Cancer Research Strategies and Cancer CareTatjana Abaffy*
Department of Molecular and Cellular Pharmacology, University of Miami, Miller School of Medicine, Miami, Florida, USA
- *Corresponding Author:
- Tatjana Abaffy
Department of Molecular and Cellular Pharmacology
University of Miami, Miller School of Medicine, Miami, Florida, USA
Tel: (305) 322-0115
E-mail: [email protected]
Received date: September 07, 2011; Accepted date: September 10, 2011; Published date: September 14, 2011
Citation: Abaffy T (2011) Cancer Research Strategies and Cancer Care. J Pharmacogenomics Pharmacoproteomics 2:e103. doi: 10.4172/2153-0645.1000e103
Copyright: © 2011 Abaffy T. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Imatinib mesylate (Gleevec) is a tyrosine kinase inhibitor currently used for treatment of BCR-ABL (Breakpoint Cluster Regionâ€“vabl ABelson murine Leukemia viral oncogene) Tyrosine Kinase (TK) positive leukemia, as well as GastroIntestinal Stromal Tumors (GIST). Imatinib represents one of the rare successful stories in drug development . Imatinib binds to the catalytic site of the kinase and traps it in an inactive conformation. This success was made possible through decades of intensive and collaborative research which led to discovery of the involvement of this protein kinase in tumor pathology. However, this success though impressive, was not immortal. A resistance to the drug developed. Drug resistance is often associated with chronic treatment with anticancer drugs and is likely due to the general genomic instability well documented in cancer. It has been shown that Activation Induced Cytidine Deaminase, AICD, the enzyme that converts cytidine to uridine, causing DNA breaks and hypermutations, also causes mutations in BCR-ABL TK resulting in Imatinib resistance. The recently revealed complexity of polyclonal resistance in patients with imatinib-resistant GIST, suggests that a single next generation drug is unlikely to inhibit all mutant clones in a given patient.