|
|
|
A new inhibitor of Bcr-abl kinase, a key therapeutic target for treating chronic myelogenous leukemia (CML), is reported in the February 2006 issue of Nature Chemical Biology. CML is a common form of leukemia that is typically characterized by two genes, BCR and ABL1, connecting together when they should be separate. The resulting fusion protein causes cellular signaling pathways to be on when they should be off and contributes to the development of CML. CML patients are developing resistance to the current clinical inhibitor of these signaling pathways, so there is a strong need to find therapeutics with alternative mechanisms of action.
Nathanael Gray and colleagues screened for new Bcr-abl inhibitors by looking for small molecules that were toxic to Bcr-abl-expressing cells but not normal cells. A compound identified in the screen was shown to selectively inhibit leukemic cell lines and use a different mechanism to bind to the protein from the current inhibitor. The highly selective Bcr-abl inhibition and distinct mode of action suggest that this inhibitor is a valuable lead for developing new CML treatments. Author contact: Nathanael Gray (Genomics Institute of the Novartis Foundation, San Diego, CA, USA)
E-mail: ngray@gnf.org Abstract available online. (C) Nature Chemical Biology press release.
Message posted by: Trevor M. D'Souza
|
|
Variants Associated with Pediatric Allergic Disorder
Mutations in PHF6 Found in T-Cell Leukemia
Genetic Risk Variant for Urinary Bladder Cancer
Antibody Has Therapeutic Effect on Mice with ALS
Regulating P53 Activity in Cancer Cells
Anti-RNA Therapy Counters Breast Cancer Spread
Mitochondrial DNA Diversity
The Power of RNA Sequencing
‘Pro-Ageing' Therapy for Cancer?
Niche Genetics Influence Leukaemia
Molecular Biology: Clinical Promise for RNA Interference
Chemoprevention Cocktail for Colon Cancer
more news ...
|