China ; epidemiology ; Humans ; Lung Neoplasms ; epidemiology ; genetics ; Risk ; Smoking

OBJECTIVETo investigate the association of the risk of prostate cancer (PCa) with the polymorphism of the CYP2E1 gene, smoking and drinking, and to explore the joint role of genes and living habits in PCa pathogenesis.

METHODSWe conducted a case-control study on 109 PCa patients and 202 age-matched non-PCa male controls, and detected the polymorphisms of CYP2E1 Rsa I and Pst I sites by PCR-RFLP using DNA from peripheral blood lymphocytes.

RESULTSThe history of deep smoking (OR = 2.29, 95% CI: 1.28 - 4.09) or heavy smoking (OR = 1.81, 95% CI: 1.02 - 3.22) was a risk factor. The CYP2E1 C1/C1 genotype significantly increased the risk of PCa (OR = 1.71, 95% CI: 1.04 - 2.82) and apparently interacted with drinking (OR = 2.21, 95% CI: 1.06 - 4.59). Heavy smokers with the C1/C1 genotype showed an increased risk of PCa (OR = 2.80, 95% CI: 1.20 - 6.56), as compared with non-smokers carrying the genotype of C1/C2 or C2/C2.

CONCLUSIONThe risk of PCa obviously increases in individuals with both the CYP2E1 C1/C1 genotype and the habit of smoking or drinking, and it has a significant positive correlation with the dose of tobacco exposure.

Aged ; Alcohol Drinking ; epidemiology ; genetics ; Case-Control Studies ; China ; epidemiology ; Cytochrome P-450 CYP2E1 ; genetics ; Genetic Predisposition to Disease ; Humans ; Male ; Middle Aged ; Polymorphism, Genetic ; Prostatic Neoplasms ; epidemiology ; genetics ; Smoking ; epidemiology ; genetics

Pancreatic cancer is an extremely life-threatening neoplasm with a case-fatality rate approaching 100%. Smoking is the major known risk factor for this cancer, explaining 19% of all cases. The nutrition and food consumption patterns play other important roles in the etiology of pancreatic cancer, explaining 35% of all cases. Epidemiological evidences on the relationship between nutrition and pancreatic cancer found consistently positive associations between the intakes of meat, carbohydrates, and dietary cholesterol and pancreatic cancer. Consistent inverse relationships with fruit and vegetable intakes and, in particular, with fiber and vitamin C, have also been noted. Many inherited germline mutations increase the risk of pancreatic cancer. In addition, several common polymorphisms in genes that associated with metabolism of environmental carcinogens, DNA repair and folate metabolism may alter the risk of pancreatic cancer. Interaction between genes and environmental factors may contribute to the risk of pancreatic cancer.
Diet ; Genetic Predisposition to Disease ; genetics ; Humans ; Occupational Exposure ; Pancreatic Neoplasms ; epidemiology ; genetics ; prevention & control ; Polymorphism, Genetic ; Risk Factors ; Smoking

OBJECTIVES: The purpose of this study was to identify any influence of socioeconomic status on smoking and smoking cessation in a situation where genetic factors are controlled. METHODS: The sample for this study was 2502 members of the twins and families cohort who participated in the Korean Healthy Twins Study from 2005 to 2009. Groups of brothers or sisters, including twins and fraternal twins, were compared in terms of smoking and smoking cessation behaviors according to differences in socioeconomic status and gender. RESULTS: In a situation with complete control of genetic factors, results showed that the daily smoking amount, cumulative smoking amount, and dependence on nicotine decreased with higher-status occupations, and the rate of smoking and amount of cumulative smoking decreased with higher levels of education. Regarding smoking cessation behavior, a higher level of education was associated with a lower smoking cessation rate, and no significant gender differences were found. CONCLUSIONS: Environmental factors had a stronger influence on smoking behavior than did genetic factors. Genetic factors had greater influence on smoking cessation than did environmental factors; however, this requires verification in further studies.
Adult ; Female ; Genetic Predisposition to Disease ; Health Behavior ; Humans ; Korea ; Male ; Sex Factors ; Smoking/*epidemiology/genetics ; *Smoking Cessation ; *Social Class ; *Social Environment ; Socioeconomic Factors

OBJECTIVETo examine the significance of individual risk on diabetes to subjects who underwent diabetes screening.

METHODS2003 asymptomatic diabetes subjects with high-risk factors of diabetes as family history, obesity, hypertension, and/or dyslipidemia, fetal giant history were screened. 5362 subjects having no risk factors but from the same community were allocated as controls.

