title: Eradication of gastric cancer is now both possible and practical.
abstract: In 1994, Helicobacter pylori was declared a human carcinogen. Evidence has now accumulated to show that at least 95% of gastric cancers are etiologically related to H. pylori. An extensive literature regarding atrophic gastritis and its effects on acid secretion, gastric microflora, and its tight association with gastric cancer has been rediscovered, confirmed, and expanded. Methods to stratify cancer risk based on endoscopic and histologic findings or serologic testing of pepsinogen levels and H. pylori testing have been developed producing practical primary and secondary gastric cancer prevention strategies. H. pylori eradication halts progressive mucosal damage. Cure of the infection in those with non-atrophic gastritis will essentially prevent subsequent development of gastric cancer. For all, the age-related progression in cancer risk is halted and likely reduced as eradication reduces or eliminates mucosal inflammation and reverses or reduces H. pylori-associated molecular events such aberrant activation-induced cytidine deaminase expression, double strand DNA breaks, impaired DNA mismatch repair and aberrant DNA methylation. Those who have developed atrophic gastritis/gastric atrophy however retain some residual risk for gastric cancer which is proportional to the extent and severity of atrophic gastritis. Primary and secondary cancer prevention starts with H. pylori eradication and cancer risk stratification to identify those at higher risk who should also be considered for secondary cancer prevention programs. Japan has embarked on population-wide H. pylori eradication coupled with surveillance targeted to those with significant remaining risk. We anticipate that countries with high gastric cancer burdens will follow their lead. We provide specific recommendations on instituting practical primary and secondary gastric cancer prevention programs as well identifying research needed to make elimination of gastric cancer both efficient and cost effective.
authors.affiliation: Department of Internal Medicine, Kawasaki Medical School, Okayama, Japan.
authors.forename: Akiko
authors.initials: A
authors.lastname: Shiotani
authors.forename: Putao
authors.initials: P
authors.lastname: Cen
authors.forename: David Y
authors.initials: DY
authors.lastname: Graham
mesh_terms: D005756:Gastritis / Q000150:complications / Q000175:diagnosis / Q000209:etiology / Q000473:pathology / Q000517:prevention & control; D016481:Helicobacter Infections / Q000150:complications / Q000175:diagnosis / Q000473:pathology / Q000517:prevention & control; D049673:History, 20th Century; D006801:Humans; D015994:Incidence; D012106:Research / Q000266:history; D012306:Risk; D013274:Stomach Neoplasms / Q000453:epidemiology / Q000209:etiology / Q000266:history / Q000517:prevention & control*
keywords: AID; Atrophic gastritis; BRCA1; CDH1; CDKN2A; CI; Cancer screening; CpG; GI; Gastric cancer; H. pylori; Helicobacter pylori; IARC; International Agency for Research on Cancer; KLF5; Krüppel-like factor 5; MGMT; MLH1; Natural history; OLGA; Operative Link on Gastritis Assessment; Pepsinogen; Prevention; Primary prevention; RUNX3; Risk; Secondary prevention; Surveillance; VCP; activation-induced cytidine deaminase; breast cancer susceptibility gene 1; cadherin-1; confidence interval; cyclin-dependent kinase inhibitor 2A; cytosine-phosphate-guanine are regions of DNA; gastrointestinal; hMLH1; human mutL homolog 1; methylated-DNA–protein-cysteine methyltransferase; mutL homolog 1; runt-related transcription factor 3; valosin-containing protein