F Prall1, U Gringmuth, H Nizze, M Barten. 1. Department of Pathology, University of Rostock, Germany. friedrich.prall@med.uni-rostock.de
Abstract
AIMS: Microvessel densities in cancers have been shown to be a prognostic factor for some types of cancer. For colorectal cancer, however, the situation is far from clear. METHODS: A consecutive series of 173 colorectal carcinomas was investigated, and to these were added 55 liver metastases originating from colorectal cancer. Microvessels were counted in hotspots (factor VIII immunostaining, 0.74 mm2). The capillary architecture was scored according to the degree of order and envelopment of the neoplastic glands. Endothelial proliferation was determined by factor VIII/Ki67 double labelling. RESULTS: Mean microvessel densities were 51.8 for colorectal carcinomas (range 8-140) and 31.9 for liver metastases (range 3-101). Stratification according to stage, depth of infiltration and nodal involvement showed a significant inverse relation with increase. Mean microvessel densities in primaries were significantly higher than in metastases. Kaplan-Meier analysis showed a significantly higher cancer-specific survival for high microvessel densities (median as cut-off) and for a more ordered microvascular architecture. Endothelial proliferation in carcinomas was significantly higher than in normal mucosa. CONCLUSIONS: Contrary to other types of cancer, for colorectal cancer high microvessel densities confer good rather than poor prognosis. We hypothesize that neoangiogenesis, though extant in colorectal cancer, is not rate-limiting in the metastatic cascade.
AIMS: Microvessel densities in cancers have been shown to be a prognostic factor for some types of cancer. For colorectal cancer, however, the situation is far from clear. METHODS: A consecutive series of 173 colorectal carcinomas was investigated, and to these were added 55 liver metastases originating from colorectal cancer. Microvessels were counted in hotspots (factor VIII immunostaining, 0.74 mm2). The capillary architecture was scored according to the degree of order and envelopment of the neoplastic glands. Endothelial proliferation was determined by factor VIII/Ki67 double labelling. RESULTS: Mean microvessel densities were 51.8 for colorectal carcinomas (range 8-140) and 31.9 for liver metastases (range 3-101). Stratification according to stage, depth of infiltration and nodal involvement showed a significant inverse relation with increase. Mean microvessel densities in primaries were significantly higher than in metastases. Kaplan-Meier analysis showed a significantly higher cancer-specific survival for high microvessel densities (median as cut-off) and for a more ordered microvascular architecture. Endothelial proliferation in carcinomas was significantly higher than in normal mucosa. CONCLUSIONS: Contrary to other types of cancer, for colorectal cancer high microvessel densities confer good rather than poor prognosis. We hypothesize that neoangiogenesis, though extant in colorectal cancer, is not rate-limiting in the metastatic cascade.
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