RESULTSThere were 131 (6.54%) diabetes identified in the screening group and 1547 (77.23%) subjects having 1 risk factor, 387 (19.27%) having 2 risk factors, 70 (3.49%) having 3 or more risk factors. There were 96 (1.79%) diabetes identified in the control group. Compared with control group, the OR (95% CI) value was 2.68 (2.20-3.25) after adjusted on age among the high risk group. The OR value of those having 1 risk factor was 2.89, but these having 3 or more risk factors increased to 4.68.

CONCLUSIONThe relation between the risk of high-risk group with diabetes and the number of risk factors of diabetes presented positive correlation. Early and regular screening for diabetes was essential in these individuals with high-risk factors.

Adult ; Aged ; China ; epidemiology ; Diabetes Mellitus, Type 2 ; epidemiology ; etiology ; genetics ; Family Health ; Female ; Glucose Tolerance Test ; Humans ; Hyperlipidemias ; epidemiology ; Hypertension ; epidemiology ; Male ; Mass Screening ; Middle Aged ; Obesity ; epidemiology ; Odds Ratio ; Prevalence ; Risk Factors ; Smoking

Glutathione S-transferase (GST) plays a key role in the detoxification of xenobiotic atherogen generated by smoking. To analyze the effect of GSTM1/T1 gene polymorphisms on the development of smoking-related coronary artery disease (CAD), 775 Korean patients who underwent coronary angiography were enrolled. The subjects were classified by luminal diameter stenosis into group A (>50%), B (20-50%), or C (<20%). GSTM1 and GSTT1 gene polymorphisms were analyzed using multiplex polymerase chain reaction (PCR) for GSTM1/T1 genes and CYP1A1 gene for internal control. Of 775 subjects, 403 patients belonged to group A. They had higher risk factors for CAD than group B (N=260) and group C (N=112). The genotype frequencies of null GSTM1 and GSTT1 showed no significant differences among 3 groups. Considering the effect of GSTM1 gene polymorphisms on the smoking-related CAD, smokers with GSTM1 null genotype had more increased risk for CAD than non-smoker with GSTM1 positive genotype (odds ratios [OR], 2.07, confidence interval [CI], 1.06-4.07). Also the effect of GSTT1 gene polymorphism on smoking-related CAD showed the same tendency as GSTM1 gene (OR, 2.00, CI, 1.05-3.84). This effect of GSTM1/T1 null genotype on smoking-related CAD was augmented when both gene polymorphisms were considered simultaneously (OR, 2.76, CI, 1.17-6.52). We concluded that GSTM1/T1 null genotype contributed to the pathogenesis of smoking-related CAD to some degree.
Aged ; Coronary Angiography ; Coronary Artery Disease/epidemiology/*genetics/radiography ; Female ; Genetic Predisposition to Disease/epidemiology ; Genotype ; Glutathione Transferase/*genetics ; Humans ; Male ; Middle Aged ; *Polymorphism, Genetic ; Risk Factors ; Severity of Illness Index ; Smoking/epidemiology/*genetics

OBJECTIVETo estimate the contribution of known identified risk factors to breast cancer incidence and mortality in China, and provide evidence to support the prevention and control of breast cancer for Chinese females.

METHODSWe calculated the proportion of breast cancer attributable to specific risk factors. Data on exposure prevalence were obtained from Meta-analyses and large-scale national surveys of representative samples of the Chinese population. Data on relative risks were obtained from Meta-analyses and large-scale prospective studies. Cancer mortality and incidence were taken from the Third National Death Survey and from cancer registries in China.

RESULTSThe first 5 risk factors of breast cancer in China were benign breast disease (RR = 2.62), family history of breast cancer (RR = 2.39), smoking (RR = 1.86), overweight (RR = 1.60) and age at menarche (RR = 1.54). The proportion of breast cancer deaths attributable to reproductive factors, lifestyle factors, benign breast disease, the use of external hormone and family history of breast cancer was 27.84%, 23.55%, 15.09%, 3.60% and 2.49%, respectively. The total population attributable fraction (PAF) was 55.95% for risk factors in our study. Overall, we estimated that 79 862 breast cancer cases and 22 456 deaths were attributed to the five risk factors in China in 2005.

CONCLUSIONSThe prevention and control of unhealthy lifestyle factors may significantly reduce the number and death of breast cancer in China.

Breast Diseases ; complications ; Breast Neoplasms ; epidemiology ; etiology ; genetics ; China ; epidemiology ; Female ; Genetic Predisposition to Disease ; Humans ; Menarche ; Meta-Analysis as Topic ; Overweight ; complications ; Risk Factors ; Smoking ; adverse effects

OBJECTIVETo determine the interaction between indoor air pollution and mEH gene polymorphisms.

