Molecular mechanisms of resistance of leukemia to imatinib mesylate

Tetsuzo Tauchi; Kazuma Ohyashiki

doi:10.1016/j.leukres.2003.10.007

Molecular mechanisms of resistance of leukemia to imatinib mesylate

Leuk Res. 2004 May:28 Suppl 1:S39-45. doi: 10.1016/j.leukres.2003.10.007.

Authors

Tetsuzo Tauchi¹, Kazuma Ohyashiki

Affiliation

¹ First Department of Internal Medicine, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan. tauchi@tokyo-med.ac.jp

PMID: 15036940
DOI: 10.1016/j.leukres.2003.10.007

Abstract

Despite high rates of hematologic and cytogenetic responses to imatinib therapy, the emergence of resistance to imatinib has been recognized as a major problem in the treatment of Ph-positive leukemia. The high frequency of BCR-ABL mutations and amplifications represents the high degree of heterogeneity in patients with advanced phase of CML, in whom multiple leukemic clones may exist. Therefore, a single inhibitor is unlikely to able to block all mutants.

Publication types

Review

MeSH terms

Benzamides
Drug Resistance, Neoplasm*
Fusion Proteins, bcr-abl / antagonists & inhibitors
Fusion Proteins, bcr-abl / genetics
Genetic Heterogeneity
Humans
Imatinib Mesylate
Leukemia / drug therapy*
Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
Mutation
Piperazines / pharmacology
Piperazines / therapeutic use*
Pyrimidines / pharmacology
Pyrimidines / therapeutic use*

Substances

Benzamides
Piperazines
Pyrimidines
Imatinib Mesylate
Fusion Proteins, bcr-abl