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PMID: 12086882 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Review

Disabling Abl-perspectives on Abl kinase regulation and cancer therapeutics.

Cancer cell ·Vol. 1 ·No. 1 ·2002-02-00 ·Pages 13-5

Sawyers CL

Abstract

Pharmacologic inhibition of the Bcr-Abl tyrosine kinase in human chronic myeloid leukemia leads to dramatic clinical responses, but relapses occur in advanced stage patients. New findings about Abl kinase domain regulation provide insight into novel strategies for targeted therapy.

MeSH Terms

Antineoplastic Agents/therapeutic use Benzamides Binding Sites Enzyme Inhibitors/therapeutic use Fusion Proteins, bcr-abl Humans Imatinib Mesylate Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy,enzymology Piperazines/therapeutic use Protein Structure, Tertiary/physiology Protein-Tyrosine Kinases/antagonists & inhibitors Pyrimidines/therapeutic use

Chemicals

Antineoplastic Agents Benzamides Enzyme Inhibitors Piperazines Pyrimidines Imatinib Mesylate Protein-Tyrosine Kinases Fusion Proteins, bcr-abl

Authors & Affiliations

1 authors, click to expand affiliations / ORCID

Sawyers Charles L

Department of Medicine, Molecular Biology Institute, UCLA School of Medicine, 90095, USA. csawyers@mednet.ucla.edu

Article Info

Journal

Cancer cell

Abbr.

Cancer Cell

ISSN

1535-6108

DOI

10.1016/s1535-6108(02)00022-3

csawyers@mednet.ucla.edu

Published

2002-02-00

Pages

13-5

Language

English

Region

United States

NLM ID

101130617

Subset

External Links

PubMed source DOI: 10.1016/s1535-6108(02)00022-3 View journal details

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Disabling Abl-perspectives on Abl kinase regulation and cancer therapeutics.

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