The high incidence of gastric cancer in Japan initially resulted in establishment of a country-wide gastric cancer screening program to detect early and treatable cancers. In 2013 countrywide Helicobacter pylori(H. py...The high incidence of gastric cancer in Japan initially resulted in establishment of a country-wide gastric cancer screening program to detect early and treatable cancers. In 2013 countrywide Helicobacter pylori(H. pylori) eradication was approved coupled with endoscopy to assess for the presence of chronic gastritis. Current data support the notion that cure of the infection in those with non-atrophic gastritis will prevent development of gastric cancer. However, while progression to more severe damage is halted in those who have already developed, atrophic gastritis/gastric atrophy remain at risk for subsequent development of gastric cancer. That risk is directly related to the extent and severity of atrophic gastritis. Methods to stratify cancer risk include those based on endoscopic assessment of the atrophic border, histologic grading, and non-invasive methods based on serologic testing of pepsinogen levels. Continued surveillance is required because those with atrophic gastritis/gastric atrophy retain considerable gastric cancer risk even after H. pylori eradication. Those who have already experienced a resectable early gastric cancer are among those at highest risk as metachronous lesions are frequent even after H. pylorieradication. We review the role of H. pylori and effect of H. pylori eradication indicating the incidence and the predictive factors on development of metachronous cancer after endoscopic therapy of early gastric cancer. Studies to refine risk markers to stratify for risk, surveillance methods, intervals, and duration after successful H. pylori eradication, and whether adjuvant therapy would change risk are needed.展开更多
The relationships among meat consumption, smoking habits, and phenotypic cytochrome P450 2A6 variation with respect to colorectal cancer risk remain unclear. In this study, the relationships among colorectal tumour ri...The relationships among meat consumption, smoking habits, and phenotypic cytochrome P450 2A6 variation with respect to colorectal cancer risk remain unclear. In this study, the relationships among colorectal tumour risk, meat consumption by questionnaire, and phenotypic P450 2A6 activity by genotyping in a case-control study (299 cases and 170 controls) were analyzed for never-smokers and ever-smokers. In never-smokers consuming ≥1 serving per day of total meat, a significant odds ratio of 4.42 (95% confidence interval, 1.29 - 15.2), adjusted by logistic regression for age and gender, was observed, compared with the group consuming ≤2 servings per week. Furthermore, in Japanese never-smokers, the susceptibility to colorectal tumours was dependent on the frequency of meat intake (trend test p = 0.011). In never-smokers who were P450 2A6 poor metabolizers and had a high frequency of meat intake, the apparent odds ratio was 3.57 (95% confidence interval, 0.30 - 42.2) compared with the P450 2A6 normal group with a low meat intake frequency. These results suggested that colorectal tumour risk was inversely associated with the phenotypic P450 2A6 activities in Japanese never-smokers with a high meat intake.展开更多
Background: Unlike with esophageal cancer, acetaldehyde levels and genetic polymorphisms in alcohol dehydrogenase have not yet been shown to be contributing factors for colorectal cancer (CRC). This study aimed to cla...Background: Unlike with esophageal cancer, acetaldehyde levels and genetic polymorphisms in alcohol dehydrogenase have not yet been shown to be contributing factors for colorectal cancer (CRC). This study aimed to clarify the mechanism of CRC development related to alcohol consumption and to the presence of genetic polymorphisms in the alcohol dehydrogenase, ADH1B and aldehyde dehydrogenase, ALDH2. Methods: This was a case-control study (221 cases and 179 controls) in patients with adenomas and intramucosal tumors who underwent endoscopic removal of all tumors. The amount of alcohol consumption was determined using a self-recorded questionnaire, and the tumor information was obtained from colonoscopy results. Blood samples were taken to analyze the following polymorphisms: ALDH2 Glu504Lys and ADH1B His48Arg. Results: The polymorphisms in ADH1B and ALDH2 had little influence on the development of colorectal adenoma or intramucosal cancer. Patients with ALDH2 (Glu/Glu) were more tolerant of alcohol than those with ALDH2 (Glu/Lys and Lys/Lys). Next, we examined certain combinations of the ADH1B genotypes. In the ALDH2 (Glu/Glu) group, an increased risk (OR = 3.4;95% CI 1.4 - 8.4;P = 0.009) was observed among moderate/heavy drinkers with ADH1B (His/His). In the ALDH2 (Glu/Lys and Lys/Lys) group, an increased risk (OR = 4.2;95% CI 1.1 - 16.7;P = 0.041) was found among moderate/heavy drinkers with ADH1B (Arg/His and Arg/Arg). Conclusions: ADH1B and ALDH2 activity may be involved in the development of CRC.展开更多
