A genomic analysis of Philadelphia chromosome-negative AML arising in patients with CML
Kilannin Krysiak(James S. McDonnell Foundation), Matt Christopher(Washington University in St. Louis), Zachary L. Skidmore(James S. McDonnell Foundation), Ryan Demeter(James S. McDonnell Foundation), Vincent Magrini(James S. McDonnell Foundation), Jason Kunisaki(James S. McDonnell Foundation), Michele O’Laughlin(James S. McDonnell Foundation), Eric J. Duncavage(Washington University in St. Louis), Christopher A. Miller(James S. McDonnell Foundation), Bradley A. Ozenberger(James S. McDonnell Foundation), Malachi Griffith(James S. McDonnell Foundation), Lukas D. Wartman(James S. McDonnell Foundation), Obi L. Griffith(James S. McDonnell Foundation)
Cited by 18Open Access
Abstract
Chronic myelogenous leukemia (CML) is characterized by the Philadelphia chromosome, an acquired clonal abnormality resulting from translocation of chromosomes 9 and 22, and the generation of the BCR-ABL fusion oncogene. The development of tyrosine kinase inhibitors (TKIs) has revolutionized the treatment of CML, as TKI therapy leads to inhibition of BCR-ABL activity, suppression of the BCR-ABL-containing clone and restoration of normal hematopoiesis in the vast majority of cases.
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