Signaling pathways in apoptosis as potential targets for cancer therapy.
Genetic instability contributes to the origin of cancer as well as to the ability of cancer cells to become resistant to various therapies. Because of this, cytotoxic rather than cytostatic therapies might be most effective against this disease. Many oncogenes and tumor suppressors mediate their effects by interfering with or inducing apoptotic signaling. Thus, apoptotic pathways might be significantly altered in cancer cells relative to untransformed cells, and these differences might present a therapeutic window that can be exploited for development of cancer drugs.
Huang
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DuPont Pharmaceuticals, 500 S. Ridgeway Ave, Glenolden, PA 19036, USA. Pearl.S.Huang@dupontpharma.com
Oliff
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D000818:Animals; D017209:Apoptosis; D051017:Apoptosis Regulatory Proteins; D002352:Carrier Proteins / Q000378:metabolism*; D016147:Genes, Tumor Suppressor; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins; D024101:Mitochondrial Proteins; D009369:Neoplasms / Q000628:therapy*; D017346:Protein Serine-Threonine Kinases; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt; D015398:Signal Transduction; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism*
D051017:Apoptosis Regulatory Proteins; D002352:Carrier Proteins; C412403:DIABLO protein, human; D047908:Intracellular Signaling Peptides and Proteins; D024101:Mitochondrial Proteins; D011518:Proto-Oncogene Proteins; D016159:Tumor Suppressor Protein p53; D017346:Protein Serine-Threonine Kinases; D051057:Proto-Oncogene Proteins c-akt