Microvessel density is associated with VEGF and α-SMA expression in different regions of human gastrointestinal carcinomas

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Abstract

Tumor angiogenesis is known to be regulated by growth factors secreted by hostand tumor cells. Despite the importance of tumor vasculature and angiogenic heterogeneityin solid tumors, few studies have compared the vasculature in different regions of humancancer. Blood vessels from different regions of carcinomas might have morphofunctionalimplications in tumor angiogenesis. In the present study, therefore, we have examined therelationship between microvascular density (MVD) and vascular endothelial growth factor(VEGF) expression and alpha smooth muscle actin (α -SMA) expression in the center ofthe tumor (CT), periphery (P) and metastasis (M) regions from gastrointestinal carcinomas(GITC), as well as the association of MVD with clinicopathological factors. Surgicallyresected specimens corresponding to the CT, P and M from 27 patients were examined forFVIII, VEGF and α -SMA by immunohistochemistry. The MVD was not significantlydifferent in the CT, P and M regions from GITC. The MVD in the VEGF positive groupwas significantly higher than in the VEGF negative group (CT, p = 0.034; P, p = 0.030; M,p = 0.032). The MVD as a function of α -SMA expression was also significantly higher inthe CT and P region compared to the M region (p = 0.0008). In conclusion, the MVDassociation with VEGF and α -SMA expression, might indicate an increase of the numberof neoformed and preexisting blood vessels uniformly or partially covered by pericytes indifferent regions of GITC, suggesting that not only MVD and VEGF are important parameters to the tumor vasculature, but also blood vessels maturation is a crucial factor for gastrointestinal tumor angiogenesis regulation and possible target of vascular therapy. © 2011 by the authors; licensee MDPI, Basel, Switzerland.

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APA

Tonino, P., & Abreu, C. (2011). Microvessel density is associated with VEGF and α-SMA expression in different regions of human gastrointestinal carcinomas. Cancers, 3(3), 3405–3418. https://doi.org/10.3390/cancers3033405

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