Novel Abl kinase inhibitors in chronic myeloid leukemia in blastic phase and Philadelphia chromosome-positive acute lymphoblastic leukemia

Ronan T Swords, Yesid Alvarado, Francis Giles

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Chronic myeloid leukemia (CML) is characterized by the presence of the Philadelphia chromosome, which is associated with a balanced translocation involving chromosomes 9 and 22 to produce a fusion gene (bcr-abl) that gives rise to a constitutively activated Abl tyrosine kinase. This kinase led to the discovery of several small-molecule inhibitors, imatinib being the first and most successful of these. Resistance to imatinib results in some patients from Abl kinase point mutations. Overcoming imatinib resistance represents one of the biggest challenges facing clinicians in the modern management of CML. In this review, we discuss the current understanding of CML pathophysiology and mechanisms of imatinib resistance and how advancing this knowledge has led to the design of novel therapies in the area of blastic phase CML and Philadelphia chromosome-positive acute lymphoblastic leukemia with previous imatinib failure.

Original languageEnglish
JournalClinical Lymphoma and Myeloma
Volume7
Issue numberSUPPL. 3
DOIs
StatePublished - Mar 1 2007
Externally publishedYes

Fingerprint

Philadelphia Chromosome
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Precursor Cell Lymphoblastic Leukemia-Lymphoma
Phosphotransferases
abl Genes
Leukemia, Myeloid, Chronic Phase
Chromosomes, Human, Pair 22
Chromosomes, Human, Pair 9
Gene Fusion
Point Mutation
Protein-Tyrosine Kinases
Imatinib Mesylate

Keywords

  • Dasatinib
  • Imatinib resistance
  • Nilotinib

ASJC Scopus subject areas

  • Cancer Research
  • Oncology
  • Hematology

Cite this

Novel Abl kinase inhibitors in chronic myeloid leukemia in blastic phase and Philadelphia chromosome-positive acute lymphoblastic leukemia. / Swords, Ronan T; Alvarado, Yesid; Giles, Francis.

In: Clinical Lymphoma and Myeloma, Vol. 7, No. SUPPL. 3, 01.03.2007.

Research output: Contribution to journalArticle

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