Accession Number : ADA506004


Title :   Mechanisms and Chemoprevention of Ovarian Carcinogenesis


Descriptive Note : Final rept. 1 Feb 2004-31 Jan 2009


Corporate Author : FOX CHASE CANCER CENTER PHILADELPHIA PA


Personal Author(s) : Cvetkovic, Dusica


Full Text : http://www.dtic.mil/get-tr-doc/pdf?AD=ADA506004


Report Date : FEB 2009


Pagination or Media Count : 38


Abstract : Ovarian cancer is the most fatal gynecological malignancy. The understanding of the early molecular events leading to ovarian cancer is important for the development of strategies for early detection and prevention. We have demonstrated that DMBA induced mutagenesis in the rat ovary, combined with gonadotropin hormone-mediated enhanced mitogenesis of the ovarian surface epithelium, produces lesions ranging from preneoplastic, early neoplastic to advanced ovarian tumors, resembling human disease. The goal of this project was to use the DMBA-gonadotropin animal model to study molecular mechanisms underlying ovarian oncogenesis and to conduct a preclinical chemoprevention trial. The original specific aims of the study were: 1) Determine the molecular genetic mechanisms underlying ovarian oncogenesis in the rat DMBA/gonadotropin model of ovarian cancer; 2) Determine the efficacy of the COX-1 inhibitor SC-560 to prevent the appearance and/or progression of DMBA-induced ovarian lesions; and 3) Study the in vivo mechanisms of the putative chemopreventive action of COX-1 inhibition. However, due to change of Principal Investigator in the last year of the study, the original research plan has been modified. Since the animal protocol pertaining to this project has been closed and the proposed chemoprevention trial in rats has not been initiated, only aim 1 is being carried out.


Descriptors :   *OVARIAN CANCER , *EPITHELIUM , *HORMONES , RESEARCH MANAGEMENT , ONCOGENESIS , MOLECULAR PROPERTIES , GENETICS , MITOSIS , MEDIATION , NEOPLASMS , GONADOTROPINS , MOLECULES , IN VIVO ANALYSIS


Subject Categories : BIOCHEMISRTY
      MEDICINE AND MEDICAL RESEARCH


Distribution Statement : APPROVED FOR PUBLIC RELEASE