Dietary Intake of Fatty Acids, Total Cholesterol, and Stomach Cancer in a Chinese Population.

To investigate the associations between dietary fatty acids and cholesterol consumption and stomach cancer (SC), we analyzed data from a population-based case-control study with a total of 1900 SC cases and 6532 controls. Dietary data and other risk or protective factors were collected by face-to-face interviews in Jiangsu Province, China, from 2003 to 2010. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using multiple unconditional logistic regression models and an energy-adjusted method. The joint associations between dietary factors and known risk factors on SC were examined. We observed positive associations between dietary saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), and total cholesterol and the development of SC, comparing the highest versus lowest quarters. Increased intakes of dietary SFAs (p-trend = 0.005; aOR, 1.11; 95% CI, 1.01-1.22 with a 7 g/day increase as a continuous variable) and total cholesterol (p-trend < 0.001; aOR, 1.13; 95% CI, 1.06-1.22 with a 250 mg/day increase as a continuous variable) were monotonically associated with elevated odds of developing SC. Our results indicate that dietary SFAs, MUFAs, and total cholesterol are associated with stomach cancer, which might provide a potential dietary intervention for stomach cancer prevention

Associations of prostate cancer risk variants with disease aggressiveness: results of the NCI-SPORE Genetics Working Group analysis of 18,343 cases

Genetic studies have identified single nucleotide polymorphisms (SNPs) associated with the risk of prostate cancer (PC). It remains unclear whether such genetic variants are associated with disease aggressiveness. The NCI-SPORE Genetics Working Group retrospectively collected clinicopathologic information and genotype data for 36 SNPs which at the time had been validated to be associated with PC risk from 25,674 cases with PC. Cases were grouped according to race, Gleason score (Gleason ≤ 6, 7, ≥ 8) and aggressiveness (non-aggressive, intermediate, and aggressive disease). Statistical analyses were used to compare the frequency of the SNPs between different disease cohorts. After adjusting for multiple testing, only PC-risk SNP rs2735839 (G) was significantly and inversely associated with aggressive (OR = 0.77; 95 % CI 0.69-0.87) and high-grade disease (OR = 0.77; 95 % CI 0.68-0.86) in European men. Similar associations with aggressive (OR = 0.72; 95 % CI 0.58-0.89) and high-grade disease (OR = 0.69; 95 % CI 0.54-0.87) were documented in African-American subjects. The G allele of rs2735839 was associated with disease aggressiveness even at low PSA levels (<4.0 ng/mL) in both European and African-American men. Our results provide further support that a PC-risk SNP rs2735839 near the KLK3 gene on chromosome 19q13 may be associated with aggressive and high-grade PC. Future prospectively designed, case-case GWAS are needed to identify additional SNPs associated with PC aggressiveness

Risk Factors of Atrophic Gastritis and Stomach Cancer in a Population-based Case-control Study in Jiangsu Province, China

