Expression of hypoxia-induced factor-1 alpha in early-stage and in metastatic oral squamous cell carcinoma
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2017
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Resumo
To investigate hypoxia-induced factor-1 alpha expression in distinct oral squamous cell carcinoma subtypes and
topographies and correlate with clinicopathological data. Hypoxia-induced factor-1 alpha expression was assessed by
immunohistochemistry in 93 cases of OSCC. Clinical and histopathological data were reviewed from medical records.
Hypoxia-induced factor-1 alpha status was distinct according to tumor location, subtype and topography affect. In
superficial oral squamous cell carcinomas, most tumor cells overexpressed hypoxia-induced factor-1 alpha, whereas
hypoxia-induced factor-1 alpha was restricted to the intratumoral region in conventional squamous cell carcinomas. All
basaloid squamous cell carcinomas exhibited downregulation of hypoxia-induced factor-1 alpha. Interestingly, metastatic
lymph nodes (91.7%, p = 0.001) and the intratumoral regions of corresponding primary tumors (58.3%, p = 0.142) showed
hypoxia-induced factor-1 alpha-positive tumor cells. Overall survival was poor in patients with metastatic lymph nodes.
Hypoxia-induced factor-1 alpha has distinct expression patterns in different oral squamous cell carcinoma subtypes
and topographies, suggesting that low oxygen tension promotes the growth pattern of superficial and conventional
squamous cell carcinoma, but not basaloid squamous cell carcinoma. Indeed, a hypoxic environment may facilitate
regional metastasis, making it a useful diagnostic and prognostic marker in primary tumors.
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Basaloid squamous cell carcinomas, Hypoxia-induced factor-1 alpha, Metastasis, Oral squamous cell carcinoma
Citação
RIBEIRO, Maisa et al. Expression of hypoxia-induced factor-1 alpha in early-stage and in metastatic oral squamous cell carcinoma. Tumor Biology, Tokyo, v. 39, n. 4, e1010428317695527, 2017. DOI: 10.1177/1010428317695527. Disponível em: https://journals.sagepub.com/doi/10.1177/1010428317695527?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed. Acesso em: 10 dez. 2024.