AIMS: Vascular invasion is a prognostic marker for many cancers, including endometrial carcinoma. Immunohistochemistry using D2-40 and CD31 antibodies makes it possible to differentiate between lymphatic vascular invasion (LVI) and blood vessel invasion (BVI). The aim was to examine lymphatic and blood vessel invasion separately and their associations with clinicopathological characteristics and prognosis. METHODS AND RESULTS: Immunohistochemistry was performed on a retrospective population-based series of endometrial carcinoma. Altogether, 31% of the 276 tumours showed lymphatic involvement, whereas 18% showed blood vessel invasion. LVI and BVI were associated with histopathological variables such as histological grade and tumour growth pattern. Patients without vascular invasion had the best prognosis and those with BVI (with or without LVI) had the worst outcome, whereas patients with LVI had an intermediate survival on univariate analysis. Multivariate models indicated that both LVI and especially BVI had independent prognostic importance. Among endometrioid carcinomas, BVI was still significant. CONCLUSIONS: Our findings support the biological importance of vascular spread through the haematogenic and lymphatic routes in endometrial cancer. The significant correlation found with clinical phenotype indicates that these markers may be relevant for patient management.
AIMS: Vascular invasion is a prognostic marker for many cancers, including endometrial carcinoma. Immunohistochemistry using D2-40 and CD31 antibodies makes it possible to differentiate between lymphatic vascular invasion (LVI) and blood vessel invasion (BVI). The aim was to examine lymphatic and blood vessel invasion separately and their associations with clinicopathological characteristics and prognosis. METHODS AND RESULTS: Immunohistochemistry was performed on a retrospective population-based series of endometrial carcinoma. Altogether, 31% of the 276 tumours showed lymphatic involvement, whereas 18% showed blood vessel invasion. LVI and BVI were associated with histopathological variables such as histological grade and tumour growth pattern. Patients without vascular invasion had the best prognosis and those with BVI (with or without LVI) had the worst outcome, whereas patients with LVI had an intermediate survival on univariate analysis. Multivariate models indicated that both LVI and especially BVI had independent prognostic importance. Among endometrioid carcinomas, BVI was still significant. CONCLUSIONS: Our findings support the biological importance of vascular spread through the haematogenic and lymphatic routes in endometrial cancer. The significant correlation found with clinical phenotype indicates that these markers may be relevant for patient management.
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