METHODSBlood samples from 222 non small cell lung cancer patients and 222 healthy people were characterized by PCR and PCR-RFLP methods. The interaction coefficients were determined through unconditional logistic regression model.

RESULTSSignificant differences in the positive rate of mEH-exon3 mutant and the heterozygote were found between case and control groups (chi(2) = 7.046, P = 0.030). But no significant difference was found in mEH-exon4 non-wild-type between groups (chi(2) = 2.674, P = 0.263). mEH-exon3 mutant (OR = 1.99; 95% CI = 1.21, 3.25) could significantly increase the risk of lung cancer. After adjusted by confounding variables, significant interactions were found between the use of coal-wall stove and the non-wild type mEH gene. The interaction coefficients were increased with the duration of exposure and quantity of coal consumed. The super multiplication models were established between non-wild type mEH gene and the exposure to soot or oil fume during cooking. The interaction coefficients were 2.75 and 7.34 respectively for exon3 and exon4. No interaction was found between non-wild type mEH gene and irritation of eye or throat during cooking.

CONCLUSIONThrough the molecular epidemiological techniques, we confirmed indoor air pollution that caused by coal burning was a noticeable lung cancer risk factor. The interaction between the polymorphisms of mEH gene and the indoor air pollution plays an important role in the carcinogenesis of lung.

Adult ; Aged ; Air Pollution, Indoor ; Carcinoma, Non-Small-Cell Lung ; epidemiology ; genetics ; China ; epidemiology ; Epoxide Hydrolases ; genetics ; Exons ; Female ; Humans ; Lung Neoplasms ; epidemiology ; Male ; Middle Aged ; Polymorphism, Genetic ; Smoking

Objective: To evaluate the association of family history with risk of major coronary events (MCE) and ischemic heart disease (IHD). Methods: After excluding participants with heart disease, stroke or cancer at baseline survey, a total of 485 784 participants from the China Kadoorie Biobank, who had no missing data on critical variables, were included in the analysis. Cox regression analysis was used to estimate the hazard ratios (HR) and 95% CI. Subgroup analyses were performed according to the baseline characteristics. Results: During a median of 7.2 years of follow-up, we documented 3 934 incident cases of MCE and 24 537 cases of IHD. In multivariable-adjusted models, family history was significantly associated with risk of MCE and IHD. The adjusted HRs (95%CI) were 1.41 (1.19-1.65) and 1.25 (1.18-1.33), respectively. History of disease among siblings was more strongly associated with early-onset MCE than parental history (HR=2.97, 95%CI: 1.80-4.88). Moreover, the association of family history with MCE and IHD was stronger in persons who were overweight or obesive, and the association between family history and MEC was stronger in smokers. Conclusion: This large-scale, prospective study indicated that family history was an independent risk factor for MCE and IHD in China. The intervention targeting major known lifestyle risk factors and the management of chronic diseases should be strengthened for Chinese population, especially for the individuals with family history were at high risk.
Asian People/statistics & numerical data* ; China/epidemiology* ; Coronary Disease/genetics* ; Humans ; Incidence ; Myocardial Ischemia/genetics* ; Overweight/ethnology* ; Proportional Hazards Models ; Prospective Studies ; Risk Assessment ; Risk Factors ; Smoking/ethnology*

Inflammation has been known to be an important underlying condition for development of various diseases including cancer. The aims of this study were to investigate whether tobacco smoke exposure increases the level of inflammation biomarkers and the GSTM1 and GSTP1 gene polymorphisms are associated with inflam matory response due to tobacco smoke exposure. We measured urinary cotinine level in 300 healthy university students. Total serum TNF-alpha levels and blood WBC counts were determined to evaluate inflammatory response. Allelic loss of the GSTM1 and the GSTP1 (Ile105Val) polymorphism were determined by PCR and RFLP. Tobacco smoke exposure was found to be associated with increase of both TNF-alpha level and WBC count. Particularly, smokers with combination of GSTM1 null and GSTP1 AG or GG genotypes showed higher TNF-alpha level than those with the other genotype combinations (p=0.07). This result suggests that smoking may induce inflammation measured as TNF-alpha level or WBC count and combinations of the GSTM1 and GSTP1 polymorphisms may modify the effect of smoking on serum TNF-alpha level.
Tumor Necrosis Factor-alpha/blood ; Students ; Smoking/*epidemiology/*genetics/immunology ; Risk Factors ; Risk Assessment/*methods ; Prevalence ; Polymorphism, Single Nucleotide/genetics ; Male ; Korea/epidemiology ; Inflammation/*epidemiology/*genetics/immunology ; Humans ; Glutathione Transferase/*genetics ; Glutathione S-Transferase pi/*genetics ; Genetic Predisposition to Disease/epidemiology/genetics ; Female ; Adult