p53 mutation and protein overexpression in the early stages of esophageal tumorigenesis utilizing endoscopically obtained biopsy specimens
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- Published online on: April 1, 1997 https://doi.org/10.3892/ijo.10.4.683
- Pages: 683-688
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Abstract
It is unclear whether p53 abnormality in the early esophageal tumorigenesis causes clonal expansion with tumor growth. In this study, we analyzed p53 abnormalities by PCR-SSCP and immunohistochemistry in 86 esophageal endoscopic biopsy specimens. Eleven of 27 specimens (39%) of mild dysplasias showed p53 mutations. Six moderate or mild dysplasias were followed by endoscopy (average 73 weeks) and continually exhibited the same p53 mutation, but none of them showed apparent tumor growth and subepithelial epithelial invasion. These results suggest that p53 mutations occur very early in the esophageal tumorigenesis and contribute to cell proliferation, but cannot be related with malignant phenotype directly.