| Literature DB >> 19095773 |
Dan Jones1, Suzanne Kamel-Reid2, David Bahler3, Henry Dong4, Kojo Elenitoba-Johnson5, Richard Press6, Neil Quigley7, Paul Rothberg8, Dan Sabath9, David Viswanatha10, Karen Weck11, James Zehnder12.
Abstract
The BCR-ABL tyrosine kinase produced by the t(9;22)(q34;q11) translocation, also known as the Philadelphia chromosome, is the initiating event in chronic myeloid leukemia (CML) and Ph+ acute lymphoblastic leukemia (ALL). Targeting of BCR-ABL with tyrosine kinase inhibitors (TKIs) has resulted in rapid clinical responses in the vast majority of patients with CML and Philadelphia chromosome+ ALL. However, long-term use of TKIs occasionally results in emergence of therapy resistance, in part through the selection of clones with mutations in the BCR-ABL kinase domain. We present here an overview of the current practice in monitoring for such mutations, including the methods used, the clinical and laboratory criteria for triggering mutational analysis, and the guidelines for reporting BCR-ABL mutations. We also present a proposal for a public database for correlating mutational status with in vitro and in vivo responses to different TKIs to aid in the interpretation of mutation studies.Entities:
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Year: 2008 PMID: 19095773 PMCID: PMC2607559 DOI: 10.2353/jmoldx.2009.080095
Source DB: PubMed Journal: J Mol Diagn ISSN: 1525-1578 Impact factor: 5.568