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Study On The Angeogenesis Regulating Molecules In Cervical Lesion

Posted on:2003-08-02Degree:DoctorType:Dissertation
Country:ChinaCandidate:J J ZhangFull Text:PDF
GTID:1104360185968709Subject:Obstetrics and gynecology
Abstract/Summary:PDF Full Text Request
BACKGROUND Cervical lesion is one of the most common gynecologic diseases , of which cervical cancer is the most serious case. In gynecologic malignancies, the incidence of cervical cancer is only secondary to breast cancer. Recent researches have shown the ascending incidence in younger women. Cervical intraepithelial neoplasia (CIN) is the pre-malignant lesion of cervical cancer, 15% of which will progress into malignant tumor .The danger of progressing into malignant tumor of CIN I , CIN II, CINIII are 15%, 30%, 45% separately . As we have known that the main pathogenesis is human papilloma virus (HPV) infection , but the successful occurrence and growth is dependent upon adequate blood supply . Neovascularization (angeogenesis), the formation of new blood vessels, can be considered to play a major role in the progression of cervical lesion. Angeogenesis is a complex procedure, which is participated by a variaty of cells and molecules, which depend on the balance of positive and negative regulators. The angeogenic factors include: vascular endothelial growth factor (VEGF),platelet-derived endothelial cell growth factor (PDECGF, PDGF),and tumor necrosis factor α (TNF- α ) , and so on.The angeogenic inhibitors include : thrombospondin-1(TSP-1) , platelet IV,interferons ,e.g. Angeogenesis takes place mostly adjacent to the mass of tumor,where the microenvironment may result in the formation of vessels. VEGF is regarded as the most important positive factor, whereas TSP-1 is another interesting endogenous inhibitor. Therefore, to investigate the expression of some angeogenesis factors is important for better understanding of pathogenesis of cervical lesion, and may provide a new treatment strategy for cervical lesion.
Keywords/Search Tags:Angeogenesis
PDF Full Text Request
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