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The role of cancer-associated inflammation in the regional dissemination of the oral squamous cell carcinoma

Abstract

The inflammation has been cited as a risk factor and also as an important promoter of a range of neoplasms, like the squamous cell carcinoma of oral cavity. Tumor-associated macrophages are important components of peritumoral cell infiltrate, that present alternatively-activated phenotype and can produce inflammatory factors that stimulate neoangiogenesis, extracellular matrix degradation and epithelia mesenchymal transition. These mechanisms and characteristics induced in the tumoral stroma are essential to the metastatic process and, particularly in the regional metastasis of oral tumors. Objectives: This study aims to investigate oral squamous cell carcinoma-associated macrophages and its role on the induction of invasive phenotype of this carcinoma, as well as its correlation with lymph node metastases. Methods. The density of intratumoral and peritumoral macrophages and the expression by tumor cells of factors that induce epithelial-mesenchymal transition will be evaluated by immunohistochemistry and further will be correlated with presence or absence of lymph node metastases. In vitro investigations will be made to evaluate the phenotype of the macrophages infiltrating samples of fresh tissues of tongue or floor of mouth squamous cell carcinoma, its role as a promoter of tumor growth and invasiveness and the role of the MIF in the polarization of tumor-associated macrophages. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
DE SOUZA RIZZO, M. BARBOSA; BRASILINO DE CARVALHO, M.; KIM, E. J.; RENDON, B. E.; NOE, J. T.; WISE, A. DARLENE; MITCHELL, R. A. Oral squamous carcinoma cells promote macrophage polarization in an MIF-dependent manner. QJM-AN INTERNATIONAL JOURNAL OF MEDICINE, v. 111, n. 11, p. 769-778, NOV 2018. Web of Science Citations: 0.

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