methylation in metastasising laryngeal cancer. PIAAZARSCHAB1 , AGNIESZKA STEMBALSKA3, MIRELA BAUS LONCAR1,. MARKUS PFISTER2, MARIA M.
ONCOLOGY REPORTS 10: 501-503, 2003
Epigenetic control of E-cadherin (CDH1) by CpG methylation in metastasising laryngeal cancer PIAAZARSCHAB 1 , AGNIESZKA STEMBALSKA 3 , MIRELA BAUS LONCAR 1 , MARKUS PFISTER 2 , MARIA M. SASIADEK 3 and NIKOLAUS BLIN 1 u n i v e r s i t y of Tübingen, Institute of Anthropology and Human Genetics, Division of Molecular Genetics, Wilhelmstr. 27, D-72074 Tübingen; d e p a r t m e n t of Otolaryngology, University Clinics, D-72076 Tübingen, Germany; 3
Department of Genetics, Wroclaw Medical University, Marcinkowskiego 1 Str., 50-368 Wroclaw, Poland Received October 21, 2002; Accepted December 2, 2002
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 l a r y n g e a l c a r c i n o m a (80 p r i m a r y t u m o r s and 18 metastases). Transcriptional silencing of the gene (CDH1) achieved by promoter methylation was tested by a mefhylationspecific PCR. In primary tumors, CDH1 methylation was noted in 4 0 % . H o w e v e r , 7 7 % of the tested metastases showed CDH1 methylation, 2 3 % remained unmethylated (p
