Tumor-associated macrophages and angiogenesis: a statistical correlation that could reflect a critical relationship in ameloblastoma.
Autor: | Guzmán-Medrano R; Departamento de Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados del IPN, A.P. 14-740, México, D.F., Mexico., Arreola-Rosales RL, Shibayama M, Silva-Olivares DA, Bologna-Molina R, Rodríguez MA |
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Jazyk: | angličtina |
Zdroj: | Pathology, research and practice [Pathol Res Pract] 2012 Nov 15; Vol. 208 (11), pp. 672-6. Date of Electronic Publication: 2012 Oct 05. |
DOI: | 10.1016/j.prp.2012.09.001 |
Abstrakt: | Neoplasm growth is determined not only by the tumor cells themselves, but also by the tumor microenvironment. Increased densities of macrophages and activation of angiogenesis have been identified as common events in the progression of several neoplasms. Ameloblastoma is one of the most frequent odontogenic tumors and an excellent model for the study of neoplasm progression due to the different clinical variants that it exhibits. Here, by immunohistochemical studies using antibodies against CD68 and CD34, we evaluated the density of macrophages and microvessels associated to 45 paraffin-embedded ameloblastomas. In solid/multicystic ameloblastoma (SMA), we observed significantly higher densities of both macrophages and microvessels than in unicystic (UA) and desmoplastic (DA) ameloblastomas. Likewise, higher densities of macrophages and microvessels were found in UA than in DA. Furthermore, a predominance of intratumoral and peritumoral macrophage infiltrates was seen in SMA, while in UA, both macrophages and microvessels were also detected in the wall of the cysts. In contrast, DA had scant macrophages and microvessels, mainly situated distant from tumoral cells. In addition, a high correlation between macrophage and microvessel densities was observed in the samples (r=0.9623). Our results suggest that these two tumor microenvironmental elements could have an important role during ameloblastoma progression. (Copyright © 2012 Elsevier GmbH. All rights reserved.) |
Databáze: | MEDLINE |
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