Gleevec: prototype or outlier?

Abstract

The protein kinase inhibitor Gleevec has proven to be spectacularly effective in the treatment of chronic myelogenous leukemia (CML). But can success such as this be achieved for genetically complex neoplasms with other drugs targeted at hyperactive oncoproteins? Although only time will tell, both theoretical and empirical arguments suggest that the success of Gleevec in CML need not be a special case. As the molecular basis of various cancers is further defined, it should be possible to develop other new drugs that, like Gleevec, specifically target cancer cells by inhibiting early events that are integral to progression to the transformed phenotype. Encouraging in this regard are cell culture experiments and animal models that suggest that cancer cells often remain dependent on, and may become addicted to, the signals resulting from such early genetic changes.

• Authors: William G Kaelin Jr
• Journal: Science's STKE : signal transduction knowledge environment (Sci STKE) Vol. 2004 Issue 225 Pg. pe12 (Mar 16 2004) ISSN: 1525-8882 [Electronic] United States
• PMID: 15039489 (Publication Type: Journal Article, Review)

Chemical References

• Antineoplastic Agents
• Benzamides
• Piperazines
• Pyrimidines
• Imatinib Mesylate
• Protein-Tyrosine Kinases

Topics

• Animals
• Antineoplastic Agents (adverse effects, pharmacokinetics, pharmacology)
• Benzamides
• Disease Models, Animal
• Humans
• Imatinib Mesylate
• Piperazines (adverse effects, pharmacokinetics, pharmacology)
• Protein-Tyrosine Kinases (antagonists & inhibitors)
• Pyrimidines (adverse effects, pharmacokinetics, pharmacology)
• Research Design (trends)