Vascular sst5 was expressed in 40% of benign and only 4.8% of malignant lesions, which may suggest that either the loss of sst5, which is postulated to have tumour suppressor actions, by benign vessels leads to the more rapid angiogenesis associated with malignancy, or that the increased production of SRIF by malignant lesions may lead to down-regulation of the vascular sst5 receptors. This evidence concerns the gene SSTR5 and neoplasm.