Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C1658953 (tumor vasculature)
 2,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

TEM1 (endosialin) expression is increased in the stroma and tumor vasculature of several common human cancers. The exact physiological role of TEM1 is still unknown since Tem1-deficient mice are viable and show only a lower rate of abdominal site-specific tumor invasion in tumor transplantation experiments. Previous studies have reported Tem1 expression in mouse embryos and adults, but did not determine the timing or location of the earliest expression, and did not examine all organ systems. Using the highly sensitive Bluo-Gal staining method for detecting temporal and spatial Tem1-lacZ activity in lacZ knock-in (+/lacZ) mice, we found that Tem1 gene expression was initially detectable in the dorsal aortic wall, the heart, the umbilical vessels, the first branchial arch, and the cephalic mesenchyme at E9.5. From E10.5 to E14.5, Tem1 gene expression was additionally seen mainly in the genital tubercle, the mesonephros, the whisker follicles, the mesenchymal tissues around the eye, and the lung. Remarkably, the kidney expressed abundant Tem1-lacZ starting from E16.5. Postnatally, Tem1 expression decreased in most organs but elevated expression persisted in the renal glomerulus and the uterus, where the expression pattern varied at different estrous cycle stages. Co-localization studies indicated that most vimentin-positive cells co-expressed Tem1-lacZ, while a large portion of CD31- or desmin-positive cells were also positive for Tem1-lacZ. Taken together, our observations suggest that Tem1 is expressed throughout embryonic and adult development in several types of mesenchymal cells closely related to blood vessels.
 ...
PMID:Gene targeting and expression analysis of mouse Tem1/endosialin using a lacZ reporter. 2140 74

Endocrine glands are well vascularized 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 hemodynamic and metabolic perturbations. Diabetic retinopathy is the most common microvascular complication of diabetes mellitus and is the leading cause of blindness. In diabetic retinopathy ischemic states and hence tissue hypoxia and angiogenesis takes place. Participation of angiogenesis and VEGF in pathogenesis of neoplastic disease is described in many papers. VEGF protein and mRNA were found in cancers of the thyroid, bronchus, lungs, esophagus, stomach, colon, liver, breast, ovary, uterus, kidney, urinary bladder, in malignant tumors of the brain, bone. In a series of reports connections between the degree of VEGF expression with tumor aggressiveness and prognosis in patients have been reported. Richly vascularized are GEP NET. In neuroendocrine tumors 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 of application the angiogenic and antiangiogenic therapy are being made. Antiangiogenic therapy (usually regarded as a form of cancer therapy) is based on: inhibitory effects of proangiogenic ligands and their receptors; stimulation or delivery of angiogenesis inhibitors; direct destruction of neoplastic tumor vasculature.
 ...
PMID:[Vascular endothelial growth factor (VEGF) in endocrinology and oncology]. 2216 82