期刊
CANCER AND METASTASIS REVIEWS
卷 34, 期 1, 页码 19-40出版社
SPRINGER
DOI: 10.1007/s10555-014-9538-9
关键词
Ovarian cancer; Targeted therapy; Angiogenesis; Anti-vascular agent; Resistance to anti-VEGF therapy
类别
资金
- US National Institutes of Health [P50CA083639, P50CA098258, CA109298, U54 CA151668, CA177909, UH2TR000943, T32CA101642, CA16672]
- Department of Defense [OC120547, OC093416]
- Ovarian Cancer Research Fund, CPRIT [RP110595]
- Bettyann Asche Murray Distinguished Professorship
- Chapman Foundation
- Meyer and Ida Gordon Foundation
- Gilder Foundation
- RGK Foundation
- Judi A. Rees Ovarian Cancer Research Fund
- Blanton-Davis Ovarian Cancer Research Program
Resistance to chemotherapy is among the most important issues in the management of ovarian cancer. Unlike cancer cells, which are heterogeneous as a result of remarkable genetic instability, stromal cells are considered relatively homogeneous. Thus, targeting the tumor microenvironment is an attractive approach for cancer therapy. Arguably, anti-vascular endothelial growth factor (anti-VEGF) therapies hold great promise, but their efficacy has been modest, likely owing to redundant and complementary angiogenic pathways. Components of platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), epidermal growth factor (EGF), and other pathways may compensate for VEGF blockade and allow angiogenesis to occur despite anti-VEGF treatment. In addition, hypoxia induced by anti-angiogenesis therapy modifies signaling pathways in tumor and stromal cells, which induces resistance to therapy. Because of tumor cell heterogeneity and angiogenic pathway redundancy, combining cytotoxic and targeted therapies or combining therapies targeting different pathways can potentially overcome resistance. Although targeted therapy is showing promise, much more work is needed to maximize its impact, including the discovery of new targets and identification of individuals most likely to benefit from such therapies.
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