Deletion of the E-cadherin gene in hepatitis B virus-positive Chinese hepatocellular carcinomas

Hepatology. 1993 Oct;18(4):757-62. doi: 10.1002/hep.1840180402.

Abstract

Frequent allele loss from chromosome 16q was recently described for human tumors of the breast, prostate gland and liver, indicating the possible presence of a tumor-suppressor gene on that chromosome arm. In this study, the chromosome 16 allele status of 38 hepatocellular carcinomas in Chinese patients was determined with restriction-fragment-length polymorphism analysis. Tumor-specific allele loss was detected in 14 (74%) of 19 patients informative for 16p markers and in 22 (85%) of 26 patients informative for 16q markers. Quantitative densitometric analysis revealed reduction to hemizygosity of the E-cadherin cell adhesion gene (localized to 16q22.1) in 18 (64%) of the 28 patients for whom quantitative data were available. Reduced expression of E-cadherin has been associated with invasion and metastasis in several human cell lines and primary tumors, and our results suggest that one mechanism of reduced E-cadherin expression is the loss of one copy of the E-cadherin gene.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Cadherins / genetics*
  • Carcinoma, Hepatocellular / genetics*
  • Carcinoma, Hepatocellular / microbiology
  • China
  • Chromosomes, Human, Pair 16*
  • Female
  • Gene Deletion*
  • Hepatitis B virus*
  • Humans
  • Liver Neoplasms / genetics*
  • Liver Neoplasms / microbiology
  • Male
  • Middle Aged
  • Mutation
  • Polymorphism, Restriction Fragment Length

Substances

  • Cadherins