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Deletion of the E‐cadherin gene in hepatitis B virus–positive chinese hepatocellular carcinomas
Author(s) -
Slagle Betty L.,
Zhou YiZhong,
Birchmeier Walter,
Scorsone Kathleen A.
Publication year - 1993
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840180402
Subject(s) - hepatocellular carcinoma , biology , allele , metastasis , gene , cadherin , tumor suppressor gene , loss of heterozygosity , cancer research , pathology , cell , microbiology and biotechnology , genetics , carcinogenesis , cancer , medicine
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‐fragmentlength 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 16p 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. (HEPATOLOGY 1993;18:757‐762).