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E‐cadherin abnormalities resulting from CPG methylation promoter in metastatic and nonmetastatic oral cancer
Author(s) -
de Moraes Renato Vieira,
Oliveira Denise Tostes,
Landman Gilles,
de Carvalho Fabrício,
Caballero Otávia,
ogaki Suely,
Nishimoto Inês,
Kowalski Luis Paulo
Publication year - 2008
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.20666
Subject(s) - immunohistochemistry , cadherin , methylation , epigenetics , carcinogenesis , dna methylation , lymph node , cancer , bisulfite sequencing , cancer research , pathology , cpg site , medicine , biology , gene expression , gene , cell , biochemistry , genetics
Background. This study aims to compare the alterations in the methylation profiles of E‐cadherin in oral cancer, especially in tumors with lowest metatastic potential. Methods. Nine oral verrucous carcinomas (VCs), 20 oral well‐differentiated squamous cell carcinomas without lymph node involvement (SCC‐pN0), and 17 with lymph node involvement (SCC‐pN+) were analyzed using methylation‐specific polymerase chain reaction and immunohistochemical expression of E‐cadherin gene. Results. The immunohistochemical expression of E‐cadherin in VC was significantly higher ( p = .016) when compared with SCC‐pN0 and SCC‐pN+ groups. The E‐cadherin gene methylation was not correlated with its abnormal immunohistochemical expression in VC and SCC‐pN0. All tumors of the SCC‐pN+ group with unmethylated E‐cadherin gene showed significant loss of E‐cadherin immunoexpression ( p = .044). Conclusions. The E‐cadherin gene methylation presence in tumors with lowest invasive and metastatic potential, such as VC, suggests the early involvement of this epigenetic event in the multistep progression of the oral carcinogenesis. © 2007 Wiley Periodicals, Inc. Head Neck, 2008