Paquette, Ronald L <br/><br/>
Frequent EVI1 translocations in myeloid blast crisis CML that evolves through tyrosine kinase inhibitors.  [electronic resource] 

 -  Cancer genetics  Jul 2011 
 - 392-7 p.  digital 
<br/><br/> Publication Type: Journal Article; Research Support, Non-U.S. Gov't 
<br/><br/><label>ISSN: </label>2210-7762 
<br/><br/><label>Standard No.: </label>10.1016/j.cancergen.2011.06.002  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Adult<br/>Aged<br/>Blast Crisis--genetics<br/>Blotting, Western<br/>DNA Breaks, Double-Stranded--drug effects<br/>DNA Repair<br/>DNA-Binding Proteins--genetics<br/>Drug Resistance, Neoplasm--genetics<br/>Evolution, Molecular<br/>Female<br/>Fusion Proteins, bcr-abl--genetics<br/>Genes, abl<br/>Humans<br/>In Situ Hybridization, Fluorescence<br/>Leukemia, Myelogenous, Chronic, BCR-ABL Positive--pathology<br/>MDS1 and EVI1 Complex Locus Protein<br/>Male<br/>Middle Aged<br/>Mutation<br/>Protein Kinase Inhibitors--therapeutic use<br/>Protein-Tyrosine Kinases--metabolism<br/>Proto-Oncogenes--genetics<br/>Transcription Factors--genetics<br/>Translocation, Genetic