722 Microvessel density and P53 overexpression in colorectal adenocarcinoma

Abstract

Cancer is an angiogenesis-dependent disease. The degree of this new vessel development is related to clinical outcome in breast carcinoma. Recent experiments suggest that wild-type p53 regulates the production of thrombospondin-I (Dameron et al., 1994) and of a glioma-derived angiogenesis inhibitor (Van Meir et al., 1994) and that mutant p53 potentiates VEGF expression (Kieser et al., 1994). We have analysed the relationship of p53 overexpression and microvessel density (MVD), as a measure of angiogenesis, in colorectal adenocarcinoma. Sections of 42 paraffin-embedded tumours were stained for CD31 (Dako) to detect endothelial cells and for p53-protein-overexpression, both wild and mutant forms, with DO7 (Biogenex). The majority (76%) of the p53-positive tumours was highly vascular (> 90 vessel/×200 field in the areas of intense neovascularisation), with a mean MVD of 114 ± 43, as compared to only 31% (χ 2 , 7.7, P This is comparable to the results of Gasparini et al. (1993) in head-and-neck squamous cell carcinoma and indicates an involvement of the p53 tumour suppressor gene in colorectal adenocarcinoma angiogenesis.