Background: Stomach cancer is a major public health burden worldwide, with 5-year survival rates ranging from 20% to 30% in most countries. However, studies have shown early diagnosis and prompt treatment leading to better survival. Atrophic gastritis is a precancerous lesion of stomach cancer, which is thought to be a reversible stage. Few studies have examined environmental risk factors and the role of genetic susceptibility of atrophic gastritis, compared to the stomach cancer endpoint. The overall objective is to evaluate potential risk factors, including Helicobacter pylori infection, tobacco smoking, alcohol drinking, dietary habits of excessive salt intake, dietary nitrate and nitrites, and observe their association with atrophic gastritis and stomach cancer individually. In addition, we examine the relationship between candidate single nucleotide polymorphisms (SNPs) from the microRNA pathway, stem cell pathway, and genomic wide association studies (GWAS) on atrophic gastritis and stomach cancer respectively.Methods: A population based case-control study was conducted in Jiangsu Province, China. In our study, 1,617 stomach cancer patients and 6,369 cancer-free controls were included for analysis. For specific aim 1, the evaluation of risk factors of atrophic gastritis, only controls (cancer-free participants) are examined. For Specific Aims 2 and 3, case-control study design was employed including both stomach cancer cases and cancer-free controls for the development of stomach cancer. Epidemiologic data were collected by face-to-face interview using a standardized questionnaire, and a 5 ml blood sample was collected at the time of the interview. Atrophic gastritis status was chemically defined using serum pepsinogen (PG) cutoffs of PG I 70ng/mL and PG I/PG II 6. Unconditional logistic regression models have been used to estimate adjusted odds ratios (ORs) and 95% confidence intervals (CIs). Potential confounding factors have been adjusted in the analyses, including age, gender, study site, average family income, education level, family history of stomach cancer, pack-years of smoking (except smoking related factors), alcohol consumption (except alcohol drinking related factors), total caloric intake (for dietary intake variables only), and H. pylori status. Additive and multiplicative interactions have been evaluated, using relative excess risk due to interaction (RERI) and ratio of odds ratios (ROR) respectively.Results: In our study, individuals with tonic supplement, having a history of drinking non-boiled water at childhood, and a moderate consumption of red meat were at higher risk of atrophic gastritis respectively, while adjusting for potential confounding factors. However, tobacco smoking, alcohol drinking, tea drinking, and dietary intake of micronutrients (vitamin A, thiamin, riboflavin, niacin, vitamin C, vitamin E, zinc, selenium) and macronutrients (protein, fat, fiber, carbohydrates) were not significantly associated with atrophic gastritis. A protective effect of frequent consumption of BBQ meat, salted meat or fish, and higher waist-to-hip ratio was observed on the odds of atrophic gastritis. For gastric cancer, tobacco smoking, alcohol drinking, a preference for salty foods, spicy foods, and high temperature foods, high vegetable intake, and high intake of certain vitamins and minerals (vitamin A, thiamin, riboflavin, vitamin C, vitamin E, zinc, selenium) were associated with higher odds of stomach cancer. H. pylori IgG seropositivity and atrophic gastritis, expressed by lower serum PG levels, were also positively associated with stomach cancer respectively. Inverse associations of light tea drinking, consumption of raw garlic and ginger, and higher intake of salted or preserved meat/fish (third quartile versus lowest quartile) were found on stomach cancer respectively. When stratifying by atrophic gastritis status, similar associations are observed for the subpopulation without atrophic gastritis, but not in those with atrophic gastritis. For genetic susceptibility markers, significant inverse associations were observed with atrophic gastritis in rs3130932 (Oct4) and rs3729629 (WNT2) from the stem cell pathway, even after semi-bayes adjustment. For the stomach cancer endpoint, rs11077 (XPO5), rs12828 (WWOX), rs4072391 (IL6R), rs11364 (HES2), and rs738722 (CHEK2) are found to be positively associated and rs2075993 (E2F2), rs2273368 (Wnt2B), rs4961280 (Ago2), rs7372209 (miR-26a1), rs1033583 (DLL1), rs1981492 (AXIN1), rs3130932 (Oct4), rs3729629 (WNT2), rs3734637 (HEY2), and rs4835761 (WNT8A) were inversely associated with stomach cancer risk overall, even after semi-bayes shrinkage. When stratifying by atrophic gastritis status, rs12828 (WWOX), rs2273368 (Wnt2B), rs9266 (KRAS) from the miRNA pathway, and rs11364 (HES2), rs2240308 (AXIN2), rs1033583 (DLL1), rs1981492 (AXIN1), rs3130932 (Oct4), rs3729629 (WNT2), rs4835761 (WNT8A), rs915894 (Notch4) from the stem cell pathway were significantly associated with stomach cancer in those without atrophic gastritis. In those with atrophic gastritis, only the rs2273368 (Wnt2B), rs3734637 (HEY2), and rs738722 (CHEK2) were associated with stomach cancer after semi-bayes adjustment. Additive interactions were observed between atrophic gastritis and rs2273368 (Wnt2B), and multiplicative interactions were observed between atrophic gastritis and rs2273368 (Wnt2B), rs11077 (XPO5), rs3130932 (Oct4), and rs738722 (CHEK2) on stomach cancer. Also interactions were found between H. pylori infection and polymorphisms of Ran (rs14035), Gemin4 (rs2740348), HEY1 (rs1046472), Ctbp2 (rs3740535), and between smoking and polymorphisms of Rbl2 (rs3929) and miR-26a1 (rs7372209), and between alcohol drinking and polymorphisms of DOCK4 (rs3801790) on the odds of stomach cancer.Conclusion: This study confirms the association between established risk factors of stomach cancer such as smoking, H. pylori infection, and atrophic gastritis, and adds evidence on the protective effects of tea drinking and raw garlic consumption. To our knowledge, it is the first study to report inverse associations between ginger consumption and stomach cancer. Furthermore, our study is one of the first studies to show association in polymorphisms in the stem cell pathway and atrophic gastritis, and interactions in H. pylori infection, smoking, and alcohol drinking with atrophic gastritis on stomach cancer respectively. Further studies on different ethnic groups and atrophic gastritis determined by the use of tissue samples should be conducted for a fuller understanding of atrophic gastritis and stomach carcinogenesis

Dietary Intake of Fatty Acids, Total Cholesterol, and Stomach Cancer in a Chinese Population.

To investigate the associations between dietary fatty acids and cholesterol consumption and stomach cancer (SC), we analyzed data from a population-based case-control study with a total of 1900 SC cases and 6532 controls. Dietary data and other risk or protective factors were collected by face-to-face interviews in Jiangsu Province, China, from 2003 to 2010. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using multiple unconditional logistic regression models and an energy-adjusted method. The joint associations between dietary factors and known risk factors on SC were examined. We observed positive associations between dietary saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), and total cholesterol and the development of SC, comparing the highest versus lowest quarters. Increased intakes of dietary SFAs (p-trend = 0.005; aOR, 1.11; 95% CI, 1.01-1.22 with a 7 g/day increase as a continuous variable) and total cholesterol (p-trend &lt; 0.001; aOR, 1.13; 95% CI, 1.06-1.22 with a 250 mg/day increase as a continuous variable) were monotonically associated with elevated odds of developing SC. Our results indicate that dietary SFAs, MUFAs, and total cholesterol are associated with stomach cancer, which might provide a potential dietary intervention for stomach cancer prevention

