AIM:To investigate the occurrence of chromosome 3,7,8,9,and 17 aneuploidies,TP53 gene deletion and p53protein expression in chronic gastritis,atrophic gastritisand gastric ulcer,and their association with H pylori in-fection.METHODS:Gastric biopsies from normal mucosa(NM,n=10),chronic gastritis(CG,n=38),atrophic gastritis(CAG,n=13)and gastric ulcer(GU,n=21)were studiedusing fluorescence in situ hybridization(FISH)and im-munohistochemical assay.A modified Giemsa stainingtechnique and PCR were used to detect H pylori.An as-sociation of the gastric pathologies and aneuploidies withH pylori infection was assessed.RESULTS:Aneuploidies were increasingly found from CG(21%)to CAG(31%)and to GU(62%),involving mainlymonosomy and trisomy 7,trisomies 7 and 8,and triso-mies 7,8 and 17,respectively.A significant associationwas found between H pylori infection and aneuploidiesin CAG(P=0.0143)and GU(P=0.0498).No TP53 dele-tion was found in these gastric lesions,but p53-positiveimmunoreactivity was detected in 45%(5/11)and 12%(2/17)of CG and GU cases,respectively.However,therewas no significant association between p53 expressionand H pylori infection.CONCLUSION:The occurrence of aneuploidies in be- nign lesions evidences chromosomal instability in earlystages of gastric carcinogenesis associated with H pyloriinfection,which may confer proliferative advantage.Theincrease of p53 protein expression in CG and GU may bedue to overproduction of the wild-type protein related toan inflammatory response in mucosa. AIM: To investigate the occurrence of chromosome 3,7,8,9, and 17 aneuploidies, TP53 gene deletion and p53 protein expression in chronic gastritis, atrophic gastritis and gastric ulcer, and their association with H pylori in-fection. METHODS: Gastric biopsies from Chronic gastritis (CG, n = 38), atrophic gastritis (CAG, n = 13) and gastric ulcer (GU, n = 21) were studied using fluorescence in situ hybridization (FISH) and im An immunohistochemical assay. A modified Giemsa staining technique and PCR were used to detect H pylori. An as-sociation of the gastric pathologies and aneuploidies with H pylori infection was assessed .RESULTS: Aneuploidies were more from found CG (21%) to CAG (31% ) and to GU (62%), involving mainly monosomy and trisomy 7, trisomies 7 and 8, and triso-mies 7,8 and 17, respectively. A significant association was found between H pylori infection and aneuploidies in CAG (P = 0.0143) and GU (P = 0.0498) .No TP53 dele-tion was found in these gastric lesions, but p53-positive immunoreactivity was det ected in 45% (5/11) and 12% (2/17) of CG and GU cases, respectively. There was no significant association between p53 expression and H pylori infection. CONCLUSION: The occurrence of aneuploidies in bengal lesions evidences chromosomal instability in early stages of gastric carcinogenesis associated with H pylori infection, which may confer proliferative advantage. The increase of p53 protein expression in CG and GU may bed to overproduction of the wild-type protein related to inflammatory response in mucosa.