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Bcl-2 expression and allelic loss of thep53 gene in gastric carcinomas

  • Original Paper
  • Clinical Oncology
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Abstract

In order to clarify the association betweenbcl-2 protein (Bcl-2) expression and genetic alteration, we investigatedp53 andDCC (deleted in the colon carcinoma gene locus) gene abnormalities in Bcl-2-positive and-negative gastric carcinomas using a polymerase chain reaction/loss of heterozygosity (LOH) assay. Bcl-2 immunoreactivity was found in 25 of 178 (14%) gastric carcinoma cases. With these 25 positive cases, the proportion 18/87 (20.6%) of the total in early stages demonstrating invasion of the mucosa and/or submucosa was significantly greater (P=0.013) than the 7/91 (7.7%) found for advanced tumors exhibiting invasion into or through the muscularis propria. However, there was no statistically significant variation between the proportions for differentiated (17/98 cases, 17.3%) and undifferentiated (8/80 cases, 10%) lesions. Sixteen Bcl-2-positive cases (9 cases were not studied because of insufficient specimen material to allow extraction of DNA) and 31 cases randomly selected from a Bcl-2-negative group were analyzed for the presence ofp53-LOH or DCC-LOH and forp53 by immunohistochemistry. The minority of the Bcl-2-positive group hadp53-LOH and were immunopositive for p53 (P=0.033,P=0.028 respectively), while no association was found in the Bcl-2-negative category. In contrast, there was no correlation at all between Bcl-2 expression and DCC-LOH although the number of informative cases analyzed was too small to allow definite conclusions. These results indicate that Bcl-2 may be predominantly expressed at an early stage in gastric carcinomas, possibly in negative association withp53 gene abnormalities.

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Abbreviations

DCC :

deleted in colon carcinoma gene locus

LOH :

loss of heterozygosity

PCR :

polymerase chain reaction

VNTR :

variable number of tandem repeats

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Saegusa, M., Takano, Y., Kamata, Y. et al. Bcl-2 expression and allelic loss of thep53 gene in gastric carcinomas. J Cancer Res Clin Oncol 122, 427–432 (1996). https://doi.org/10.1007/BF01212883

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  • DOI: https://doi.org/10.1007/BF01212883

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