title: Evaluation of angiogenesis, p-53 tissue protein expression and serum VEGF in patients with endometrial cancer.
abstract: Endometrial carcinoma occurs mostly in post-menopausal women. Classical methods of prognostication, as FIGO stage and histopathologic grade, could be improved by applying additional techniques, utilizing molecular biology and immunochemistry. p-53 tumor suppressor gene, the most commonly mutated gene in human cancers has been shown to play an important role in the biology of gynecologic carcinomas. Angiogenesis, a process of formation of new vessels, being connected to tumors progression and metastatic potential was shown to be linked with tumor suppressor genes expression. The aim of the study was to evaluate relationships between intensity of tumor angiogenesis, serum levels of Vascular Endothelial Growth Factor (VEGF) and tissue p-53 protein expression in endometrial adenocarcinoma. Angiogenic Point's Density (APD) was calculated in hot spots areas using the morphometric appliance. For detection of p53 protein in tumor samples, LSAB + Kit Alkaline Phosphatase (DAKO) was used. VEGF levels were assessed in patient's blood sampled before the operation. Overexpression of p53 protein was found in tumor tissue in 35.2% of cases and mean angiogenic points density was greater in p53 positive cases. Serum levels of VEGF were above the cut off level in 54.5% of patients, in those cases angiogenesis was also elevated. In cases of p53 overexpression, VEGF levels tended to be greater as compared with p53 negative cases. In conclusion, our study demonstrated that angiogenesis was more intensive in p53 positive cases, confirming the hypothesis of tumor suppressor-gene regulation of the process of neovascularization. Serum levels of VEGF were borderline-significantly higher in cases of p53 overexpression, they were also correlated to the angiogenesis. Joint assessment of angiogenesis and tumor suppressor genes expression may contribute to reliable evaluation of the biology of endometrial carcinoma.
authors.affiliation: Department of Pathophysiology of Pregnancy, Medical University of Bialystok, 15-276, Poland.
authors.forename: A
authors.initials: A
authors.lastname: Mazurek
authors.forename: P
authors.initials: P
authors.lastname: Pierzyński
authors.forename: P
authors.initials: P
authors.lastname: Kuć
authors.forename: P
authors.initials: P
authors.lastname: Kopinski
authors.forename: S
authors.initials: S
authors.lastname: Terlikowski
authors.forename: W
authors.initials: W
authors.lastname: Niklińska
authors.forename: J
authors.initials: J
authors.lastname: Trojan
authors.forename: T
authors.initials: T
authors.lastname: Laudański
mesh_terms: D000230:Adenocarcinoma / Q000098:blood supply / Q000473:pathology*; D000368:Aged; D046508:Culture Techniques; D016889:Endometrial Neoplasms / Q000098:blood supply / Q000473:pathology*; D005260:Female; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor; D006801:Humans; D007150:Immunohistochemistry; D008875:Middle Aged; D009389:Neovascularization, Pathologic; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis*; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
chemical_list: D016159:Tumor Suppressor Protein p53; D042461:Vascular Endothelial Growth Factor A