Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vulvar intraepithelial neoplasia (VIN) has been reported to be a precursor of invasive vulvar cancer. Switching to the angiogenic phenotype is considered a key step in tumor growth. Microvessel density (MVD) and vascular endothelial growth factor (VEGF), a highly angiogenic peptide, are important parameters of tumor angiogenesis. Forty-three histologic slides with 38 VIN I-III lesions were immunohistochemically stained for factor VIII-related antigen (F8-RA) and 44 slides with 37 VIN I-III for VEGF, since F8-RA reliably highlights tumor microvessels. Determination of MVD and VEGF expression was done by counting microvessels and VEGF-positive cells at a magnification of 200x and 400x. The highest concentration of F8-RA-stained MVD and VEGF expression was found at a small subepithelial area at the border of the VIN lesion to the stroma underneath but concentrations were low in all specimens of normal epithelium. High VEGF expression was significantly correlated to high MVD. For both MVD and VEGF expression the differences between VIN I and VIN III and between VIN II and VIN III were statistically significant (P < 0.0001). VIN III lesions are the clinical relevant precursors of invasive cancer of the vulva, as outlined by intense expression of VEGF protein and a highly dense network of microvessels underlying the dysplastic epithelium.
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PMID:Angiogenesis in vulvar intraepithelial neoplasia. 906 59

Angiogenesis plays an important role both in progression of solid tumors and in metastasizing. An invasive growth of a neoplasm is mainly connected with appearing of blood vessels within a tumor. Inhibition of angiogenesis in solid neoplasms may deter both tumor growth and metastases. New treatment strategies based on suppressing of angiogenesis and selective damaging of neoplastic blood vessels may prove to be as efficient as those based on direct destruction of neoplastic cells. One of important angiogenic factors is vascular endothelial growth factor (VEGF), which is produced by neoplastic cells and shows high promitotic activity almost entirely for endothelial cells (paracrine activity). We decided to investigate VEGF expression in precancerous lesions as well as in squamous cancers of vulva. Our material included 31 cases of vulvar squamous cancer, 28 cases of VIN (vulvar intraepithelial neoplasia) III, 10 VIN II cases and 12 VIN I cases. A diagnosis was established according to WHO criteria on the ground of post-operative histopathological examination complemented with proliferation index estimated by the use of MIB-1 antibody. Immunohistochemical examinations were performed on paraffin-embedded material, using MIB-1 antibody (Immunotech), VEGF antibody (Santa Cruz), Goat serum Normal (DAKO), DAKO StreptAB-Complex/HRP Duet, Mouse/Rabbit DAKO DAB Chromogen Tablets, TBS (Sigma). Positive cytoplasmic expression of anti-VEGF polyclonal antibody (diffuse and/or focal and of various intensity) was observed in almost all samples from precancerous and cancerous lesions. The expression was especially strong and diffuse in all cancer cases; in cases of VIN it was mainly focal and weak.
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PMID:Expression of vascular endothelial growth factor (VEGF) in vulvar squamous cancer and VIN. 1592 Oct 7