title: Helicobacter pylori infection enhances glandular stomach carcinogenesis in Mongolian gerbils treated with chemical carcinogens.
abstract: Helicobacter pylori (Hp) is thought to be a stomach carcinogen from epidemiological findings. To determine the effects of infection with the bacteria on experimental carcinogenesis, a study of the glandular stomach of Mongolian gerbils (MGs) was performed. Male MGs were treated with N-methyl-N'-nitro-N-nitrosoguanidine followed by inoculation with Hp or infected with Hp followed by N-methyl-N'-nitro-N-nitrosoguanidine administration. Animals were killed at week 50, and their excised stomachs underwent microbiological and histopathological examinations. In addition, a serological investigation was performed. The incidences of adenocarcinomas were significantly higher in animals treated with 60 or 300 p.p.m. N-methyl-N'-nitro-N-nitrosoguanidine for 10 weeks followed by Hp inoculation or Hp followed by 20 p.p.m. N-methyl-N'-nitro-N-nitrosoguanidine for 30 weeks than in the respective controls. Moreover, tumour-bearing animals had higher titres of anti-Hp antibodies than tumour-free animals. Of interest was the finding that a dose of 100 p.p.m. N-methyl-N'-nitro-N-nitrosoguanidine given to infected gerbils eradicated the Hp in about half the animals, with a concomitant reduction in the promoting effect. No tumours were found in animals infected with Hp without N-methyl-N'-nitro-N-nitrosoguanidine or non-treated gerbils. Hp infection enhances glandular stomach carcinogenesis in MGs treated with N-methyl-N'-nitro-N-nitrosoguanidine. Animals with high titres of anti-Hp antibodies are at greatest risk of developing neoplasms.
authors.affiliation: Laboratory of Pathology, Aichi Cancer Center Research Institute, Nagoya, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Shimizu
authors.forename: K
authors.initials: K
authors.lastname: Inada
authors.forename: H
authors.initials: H
authors.lastname: Nakanishi
authors.forename: T
authors.initials: T
authors.lastname: Tsukamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Ikehara
authors.forename: M
authors.initials: M
authors.lastname: Kaminishi
authors.forename: S
authors.initials: S
authors.lastname: Kuramoto
authors.forename: A
authors.initials: A
authors.lastname: Sugiyama
authors.forename: T
authors.initials: T
authors.lastname: Katsuyama
authors.forename: M
authors.initials: M
authors.lastname: Tatematsu
mesh_terms: D000230:Adenocarcinoma / Q000139:chemically induced / Q000209:etiology* / Q000382:microbiology; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D002273:Carcinogens / Q000633:toxicity*; D002454:Cell Differentiation; D003043:Cocarcinogenesis; D004334:Drug Administration Schedule; D004487:Edema / Q000209:etiology; D005753:Gastric Mucosa / Q000187:drug effects / Q000382:microbiology / Q000473:pathology; D005756:Gastritis / Q000150:complications* / Q000382:microbiology; D006471:Gastrointestinal Hemorrhage / Q000209:etiology; D005849:Gerbillinae; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori / Q000276:immunology / Q000472:pathogenicity*; D006965:Hyperplasia; D008297:Male; D008679:Metaplasia; D008769:Methylnitronitrosoguanidine / Q000008:administration & dosage / Q000633:toxicity*; D011230:Precancerous Conditions / Q000382:microbiology*; D013047:Specific Pathogen-Free Organisms; D013274:Stomach Neoplasms / Q000139:chemically induced / Q000209:etiology* / Q000382:microbiology; D013276:Stomach Ulcer / Q000150:complications / Q000382:microbiology; D013997:Time Factors
chemical_list: D000907:Antibodies, Bacterial; D002273:Carcinogens; D008769:Methylnitronitrosoguanidine