The DOI matches its Crossref record; 68 of the 68 references it cites were found in a registry or an index.
Recent advances in understanding the cell death pathways activated by anticancer therapy
Abstract
Over the past two decades, the role of apoptosis in the cytotoxicity of anticancer drugs has become clear. Apoptosis may occur via a death receptor‐dependent (extrinsic) or independent (intrinsic or mitochondrial) pathway. Mitochondria play a central role in cell death in response to DNA damage, and mediate the interaction(s) of various cytoplasmic organelles, including the endoplasmic reticulum, Golgi apparatus, and lysosomes. The mitochondrial pathway of cell death is mediated by Bcl‐2 family proteins, a group of antiapoptotic and proapoptotic proteins that regulate the passage of small molecules, such as cytochrome c, Smac/Diablo, and apoptosis‐inducing factor, which activates caspase cascades, through the mitochondrial transition pore. In addition, apoptosis can induce autophagic cell death via crosstalk between the two pathways upon treatment with anticancer drugs. The current review focused on recent advances surrounding the mechanism(s) of cell death induced by anticancer agents and discussed potential molecular targets for enhancing the chemotherapeutic effect(s) of anticancer agents. Cancer 2005. © 2005 American Cancer Society.
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Cites
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Cited by
Role of mitochondria as the gardens of cell death
Kim, R., Emi, M., & Tanabe, K. (2006) · Cancer Chemotherapy and Pharmacology · doi:10.1007/s00280-005-0111-7 · Cited by 326
Self-citationChen, T., & Wong, Y.-S. (2008) · Journal of Agricultural and Food Chemistry · doi:10.1021/jf073399k · Cited by 157
Lee, S. Y., Park, S.-H., Lee, S. W., Lee, S. H., Son, M. K., Choi, Y. H., Chung, W. T., & Yoo, Y. H. (2014) · Archives of Pharmacal Research · doi:10.1007/s12272-014-0365-x · Cited by 17
Metadata
- Authors
- Kim, R.
- Venue
- Cancer
- Publisher
- Wiley
- Published
- 2005-03
- Volume
- 103
- Issue
- 8
- Pages
- 1551-1560
- ISSN
- 0008-543X (ISSN-L)
- 1097-0142
- OpenAlex
- W1992844265
- Cited by
- 314
- References
- 68
- FWCI
- 10.60
- Type
- journal article
- Language
- en
- Open access
- closed
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