Index-based dietary patterns and stomach cancer in a Chinese population

ObjectivesDietary factors are of importance in the development of stomach cancer. This study aims to examine index-based dietary patterns associated with stomach cancer in a Chinese population.MethodsUsing data from a population-based case-control study conducted in Jiangsu Province, China, we included a total of 8432 participants (1900 stomach cancer cases and 6532 controls). Dietary data collected by food frequency questionnaire was evaluated by modified Chinese Healthy Eating Index-2016 (mCHEI-2016) and the US Healthy Eating Index-2015 (HEI-2015). Multiple logistic regression analyses were applied to examine the association of mCHEI-2016 and HEI-2015 with stomach cancer while adjusting for potential confounders. The possible interactions between mCHEI-2016 or HEI-2015 and established risk factors were explored.ResultsAmong nonproxy interviews, after adjusting for potential confounding factors, a higher score of sodium, reflecting lower intake per day, was inversely associated with stomach cancer [odds ratio (OR), 0.95; 95% CI, 0.91-0.99 for mCHEI-2016; OR, 0.97; 95% CI, 0.94-0.99 for HEI-2015]. No clear associations with stomach cancer were identified for total scores of HEI-2015 (OR, 0.98; 95% CI, 0.87-1.10 with a 10-point increase, P trend = 0.98) and mCHEI-2016 (OR, 1.05; 95% CI, 0.94-1.17 with a 10-point increase, P trend = 0.22). However, the relation between stomach cancer and the mCHEI-2016 was modified by BMI, with a possible inverse association in normal-weight subjects.ConclusionsOur findings highlight that reduced intake of dietary sodium would prevent the development of stomach cancer. The data indicate a heterogeneity between normal weight and overweight's dietary factors in relation to stomach cancer

Associations of prostate cancer risk variants with disease aggressiveness: results of the NCI-SPORE Genetics Working Group analysis of 18,343 cases.

Genetic studies have identified single nucleotide polymorphisms (SNPs) associated with the risk of prostate cancer (PC). It remains unclear whether such genetic variants are associated with disease aggressiveness. The NCI-SPORE Genetics Working Group retrospectively collected clinicopathologic information and genotype data for 36 SNPs which at the time had been validated to be associated with PC risk from 25,674 cases with PC. Cases were grouped according to race, Gleason score (Gleason ≤ 6, 7, ≥ 8) and aggressiveness (non-aggressive, intermediate, and aggressive disease). Statistical analyses were used to compare the frequency of the SNPs between different disease cohorts. After adjusting for multiple testing, only PC-risk SNP rs2735839 (G) was significantly and inversely associated with aggressive (OR = 0.77; 95 % CI 0.69-0.87) and high-grade disease (OR = 0.77; 95 % CI 0.68-0.86) in European men. Similar associations with aggressive (OR = 0.72; 95 % CI 0.58-0.89) and high-grade disease (OR = 0.69; 95 % CI 0.54-0.87) were documented in African-American subjects. The G allele of rs2735839 was associated with disease aggressiveness even at low PSA levels (&lt;4.0 ng/mL) in both European and African-American men. Our results provide further support that a PC-risk SNP rs2735839 near the KLK3 gene on chromosome 19q13 may be associated with aggressive and high-grade PC. Future prospectively designed, case-case GWAS are needed to identify additional SNPs associated with PC aggressiveness

Associations of prostate cancer risk variants with disease aggressiveness: results of the NCI-SPORE Genetics Working Group analysis of 18,343 cases

Genetic studies have identified single nucleotide polymorphisms (SNPs) associated with the risk of prostate cancer (PC). It remains unclear whether such genetic variants are associated with disease aggressiveness. The NCI-SPORE Genetics Working Group retrospectively collected clinicopathologic information and genotype data for 36 SNPs which at the time had been validated to be associated with PC risk from 25,674 cases with PC. Cases were grouped according to race, Gleason score (Gleason ≤ 6, 7, ≥ 8) and aggressiveness (non-aggressive, intermediate, and aggressive disease). Statistical analyses were used to compare the frequency of the SNPs between different disease cohorts. After adjusting for multiple testing, only PC-risk SNP rs2735839 (G) was significantly and inversely associated with aggressive (OR = 0.77; 95 % CI 0.69-0.87) and high-grade disease (OR = 0.77; 95 % CI 0.68-0.86) in European men. Similar associations with aggressive (OR = 0.72; 95 % CI 0.58-0.89) and high-grade disease (OR = 0.69; 95 % CI 0.54-0.87) were documented in African-American subjects. The G allele of rs2735839 was associated with disease aggressiveness even at low PSA levels (&lt;4.0 ng/mL) in both European and African-American men. Our results provide further support that a PC-risk SNP rs2735839 near the KLK3 gene on chromosome 19q13 may be associated with aggressive and high-grade PC. Future prospectively designed, case-case GWAS are needed to identify additional SNPs associated with PC aggressiveness