title: Tumor angiogenesis and molecular target therapy in ovarian carcinomas.
abstract: Growth of solid tumors depends on angiogenesis, the process by which new blood vessels develop from the endothelium of a pre-existing vasculature. Tumors promote angiogenesis by secreting various angiogeneic factors, and newly formed blood vessels induce tumor cell proliferation and invasiveness. Ovarian carcinomas have a poor prognosis, often associated with multifocal intraperitoneal dissemination accompanied by intense neovascularization. The degree of angiogenesis of ovarian carcinomas may directly influence the clinical course of the disease. Although a growing body of evidence indicates that angiogenic intensity may play a prognostic role in gynecological malignancies including ovarian carcinomas, the related biological mechanisms remain to be further elucidated. In this review, we describe current knowledge pertaining to mechanisms and regulation of angiogenesis in ovarian carcinomas with special reference to our recent research results.
authors.affiliation: Department of Obstetrics and Gynecology, Osaka Medical College, 2-7 Daigakumachi, Takatsuki, Osaka 569-8686, Japan. gyn017@poh.osaka-med.ac.jp
authors.forename: Masatsugu
authors.initials: M
authors.lastname: Ueda
authors.forename: Yoshito
authors.initials: Y
authors.lastname: Terai
authors.forename: Koji
authors.initials: K
authors.lastname: Kanda
authors.forename: Masanori
authors.initials: M
authors.lastname: Kanemura
authors.forename: Mikio
authors.initials: M
authors.lastname: Takehara
authors.forename: Hikari
authors.initials: H
authors.lastname: Futakuchi
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Yamaguchi
authors.forename: Masayuki
authors.initials: M
authors.lastname: Yasuda
authors.forename: Koji
authors.initials: K
authors.lastname: Nishiyama
authors.forename: Minoru
authors.initials: M
authors.lastname: Ueki
mesh_terms: D043925:Angiogenesis Inducing Agents; D020533:Angiogenesis Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D042501:Angiogenic Proteins / Q000235:genetics / Q000502:physiology; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D000068258:Bevacizumab; D002277:Carcinoma / Q000098:blood supply* / Q000235:genetics / Q000473:pathology / Q000628:therapy*; D049109:Cell Proliferation; D016326:Extracellular Matrix Proteins; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D015316:Genetic Therapy; D006801:Humans; D020778:Matrix Metalloproteinase 2 / Q000235:genetics / Q000502:physiology; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D009389:Neovascularization, Pathologic / Q000235:genetics*; D010051:Ovarian Neoplasms / Q000098:blood supply* / Q000235:genetics / Q000473:pathology / Q000628:therapy*; D010455:Peptides / Q000494:pharmacology / Q000627:therapeutic use; D016337:RNA, Catalytic / Q000494:pharmacology / Q000627:therapeutic use; D014407:Tumor Cells, Cultured; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors / Q000235:genetics / Q000502:physiology
chemical_list: D043925:Angiogenesis Inducing Agents; D020533:Angiogenesis Inhibitors; D042501:Angiogenic Proteins; C121301:Angiozyme; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D016326:Extracellular Matrix Proteins; D010455:Peptides; D016337:RNA, Catalytic; C429104:SPON1 protein, human; D042461:Vascular Endothelial Growth Factor A; D000068258:Bevacizumab; D020778:Matrix Metalloproteinase 2