文摘The high incidence of gastric cancer in Japan initially resulted in establishment of a country-wide gastric cancer screening program to detect early and treatable cancers. In 2013 countrywide Helicobacter pylori(H. pylori) eradication was approved coupled with endoscopy to assess for the presence of chronic gastritis. Current data support the notion that cure of the infection in those with non-atrophic gastritis will prevent development of gastric cancer. However, while progression to more severe damage is halted in those who have already developed, atrophic gastritis/gastric atrophy remain at risk for subsequent development of gastric cancer. That risk is directly related to the extent and severity of atrophic gastritis. Methods to stratify cancer risk include those based on endoscopic assessment of the atrophic border, histologic grading, and non-invasive methods based on serologic testing of pepsinogen levels. Continued surveillance is required because those with atrophic gastritis/gastric atrophy retain considerable gastric cancer risk even after H. pylori eradication. Those who have already experienced a resectable early gastric cancer are among those at highest risk as metachronous lesions are frequent even after H. pylorieradication. We review the role of H. pylori and effect of H. pylori eradication indicating the incidence and the predictive factors on development of metachronous cancer after endoscopic therapy of early gastric cancer. Studies to refine risk markers to stratify for risk, surveillance methods, intervals, and duration after successful H. pylori eradication, and whether adjuvant therapy would change risk are needed.
文摘The relationships among meat consumption, smoking habits, and phenotypic cytochrome P450 2A6 variation with respect to colorectal cancer risk remain unclear. In this study, the relationships among colorectal tumour risk, meat consumption by questionnaire, and phenotypic P450 2A6 activity by genotyping in a case-control study (299 cases and 170 controls) were analyzed for never-smokers and ever-smokers. In never-smokers consuming ≥1 serving per day of total meat, a significant odds ratio of 4.42 (95% confidence interval, 1.29 - 15.2), adjusted by logistic regression for age and gender, was observed, compared with the group consuming ≤2 servings per week. Furthermore, in Japanese never-smokers, the susceptibility to colorectal tumours was dependent on the frequency of meat intake (trend test p = 0.011). In never-smokers who were P450 2A6 poor metabolizers and had a high frequency of meat intake, the apparent odds ratio was 3.57 (95% confidence interval, 0.30 - 42.2) compared with the P450 2A6 normal group with a low meat intake frequency. These results suggested that colorectal tumour risk was inversely associated with the phenotypic P450 2A6 activities in Japanese never-smokers with a high meat intake.
文摘Background: Unlike with esophageal cancer, acetaldehyde levels and genetic polymorphisms in alcohol dehydrogenase have not yet been shown to be contributing factors for colorectal cancer (CRC). This study aimed to clarify the mechanism of CRC development related to alcohol consumption and to the presence of genetic polymorphisms in the alcohol dehydrogenase, ADH1B and aldehyde dehydrogenase, ALDH2. Methods: This was a case-control study (221 cases and 179 controls) in patients with adenomas and intramucosal tumors who underwent endoscopic removal of all tumors. The amount of alcohol consumption was determined using a self-recorded questionnaire, and the tumor information was obtained from colonoscopy results. Blood samples were taken to analyze the following polymorphisms: ALDH2 Glu504Lys and ADH1B His48Arg. Results: The polymorphisms in ADH1B and ALDH2 had little influence on the development of colorectal adenoma or intramucosal cancer. Patients with ALDH2 (Glu/Glu) were more tolerant of alcohol than those with ALDH2 (Glu/Lys and Lys/Lys). Next, we examined certain combinations of the ADH1B genotypes. In the ALDH2 (Glu/Glu) group, an increased risk (OR = 3.4;95% CI 1.4 - 8.4;P = 0.009) was observed among moderate/heavy drinkers with ADH1B (His/His). In the ALDH2 (Glu/Lys and Lys/Lys) group, an increased risk (OR = 4.2;95% CI 1.1 - 16.7;P = 0.041) was found among moderate/heavy drinkers with ADH1B (Arg/His and Arg/Arg). Conclusions: ADH1B and ALDH2 activity may be involved in the development of CRC.
