A1 Refereed original research article in a scientific journal
Expression and Role of E-Cadherin, β-Catenin, and Vimentin in Human Papillomavirus–Positive and Human Papillomavirus–Negative Oropharyngeal Squamous Cell Carcinoma
Authors: Hesham Mohamed, Caj Haglund, Lauri Jouhi, Timo Atula, Jaana Hagström, Antti Mäkitie
Publisher: SAGE PUBLICATIONS LTD
Publication year: 2020
Journal: Journal of Histochemistry and Cytochemistry
Journal name in source: JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY
Journal acronym: J HISTOCHEM CYTOCHEM
Article number: ARTN 0022155420950841
Volume: 68
Issue: 9
First page : 595
Last page: 606
Number of pages: 12
ISSN: 0022-1554
eISSN: 1551-5044
DOI: https://doi.org/10.1369/0022155420950841
Self-archived copy’s web address: https://research.utu.fi/converis/portal/detail/Publication/50423123
Oropharyngeal squamous cell carcinoma (OPSCC) is subclassified by the World Health Organization into two different entities: human papillomavirus (HPV)-positive and HPV-negative tumors. HPV infection promotes the epithelial-to-mesenchymal transition (EMT) and transformation of keratinocyte stem cells into cancer stem cells. EMT is a crucial process in the carcinogenesis of epithelial-derived malignancies, and we aimed to study the role of its markers in OPSCC. This study consists of 202 consecutive OPSCC patients diagnosed and treated with curative intent. We examined E-cadherin, beta-catenin, and vimentin expression using immunohistochemistry and compared these with tumor and patient characteristics and treatment outcome. We found that the cell-membranous expression of beta-catenin was stronger in HPV-positive than in HPV-negative tumors, and it was stronger in the presence of regional metastasis. The stromal vimentin expression was stronger among HPV-positive tumors. A high E-cadherin expression was associated with tumor grade. No relationship between these markers and survival emerged. In conclusion, beta-catenin and vimentin seem to play different roles in OPSCC: the former in the tumor tissue itself, and the latter in the tumor stroma. HPV infection may exploit the beta-catenin and vimentin pathways in carcinogenic process. More, beta-catenin may serve as a marker for the occurrence of regional metastasis:
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