Aims. To evaluate the vascularization in basal cell carcinomas (BCCs) and squamous cell carcinomas (SCCs) of the skin. Methods. We performed CD31 (i.e., panendothelial marker) and CD105 (i.e., proliferating endothelium marker) immunostaining on samples of 70 SCCs and 70 BCCs of the skin. We evaluated the relative blood vessel area using the Chalkley counting method in each histologic subtype of these tumours. We calculated the degree of proliferation of blood vessel endothelium dividing CD105-Chalkley score by CD31-Chalkley score. Results. We found significantly higher peritumoral and intratumoral blood vessel area in SCC when compared to BCC (both with CD31 and CD105). Chalkley counts differed significantly between groups with different BCC histologic subtypes and SCC with different grade of differentiation. Surprisingly, the degree of proliferation of blood vessel endothelium was higher in BCC when compared to SCC. Conclusions. While SCC exhibited significantly higher intratumoral and peritumoral blood vessel areas compared to BCC, the relatively low rate of proliferating endothelium in this tumour type suggests the existence of endothelial-sprouting-independent mechanisms of vascularization in SCC. 1. Introduction Basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) of the skin are the most common human solid malignant tumours. One of the key biological processes that appear to be relevant to the establishment and prognosis of most forms of cancer, including skin cancer, is angiogenesis [1]. Using the mouse model Eichten et al. demonstrated that during squamous skin carcinogenesis blood vessels undergo increase in endothelial cell proliferation, vessel diameter, vessel density and leakage [2]. Although several studies evaluated the role of microvessel density in the progression of epithelial skin cancer, the proliferation of vascular endothelium or blood vessel area (BVA) has not yet been investigated. For many years, the process of tumour vascularization was thought to proceed mainly through the sprouting of new blood vessels from the preexisting vasculature. However, in recent years, additional endothelial-sprouting-independent mechanisms have been described, such as vascular cooption, intussusceptive angiogenesis, mosaic vessels, vasculogenesis, and/or vasculogenic mimicry [3]. The quantification of angiogenesis is complicated by the fact this is dynamic process. Two international consensus on quantification of angiogenesis in solid tumours were published [4, 5], considering the Chalkley counting technique as a more reproducible and
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