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    Oncol Rep. 2003 Mar-Apr;10(2):501-3.

    Epigenetic control of E-cadherin (CDH1) by CpG methylation in metastasising laryngeal cancer.

    Azarschab P, Stembalska A, Loncar MB, Pfister M, Sasiadek MM, Blin N.

    Source

    University of Tübingen, Institute of Anthropology and Human Genetics, Division of Molecular Genetics, D-72074 Tübingen, Germany.

    Abstract

    Intercellular adhesion is promoted by many-fold structures formed by interacting molecules. One prominent protein family, called cadherins, consists of calcium-dependent proteins contributing to cell differentiation, migration and extracellular signal transduction. E-cadherin, regularly expressed in epithelial tissues, displays aberrant activity patterns in a variety of tumors. We have explored the mode of E-cadherin regulation in 98 biopsy samples from 76 patients with laryngeal carcinoma (80 primary tumors and 18 metastases). Transcriptional silencing of the gene (CDH1) achieved by promoter methylation was tested by a methylation-specific PCR. In primary tumors, CDH1 methylation was noted in 40%. However, 77% of the tested metastases showed CDH1 methylation, 23% remained unmethylated (p<0.01). These data suggest that the E-cadherin promoter is subjected to epigenetic control connected with biological aggressiveness of laryngeal cancer in advanced steps of neoplastic transformation.

    PMID:
    12579297
    [PubMed - indexed for MEDLINE]

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