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Tumor-associated Macrophages, Angiogenesis, and Tumor Cell Migration in Oral Squamous Cell Carcinoma

OBJECTIVE: To investigate the relationship between tumor-associated macrophages (TAMs), neovascularization, and tumor cell migration in oral squamous cell carcinoma (OSCC) of an African subpopulation. MATERIALS AND METHODS: Twenty OSCC paraffin blocks underwent immunohistochemistry to TAM1 (CCR7), T...

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Detalles Bibliográficos
Autores principales: Udeabor, Samuel E., Adisa, Akinyele O., Orlowska, Anna, Sader, Robert A., Ghanaati, Shahram
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5676408/
https://www.ncbi.nlm.nih.gov/pubmed/29063902
http://dx.doi.org/10.4103/aam.aam_8_17
Descripción
Sumario:OBJECTIVE: To investigate the relationship between tumor-associated macrophages (TAMs), neovascularization, and tumor cell migration in oral squamous cell carcinoma (OSCC) of an African subpopulation. MATERIALS AND METHODS: Twenty OSCC paraffin blocks underwent immunohistochemistry to TAM1 (CCR7), TAM2 (CD206), Twist, E-cadherin, N-cadherin, and CD34. The relative percentage of CCR7 + and CD206 + cells to overall immune cell population was calculated for three high power fields and an average was taken. TAM-related microvessel density (MVD) was determined as the mean of the three recorded values. Cases that had no CD34 + vessels adjacent to the TAMs region were regarded as having an MVD score of 0. RESULTS: Ten cases (50%) expressed greater CCR7 activity than CD206, seven cases (35%) expressed approximately equal activity of CCR7 and CD206, while three cases (15%) expressed greater activity of CD206 than CCR7. Twist expression was strong in some cases with strong N-cadherin and weak E-cadherin, but the expression of Twist was not consistently high in all cases that expressed strong N-cadherin and weak E-cadherin. CONCLUSIONS: TAMs distribution suggested antitumor activity and the potential for tumor metastasis was only partly due to Twist-mediated epithelial–mesenchymal transition.