BACKGROUND: Stomach cancer is generally thought to evolve through a series of gastric mucosal changes, but the determinants of the precancerous lesions are not well understood. PURPOSE: Our purpose was to assess risk factors for intestinal metaplasia and gastric dysplasia arising from chronic atrophic gastritis in a general population at high risk for stomach cancer. METHODS: A population-based gastroscopic screening of more than 3000 residents was conducted in a county in China with one of the world's highest rates of stomach cancer. Information on the lifestyle and other characteristics of the participants was obtained by interview, and responses were compared between those in whom the most advanced gastric lesion was dysplasia or intestinal metaplasia versus those with chronic atrophic gastritis. RESULTS: Cigarette smoking was found to nearly double the risk of transition to dysplasia and to be a mild risk factor for intestinal metaplasia. Smoking accounted almost entirely for the 55% higher prevalence of dysplasia among men than among women. Risk of transition to dysplasia had a weak association with several dietary factors and was increased among those participants with a family history of stomach cancer and with blood type A. CONCLUSIONS: The findings provide strong evidence for a role of tobacco consumption and offer clues to other environmental and genetic factors involved in the process of gastric carcinogenesis.
BACKGROUND:Stomach cancer is generally thought to evolve through a series of gastric mucosal changes, but the determinants of the precancerous lesions are not well understood. PURPOSE: Our purpose was to assess risk factors for intestinal metaplasia and gastric dysplasia arising from chronic atrophic gastritis in a general population at high risk for stomach cancer. METHODS: A population-based gastroscopic screening of more than 3000 residents was conducted in a county in China with one of the world's highest rates of stomach cancer. Information on the lifestyle and other characteristics of the participants was obtained by interview, and responses were compared between those in whom the most advanced gastric lesion was dysplasia or intestinal metaplasia versus those with chronic atrophic gastritis. RESULTS: Cigarette smoking was found to nearly double the risk of transition to dysplasia and to be a mild risk factor for intestinal metaplasia. Smoking accounted almost entirely for the 55% higher prevalence of dysplasia among men than among women. Risk of transition to dysplasia had a weak association with several dietary factors and was increased among those participants with a family history of stomach cancer and with blood type A. CONCLUSIONS: The findings provide strong evidence for a role of tobacco consumption and offer clues to other environmental and genetic factors involved in the process of gastric carcinogenesis.
Authors: David K van der Poorten; Duncan McLeod; Golo Ahlenstiel; Scott Read; Avelyn Kwok; Cositha Santhakumar; Milan Bassan; Suzanne Culican; David Campbell; Sue W J Wong; Louise Evans; Bilel Jideh; Alisa Kane; Constance H Katelaris; Karuna Keat; Yanna Ko; Jessie A Lee; Sandhya Limaye; Ming Wei Lin; Ari Murad; Martina Rafferty; Dan Suan; Sanjay Swaminathan; Sean D Riminton; Catherine Toong; Lucinda J Berglund Journal: J Clin Immunol Date: 2018-09-15 Impact factor: 8.317
Authors: Abraham M Y Nomura; Lynne R Wilkens; Brian E Henderson; Meira Epplein; Laurence N Kolonel Journal: Cancer Causes Control Date: 2011-10-29 Impact factor: 2.506
Authors: Jung H Yoon; Sung S Choi; Olga Kim; Won S Choi; Yong K Park; Suk W Nam; Jung Y Lee; Won S Park Journal: Mod Pathol Date: 2016-01-08 Impact factor: 7.842