DISSECTING COX-1 RELATED GENE PATHWAYS IN OVARIAN CANCER

剖析卵巢癌中 COX-1 相关基因通路

• 批准号: 8166236
• 负责人: DEOK-SOO SON
• 金额: $ 12.66万
• 依托单位: MEHARRY MEDICAL COLLEGE
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-09-08 至 2011-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8166236
• 关键词: 1-Phosphatidylinositol 3-Kinase; Arachidonic Acids; Biological Markers; Cancer Etiology; Cells; Cessation of life; Computer Retrieval of Information on Scientific Projects Database; Disease; EGF gene; Enzymes; Funding; Future; Genes; Goals; Grant; Institution; Malignant neoplasm of ovary; Molecular; Ovarian; Ovary; PTGS2 gene; Pathway interactions; Pilot Projects; Prostaglandin H2; Proto-Oncogene Proteins c-akt; Research; Research Personnel; Resources; Signal Transduction; Source; Survival Rate; United States National Institutes of Health; Woman; anticancer research; base; cancer cell; carcinogenesis; cyclooxygenase 1; ovarian neoplasm; programs; response; tumor; tumor growth; tumor progression

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. NOTE: Tables and Figures were uploaded with Program Summary. PILOT PROJECT  Dissecting COX-1 Related Gene Pathways in Ovarian Cancer Ovarian cancer is the fifth leading cause of cancer deaths among women with little change in survival rates over the past 30 years. It is typically asymptomatic until tumors have spread far beyond the ovaries. Cyclooxygenase-1 (COX-1), an enzyme that convert arachidonic acid to prostaglandin H2, is highly expressed in ovarian cancers, compared with COX-2. The goal of this research is to determine the specific contributions of COX-1 to ovarian carcinogenesis. Hypothesis and Aims: The long-range goal of this research is to determine the specific contributions of COX-1 to ovarian carcinogenesis. We hypothesize that COX-1 expression modulates phosphatidylinositol 3 kinase/protein kinase B (PI3K/Akt) signaling that is involved in ovarian tumor growth and progression. We explore molecular mechanisms of PI3K/Akt signaling in response to EGF comparing COX-1 positive cells to COX-1 negative ovarian cancer cells. Significance: If we determine that COX-1 is indeed a prominent factor in tumor progression in ovarian cancer, this research may provide the basis for its future use as a biomarker and target for therapy in the management of this deadly disease.

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