Genetic alterations in benign lesions: Chronic gastritis and gastric ulcer

• Autor(a) principal: Gobbo César, Ana Cristina [UNESP]
• Data de Publicação: 2006
• Outros Autores: de Freitas Calmon, Marília [UNESP], Cury, Patrícia Maluf, Caetano, Alaor, Borim, Aldenis Albaneze, Silva, Ana Elizabete [UNESP]
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://www.wjgnet.com/1007-9327/abstract_en.asp?f=625&v=12; http://hdl.handle.net/11449/68765
• topic: Aneuploidies; Gastric ulcer; Gastritis; p53 protein; TP53 gene; protein p53; adolescent; adult; aged; aneuploidy; atrophic gastritis; bacterium detection; cell proliferation; child; chromosomal instability; chromosome 17; chromosome 3; chromosome 7; chromosome 8; chromosome 9; chronic gastritis; controlled study; correlation analysis; disease association; female; fluorescence in situ hybridization; gene deletion; Giemsa stain; Helicobacter infection; Helicobacter pylori; human; human tissue; immunohistochemistry; immunoreactivity; inflammation; major clinical study; male; monosomy 7; nonhuman; polymerase chain reaction; protein expression; protein synthesis; stomach biopsy; stomach carcinogenesis; stomach mucosa; stomach ulcer; trisomy; trisomy 17; trisomy 7; trisomy 8; wild type; Adult; Aged; Aged, 80 and over; Aneuploidy; Child, Preschool; Chronic Disease; Female; Gene Deletion; Genes, p53; Helicobacter Infections; Humans; In Situ Hybridization, Fluorescence; Male; Middle Aged; Stomach Ulcer; Tumor Suppressor Protein p53

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 infection. 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 studied using fluorescence in situ hybridization (FISH) and immunohistochemical assay. A modified Giemsa staining technique and PCR were used to detect H pylori. An association of the gastric pathologies and aneuploidies with H pylori infection was assessed. Results: Aneuploidies were increasingly found from CG (21%) to CAG (31%) and to GU (62%), involving mainly monosomy and trisomy 7, trisomies 7 and 8, and trisomies 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 deletion was found in these gastric lesions, but p53-positive immunoreactivity was detected in 45% (5/11) and 12% (2/17) of CG and GU cases, respectively. However, there was no significant association between p53 expression and H pylori infection. Conclusion: The occurrence of aneuploidies in benign 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 be due to overproduction of the wild-type protein related to an inflammatory response in mucosa. © 2006 The WJG Press. All rights reserved.