Expression of Basic Fibroblast Growth Factor, Vascular Endothelial Growth Factor, and Thrombospondin‐1 Related to Microvessel Density in Nonaggressive and Aggressive Basal Cell Carcinomas

Abstract

The aggressive forms of basal cell carcinoma (BCC) are biologically different in a number of features from their nonaggressive counterparts. The expression of basic Fibroblast Growth Factor (bFGF), Vascular Endothelial Growth Factor (VEGF), and Thrombospondin-1 (TSP-1) was examined in primary culture samples of nonaggressive and aggressive BCCs. We studied the relationship between neoangiogenesis by counting microvessels, tumor aggressiveness, and the expression of three different angiogenic factors. bFGF mRNA was detectable in all BCC samples, but there was no significant difference in the levels of expression between the two types. VEGF mRNA was also detectable in all BCC samples. VEGF expression in the aggressive type was approximately 3.5-fold higher than in the nonaggressive type. TSP-1 expression was variable and not related to the type of BCC. The mean value of microvessel density (MVD) was significantly higher for the aggressive type than for the nonaggressive type. There was a significant correlation between VEGF levels and MVD. No significant relationships were found between bFGF, TSP-1 mRNA expression, and MVD. In conclusion, the results of present study suggest that VEGF expression and angiogenesis might play important roles in the progression to aggressive BCC.

Sequential effects of photodynamic treatment of basal cell carcinoma

“…Cancer nests show the expression of cytokines and chemotactic molecules too. Expression of IL‐6, GM‐CSF, IL‐8, VEGF and SCF has already been described in untreated BCC in vivo 12,14–18 or in vitro 19,20 . Our BCC cells express IL‐8, GM‐CSF, bFGF, VEGF, SCF and little IL‐6 at baseline, which are growth factors capable of exerting chemotactic activity on the inflammatory infiltrate, as well as autocrine or paracrine effects.…”

“…SCF can exert an autocrine and paracrine (on mast cells especially) activity 23 that seems to be related to the presence of mast cells in the infiltrate. bFGF exhibits autocrine mitogenic effects on BCC cells, 20 and it is reduced in animal models after PDT therapy 24 . VEGF reactivity is related to the strong vascularity of BCC; while systemic PDT showed a clear induction of VEGF on mammary cancer cells in vitro 25 as a consequence of microvascular shutdown, topical ALA‐PDT is not able to induce microvascular damage 4 .…”

“…Expression of IL-6, GM-CSF, IL-8, VEGF and SCF has already been described in untreated BCC in vivo 12,[14][15][16][17][18] or in vitro. 19,20 Our BCC cells express IL-8, GM-CSF, bFGF, VEGF, SCF and little IL-6 at baseline, which are growth factors capable of exerting chemotactic activity on the inflammatory infiltrate, as well as autocrine or paracrine effects. The cytokine detection results in an explanation of the sequential composition of infiltrating cell according to time points.…”

Upregulated periostin promotes angiogenesis in keloids through activation of the ERK 1/2 and focal adhesion kinase pathways, as well as the upregulated expression of VEGF and angiopoietin-1

“…Although keloids are defined as a dermal benign disorder, their behavior resembles that of tumor cells, with keloids exhibiting biological characteristics of tumor cells, including bioenergetics, hyperproliferation and invasion ( 21 , 22 ). The induction of angiogenesis is considered important in the cascade of tumor invasion ( 23 ). To maintain the invasive characteristics and ability to recur, tumor-like keloids require the generation of numerous new blood vessels to maintain a steady supply of oxygen and nutrients.…”

Decreased expression of thymidine phosphorylase/platelet‐derived endothelial cell growth factor in basal cell carcinomas

“…However, lack of TP immunodetection, as shown here for BCC cells, has been exceptionally described in tumor cells (27,28). The angiogenic factors expression has been poorly investigated in BCC (29). Vascular endothelial growth factor that exerts, along with TP, a cooperative role in the neovascularization of numerous human cancers (8) is downregulated in most BCCs (as compared with SCC) (30,31).…”