Chemoresistance in human ovarian cancer: The role of apoptotic regulators

被引:143
作者
Michael Fraser
Brendan Leung
Arezu Jahani-Asl
Xiaojuan Yan
Winston E Thompson
Benjamin K Tsang
机构
[1] Dept. Obstet./Gynecol./Molec. Med., University of Ottawa, Ottawa Health Research Institute, Ottawa
[2] Dept. of Obstetrics and Gynecology, Cooperative Repro. Sci. Res. Center, Morehouse School of Medicine, Atlanta
关键词
Ovarian Cancer; Ovarian Cancer Cell; Human Ovarian Cancer Cell; Sporadic Breast Cancer; Death Effector Domain;
D O I
10.1186/1477-7827-1-66
中图分类号
学科分类号
摘要
Ovarian cancer is among the most lethal of all malignancies in women. While chemotherapy is the preferred treatment modality, chemoresistance severely limits treatment success. Recent evidence suggests that deregulation of key pro- and anti-apoptotic pathways is a key factor in the onset and maintenance of chemoresistance. Furthermore, the discovery of novel interactions between these pathways suggests that chemoresistance may be multi- factorial. Ultimately, the decision of the cancer cell to live or die in response to a chemotherapeutic agent is a consequence of the overall apoptotic capacity of that cell. In this review, we discuss the biochemical pathways believed to promote cell survival and how they modulate chemosensitivity. We then conclude with some new research directions by which the fundamental mechanisms of chemoresistance can be elucidated. © 2003 Frazer et al; licensee BioMed Central Ltd.
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页数:13
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共 114 条
[1]  
(2003)
[2]  
Eltabbakh G.H., Awtrey C.S., Current treatment for ovarian cancer, Expert Opin. Pharmacother., 2, pp. 109-124, (2001)
[3]  
Yuan Z.Q., Sun M., Feldman R.I., Wang G., Ma X., Jiang C., Coppola D., Nicosia S.V., Cheng J.Q., Frequent activation of AKT2 induction of apoptosis by inhibition of phosphoinositide-3-OH kinase/Akt pathway in human ovarian cancer, Oncogene, 19, pp. 2324-2330, (2000)
[4]  
Lasky T., Silbergeld E., P53 mutations associated with breast, colorectal, liver, lung, and ovarian cancers, Environ. Health Perspect., 104, pp. 1324-1331, (1996)
[5]  
Gatti L., Supino R., Perego P., Pavesi R., Caserini C., Carenini N., Righetti S.C., Zuco V., Zunino F., Apoptosis growth arrest induced by platinum compounds in U2-OS cells reflect a specific DNA damage recognition associated with a different p53-mediated response, Cell Death Differ., 9, pp. 1352-1359, (2002)
[6]  
Servidei T., Ferlini C., Riccardi A., Meco D., Scambia G., Segni G., Manzotti C., Riccardi R., The novel trinuclear platinum complex BBR3464 induces a cellular response different from cisplatin, Eur. J. Cancer, 37, pp. 930-938, (2001)
[7]  
Schneiderman D., Kim J.-M., Senterman M., Tsang B.K., Sustained suppression of Fas ligand expression in cisplatin-resistant human ovarian surface epithelial cancer cells, Apoptosis, 4, pp. 271-282, (1999)
[8]  
Li J., Feng Q., Kim J.M., Schneiderman D., Liston P., Li M., Vanderhyden B., Faught W., Fung M.F., Senterman M., Korneluk R.G., Tsang B.K., Human ovarian cancer cisplatin resistance: Possible role of inhibitor of apoptosis proteins, Endocrinology, 142, pp. 370-380, (2001)
[9]  
Jesenberger V., Jentsch S., Deadly encounter: Ubiquitin meets apoptosis, Nat. Rev. Mol. Cell Biol., 3, pp. 112-121, (2002)
[10]  
Verhagen A.M., Coulson E.J., Vaux D.L., Inhibitor of apoptosis proteins their relatives: IAPs other BIRPs, Genome. Biol., 2, (2001)