Interrelationship between TP53 gene deletion, protein expression and chromosome 17 aneusomy in gastric adenocarcinoma
1 Human's Cytogenetics Laboratory, Institute of Biological Sciences, Federal University of Pará, Av Augusto Correa 01, 66075-900, Belém, PA, Brazil
2 Biology Department, Campus Ministro Reis Velloso/Parnaíba, Federal University of Piauí, PI, Brazil
3 Genetics Division, Department of Morphology, Federal University of São Paulo, São Paulo, SP, Brazil
4 Molecular's Genetics Laboratory, Department of Pathology, Medical School, Federal University of Ceará, Fortaleza, CE, Brazil
5 João de Barros Barreto University Hospital, Federal University of Pará, Belém, PA, Brazil
BMC Gastroenterology 2009, 9:55 doi:10.1186/1471-230X-9-55Published: 20 July 2009
This study evaluates the existence of numerical alterations of chromosome 17 and TP53 gene deletion in gastric adenocarcinoma. The p53 protein expression was also evaluated, as well as, possible associations with clinicopathological characteristics.
Dual-color fluorescence in situ hybridization and immunostaining were performed in twenty gastric cancer samples of individuals from Northern Brazil.
Deletion of TP53 was found in all samples. TP53 was inactivated mainly by single allelic deletion, varying to 7–39% of cells/case. Aneusomy of chromosome 17 was observed in 85% of cases. Chromosome 17 monosomy and gain were both observed in about half of cases. Cells with gain of chromosome 17 frequently presented TP53 deletion. The frequency of cells with two chr17 and one TP53 signals observed was higher in diffuse than in intestinal-type GC. Immunoreactivity of p53 was found only in intestinal-type samples. The frequency of cells with two chr17 and two TP53 signals found was higher in samples with positive p53 expression than in negative cases in intestinal-type GC.
We suggest that TP53 deletion and chromosome 17 aneusomy is a common event in GC and other TP53 alterations, as mutation, may be implicated in the distinct carcinogenesis process of diffuse and intestinal types.