Vol 62, No 5 (2011)
Review paper
Published online: 2011-11-08
Vascular endothelial growth factor (VEGF) — part 2: in endocrinology and oncology
Endokrynol Pol 2011;62(5):456-464.
Abstract
Endocrine glands are well vascularised and the structure of their vessels facilitates the exchange of various substances, including hormones.
These glands are a frequent experimental model in research on VEGF and angiogenesis. VEGF participates in the pathogenesis
of diabetes. Diabetic nephropathy is in essence a microvascular disease that develops as a result of a confluence of haemodynamic and
metabolic perturbations. Diabetic retinopathy is the commonest microvascular complication of diabetes mellitus and is the leading cause of
blindness. In diabetic retinopathy, ischaemic states, and hence tissue hypoxia and angiogenesis, take place. The participation of angiogenesis
and VEGF in the pathogenesis of neoplastic disease has been described in many papers. VEGF protein and mRNA have been found
in cancers of the thyroid, bronchus, lungs, oesophagus, stomach, colon, liver, breast, ovary, uterus, kidney, and urinary bladder, and in
malignant tumours of the brain and bone. There have been many reports of the connections between the degree of VEGF expression and
tumour aggression and prognosis in patients. Richly vascularised are GEP NET. In neuroendocrine tumours, strong expression of VEGF,
Flt-1 and KDR in relation to the unchanged surrounding tissues has been demonstrated. Depending on the disease entity or the degree of
its severity, attempts to apply angiogenic and antiangiogenic therapy have being made. Antiangiogenic therapy (usually regarded as a form
of cancer therapy) is based on: 1. inhibitory effects of proangiogenic ligands and their receptors; 2. stimulation or delivery of angiogenesis
inhibitors; and 3. direct destruction of neoplastic tumour vasculature. (Pol J Endocrinol 2011; 62 (5): 456–464)
Keywords: VEGFangiogenesisKDRFlt-1endocrine glandspituitarythyroiddiabetes mellitusliverGEP NETcancerneoplasmhepatocellular carcinomaoncologygrowth factor