Histopathology · 2014
Vascular endothelial growth factor A (VEGFA) expression in mycosis fungoides.
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Pileri Alessandro, Agostinelli Claudio, Righi Simona, Fuligni Fabio, Bacci Francesco, Sabattini Elena, Patrizi Annalisa, Pileri Stefano A, Piccaluga Pier Paolo
Аннотация
AIMS: High levels of vascular endothelial growth factor A (VEGFA) seem to herald a worse prognosis in mycosis fungoides (MF). In this study, we aimed to characterize more clearly VEGFA gene and protein expression in MF.
METHODS AND RESULTS: First, we compared VEGFA mRNA levels in MF and in normal T lymphocyte samples; significantly higher VEGFA levels were found in MF. We then studied VEGFA expression in different normal T cell subsets, focusing on CD4(+) , CD8(+) , resting and activated T lymphocytes. We applied the gene signatures of the normal T cell subsets to MF samples and found that activated T lymphocytes represented the closest normal counterpart of the tumour. However, VEGFA mRNA levels were significantly higher in MF than in activated normal T cells, suggesting that VEGFA overexpression in MF represents an attribute acquired during neoplastic transformation: no significant VEGFA expression differences were recorded between early and advanced stages. Gene expression profile results were supported by immunohistochemistry in routine sections from 27 MF cases.
CONCLUSIONS: For the first time, we demonstrate VEGFA expression in MF cells, suggesting that the VEGF pathway may be implicated in MF pathogenesis and can represent a novel therapeutic target.
METHODS AND RESULTS: First, we compared VEGFA mRNA levels in MF and in normal T lymphocyte samples; significantly higher VEGFA levels were found in MF. We then studied VEGFA expression in different normal T cell subsets, focusing on CD4(+) , CD8(+) , resting and activated T lymphocytes. We applied the gene signatures of the normal T cell subsets to MF samples and found that activated T lymphocytes represented the closest normal counterpart of the tumour. However, VEGFA mRNA levels were significantly higher in MF than in activated normal T cells, suggesting that VEGFA overexpression in MF represents an attribute acquired during neoplastic transformation: no significant VEGFA expression differences were recorded between early and advanced stages. Gene expression profile results were supported by immunohistochemistry in routine sections from 27 MF cases.
CONCLUSIONS: For the first time, we demonstrate VEGFA expression in MF cells, suggesting that the VEGF pathway may be implicated in MF pathogenesis and can represent a novel therapeutic target.