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Interrelationships among chromosome aneuploidy, promoter hypermethylation, and protein expression of the CDKN2A gene in individuals from northern Brazil with gastric adenocarcinoma.
Guimarães, Adriana Costa; Lima, Eleonidas Moura; Khayat, André Salim; Girão Faria, Mário Henrique; Barem Rabenhorst, Silvia Helena; Pitombeira, Márcia Valéria; Assumpção, Paulo Pimentel; de Oliveira Bahia, Marcelo; Lima de Lima, Patrícia Danielle; de Arruda Cardoso Smith, Marília; Burbano, Rommel Rodríguez.
Afiliação
  • Guimarães AC; Human Cytogenetics and Toxicological Genetics Laboratory, Institute of Biological Sciences, Federal University of Pará, Campus Universitário do Guamá, Av. Augusto Correa, 01, CEP 66075-900, Belém, PA, Brazil.
Cancer Genet Cytogenet ; 179(1): 45-51, 2007 Nov.
Article em En | MEDLINE | ID: mdl-17981214
Numerical alterations of chromosome 9, the status of promoter methylation and protein expression of the CDKN2A gene (aliases include p16 and p16(INK4a)), the possible association with gain of chromosome X, and the interrelation of these findings with clinic and pathological characteristics were investigated in gastric adenocarcinomas. Fluorescence in situ hybridization analysis with centromeric DNA probes, immunohistochemical staining, and methylation-specific polymerase chain reaction assays were performed in 15 gastric adenocarcinomas samples from individuals from northern Brazil. Aneuploidies of chromosomes X and 9 were found in all samples, both intestinal and diffuse type. Monosomy of chromosome 9 and gain of a copy of chromosome X (in both sexes) were observed in 100% of cases. Hypermethylation frequency and protein expression of CDKN2A were also found in all cases analyzed. No association of genetic and epigenetic alterations with histological type, tumor aggressiveness, and invasion was found (P > 0.05), which may be attributable to small sample size. There was a high level of association between absence of p16 protein expression levels, CDKN2A gene promote hypermethylation, and chromosome 9 aneuploidy (100% of cases). Thus, in the present samples, the apparent mechanisms behind p16 silencing include loss of chromosome 9 and promoter region hypermethylation.
Assuntos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Neoplasias Gástricas / Adenocarcinoma / Regiões Promotoras Genéticas / Metilação de DNA / Genes p16 / Inibidor p16 de Quinase Dependente de Ciclina / Aneuploidia Limite: Adult / Aged / Female / Humans / Male / Middle aged País/Região como assunto: America do sul / Brasil Idioma: En Revista: Cancer Genet Cytogenet Ano de publicação: 2007 Tipo de documento: Article País de afiliação: Brasil País de publicação: Estados Unidos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Neoplasias Gástricas / Adenocarcinoma / Regiões Promotoras Genéticas / Metilação de DNA / Genes p16 / Inibidor p16 de Quinase Dependente de Ciclina / Aneuploidia Limite: Adult / Aged / Female / Humans / Male / Middle aged País/Região como assunto: America do sul / Brasil Idioma: En Revista: Cancer Genet Cytogenet Ano de publicação: 2007 Tipo de documento: Article País de afiliação: Brasil País de publicação: Estados Unidos