You are currently viewing the abstract.
View Full TextLog in to view the full text
AAAS login provides access to Science for AAAS members, and access to other journals in the Science family to users who have purchased individual subscriptions.
More options
Download and print this article for your personal scholarly, research, and educational use.
Buy a single issue of Science for just $15 USD.
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.
