japan, Singapore, Taiwan, and Hong Kong. We genotyped the most promising variants (associated at P < 5 × 10-6) in an additional 1,099 cases and 2,913 controls. We identified three new susceptibility loci at 10q25.2 (rs7086803, P = 3.54 × 10-18), 6q22.2 (rs9387478, P = 4.14 × 10-10) and 6p21.32 (rs2395185, P = 9.51 × 10-9). We also confirmed associations reported for loci at 5p15.33 and 3q28 and a recently reported finding at 17q24.3. We observed no evidence of association for lung cancer at 15q25 in never-smoking women in Asia, providing strong evidence that this locus is not associated with lung cancer independent of smoking.

Known genetic loci explain only a small proportion of the familial relative risk of colorectal cancer (CRC). We conducted the largest genome-wide association study in East Asians with 14,963 CRC cases and 31,945 controls and identified six new loci associated with CRC risk (P = 3.42 × 10−8 to 9.22 × 10−21) at 10q22.3, 10q25.2, 11q12.2, 12p13.31, 17p13.3 and 19q13.2. Two of these loci map to genes (TCF7L2 and TGFB1) with established roles in colorectal tumorigenesis. Four other loci are located in or near genes involved in transcription regulation (ZMIZ1), genome maintenance (FEN1), fatty acid metabolism (FADS1 and FADS2), cancer cell motility and metastasis (CD9) and cell growth and differentiation (NXN). We also found suggestive evidence for three additional loci associated with CRC risk near genome-wide significance at 8q24.11, 10q21.1 and 10q24.2. Furthermore, we replicated 22 previously reported CRC loci. Our study provides insights into the genetic basis of CRC and suggests new biological pathways.

This uniquely large pooled analysis confirms that current cigarette smoking is associated with a twofold increased risk of pancreatic cancer and that the risk increases with the number of cigarettes smoked and duration of smoking. Risk of pancreatic cancer reaches the level of never smokers ∼20 years after quitting.

This population-based, case-control study of esophageal cancer in urban Shanghai suggests a protective effect of green tea consumption. Although these findings are consistent with studies in laboratory animals, indicating that green tea can inhibit esophageal carcinogenesis, further investigations are definitely needed.