No association between alcohol consumption and pancreatic cancer even among individuals genetically susceptible to the carcinogenicity of alcohol.

Inconsistent results have been reported for the association between alcohol use and pancreatic cancer, particularly at low levels of alcohol consumption. Individuals genetically susceptible to the carcinogenic effect of alcohol might have higher pancreatic cancer risk after drinking alcohol. The current study investigated the association between alcohol use and pancreatic cancer with 419 pancreatic cancer cases and 963 controls recruited by a hospital-based case-control study in Taiwan. Gene-environment interaction between alcohol use and polymorphisms of two ethanol-metabolizing genes, ADH1B and ALDH2, on pancreatic risk was evaluated. Our results showed no significant association between alcohol drinking and an increased pancreatic cancer risk, even at high levels of alcohol consumption. Even among those genetically susceptible to the carcinogenic effect of alcohol (carriers of ADH1B*2/*2(fast activity) combined with ALDH2*1/*2(slow activity) or ALDH2*2/*2(almost non-functional)), no significant association between alcohol use and pancreatic cancer was observed. Overall, our results suggested that alcohol drinking is not a significant contributor to the occurrence of pancreatic cancer in Taiwan.

Validation of genome-wide association study-identified single nucleotide polymorphisms in a case-control study of pancreatic cancer from Taiwan.

BACKGROUND: Due to differences in genetic background, it is unclear whether the genetic loci identified by the previous genome-wide association studies (GWAS) of pancreatic cancer also play significant roles in the development of pancreatic cancer among the Taiwanese population. METHODS: This study aimed to validate the 25 pancreatic cancer GWAS-identified single nucleotide polymorphisms (SNPs) in a case-control study (278 cases and 658 controls) of pancreatic cancer conducted in Taiwan. Statistical analyses were conducted to determine the associations between the GWAS-identified SNPs and pancreatic cancer risk. Gene-environment interaction analysis was conducted to evaluate the interactions between SNPs and environmental factors on pancreatic cancer risk. RESULTS: Among the 25 GWAS-identified SNPs, 7 (rs2816938 (~ 11 kb upstream of NR5A2), rs10094872 (~ 28 kb upstream of MYC), rs9581943 (200 bp upstream of PDX1) and 4 chromosome 13q22.1 SNPs: rs4885093, rs9573163, rs9543325, rs9573166) showed a statistically significant association with pancreatic cancer risk in the current study. Additional analyses showed two significant gene-environment interactions (between poor oral hygiene and NR5A2 rs2816938 and between obesity and PDX1 rs9581943) on the risk of pancreatic cancer. CONCLUSIONS: The current study confirmed the associations between 7 of the 25 GWAS-identified SNPs and pancreatic risk among the Taiwanese population. Furthermore, pancreatic cancer was jointly influenced by lifestyle and medical factors, genetic polymorphisms, and gene-environment interaction. Additional GWAS is needed to determine the genetic polymorphisms that are more relevant to the pancreatic cancer cases occurring in Taiwan.

The relationship between different glycemic statuses and colon polyps in a Taiwanese population.

BACKGROUND: While diabetes is considered as a risk factor for colorectal cancer, there are few studies that address the association between glycemic statuses and different colon polyps, ranging from non-neoplastic polyps to advanced adenomatous polyps. METHODS: A total of 6,348 participants, consisting of 3,777 men and 2,571 women, with a mean age of 50.5 years, were included for final analysis after excluding subjects with a past history of colorectal cancer, colon polyps/polypectomy, familial adenomatous polyposis, and colorectomy, or missing data. Diabetes and pre-diabetes were defined using the 2011 American Diabetes Association criteria. Subjects were classified into four groups: polyp-free, non-neoplastic polyps, non-advanced and advanced adenomatous polyps. RESULTS: There were significant differences in the prevalence of diabetes and pre-diabetes among groups with different kinds of colon polyps. In addition, significant differences were also noted in age, total cholesterol, body mass index, triglyceride, high density lipoprotein-cholesterol, fasting plasma glucose, and the prevalence of male gender, hypertension, obesity, current smoking and alcohol drinking among groups. In the multinomial logistic regression analyses, diabetes was related to both non-advanced and advanced adenomatous polyps, while pre-diabetes was only related to non-advanced adenomatous polyps. In addition, age ≥65 years and male gender were associated with both non-advanced and advanced adenomatous polyps, while hypertension and current smoking were independently related to advanced and non-advanced adenomatous polyps, respectively. CONCLUSIONS: Diabetes, but not pre-diabetes, was associated with a higher risk of advanced adenomatous polyps. In addition, both diabetes and pre-diabetes were important correlates of non-advanced adenomatous polyps.