Kashkar, Hamid (2010). X-linked Inhibitor of Apoptosis: A Chemoresistance Factor or a Hollow Promise. Clin. Cancer Res., 16 (18). S. 4496 - 4503. PHILADELPHIA: AMER ASSOC CANCER RESEARCH. ISSN 1078-0432

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Abstract

The X-linked inhibitor of apoptosis (XIAP) is the only cellular protein that has evolved to potently inhibit the enzymatic activity of mammalian caspases and promotes resistance to apoptosis. Given its role in apoptosis and its frequently elevated expression in malignant cells, XIAP has garnered the most attention as a promising therapeutic target in cancer to overcome drug resistance. Accordingly, XIAP is thought to render tumor cells resistant to chemotherapy through its ability to inhibit caspases, and it is on this basis that XIAP has been proposed as an important adverse biomarker for chemoresistance in cancer patients. Here, the current understanding of the role of XIAP in cancer is reviewed. Further, the notion is explored that the elevated XIAP expression frequently observed in malignant tissues is, at least, not exclusively responsible for the resistance of tumor cells to conventional therapeutic treatment; rather, the function of XIAP seems to be conducive to the process of malignant transformation and/or progression. Clin Cancer Res; 16(18); 4496-502. (c) 2010 AACR.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Kashkar, HamidUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-496554
DOI: 10.1158/1078-0432.CCR-10-1664
Journal or Publication Title: Clin. Cancer Res.
Volume: 16
Number: 18
Page Range: S. 4496 - 4503
Date: 2010
Publisher: AMER ASSOC CANCER RESEARCH
Place of Publication: PHILADELPHIA
ISSN: 1078-0432
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
ALPHA-DEPENDENT APOPTOSIS; PROGRAMMED CELL-DEATH; NF-KAPPA-B; PROMOTES APOPTOSIS; MEDIATED APOPTOSIS; XIAP EXPRESSION; TRANSGENIC MICE; CYTOCHROME-C; IAP GENE; PROTEINMultiple languages
OncologyMultiple languages
URI: http://kups.ub.uni-koeln.de/id/eprint/49655

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