Chronic myelogenous leukaemia - New therapeutic principles

Michael E. O'Dwyer; Brian J. Druker

doi:10.1046/j.1365-2796.2001.00823.x

Chronic myelogenous leukaemia - New therapeutic principles

Michael E. O'Dwyer
, Brian J. Druker

Oregon Health and Science University

Research output: Contribution to a Journal (Peer & Non Peer) › Review article › peer-review

49 Citations (Scopus)

Abstract

The deregulated tyrosine kinase activity of the BCR-ABL fusion protein is the cause of malignant transformation in almost all cases of chronic myelogenous leukaemia (CML), making BCR-ABL an ideal target for pharmacological inhibition. Signal transduction inhibitor (STI571) (formerly 2CGP57 148B), is an ABL specific, tyrosine kinase inhibitor. In preclinical studies, it has been shown to selectively kill BCR-ABL expressing cells, both in-vitro and in vivo. The results of clinical studies to date are highly encouraging and STI571 promises to be an important addition to the therapy of CML.

Original language	English
Pages (from-to)	3-9
Number of pages	7
Journal	Journal of Internal Medicine
Volume	250
Issue number	1
DOIs	https://doi.org/10.1046/j.1365-2796.2001.00823.x
Publication status	Published - 2001
Externally published	Yes

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

BCR-ABL
Chronic myelogenous leukaemia
Signal transduction
STI571
Therapy
Tyrosine kinase inhibitor

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10.1046/j.1365-2796.2001.00823.x

Cite this

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title = "Chronic myelogenous leukaemia - New therapeutic principles",

abstract = "The deregulated tyrosine kinase activity of the BCR-ABL fusion protein is the cause of malignant transformation in almost all cases of chronic myelogenous leukaemia (CML), making BCR-ABL an ideal target for pharmacological inhibition. Signal transduction inhibitor (STI571) (formerly 2CGP57 148B), is an ABL specific, tyrosine kinase inhibitor. In preclinical studies, it has been shown to selectively kill BCR-ABL expressing cells, both in-vitro and in vivo. The results of clinical studies to date are highly encouraging and STI571 promises to be an important addition to the therapy of CML.",

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AU - O'Dwyer, Michael E.

AU - Druker, Brian J.

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N2 - The deregulated tyrosine kinase activity of the BCR-ABL fusion protein is the cause of malignant transformation in almost all cases of chronic myelogenous leukaemia (CML), making BCR-ABL an ideal target for pharmacological inhibition. Signal transduction inhibitor (STI571) (formerly 2CGP57 148B), is an ABL specific, tyrosine kinase inhibitor. In preclinical studies, it has been shown to selectively kill BCR-ABL expressing cells, both in-vitro and in vivo. The results of clinical studies to date are highly encouraging and STI571 promises to be an important addition to the therapy of CML.

AB - The deregulated tyrosine kinase activity of the BCR-ABL fusion protein is the cause of malignant transformation in almost all cases of chronic myelogenous leukaemia (CML), making BCR-ABL an ideal target for pharmacological inhibition. Signal transduction inhibitor (STI571) (formerly 2CGP57 148B), is an ABL specific, tyrosine kinase inhibitor. In preclinical studies, it has been shown to selectively kill BCR-ABL expressing cells, both in-vitro and in vivo. The results of clinical studies to date are highly encouraging and STI571 promises to be an important addition to the therapy of CML.

KW - BCR-ABL

KW - Chronic myelogenous leukaemia

KW - Signal transduction

KW - STI571

KW - Therapy

KW - Tyrosine kinase inhibitor

UR - https://www.scopus.com/pages/publications/0035724240

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DO - 10.1046/j.1365-2796.2001.00823.x

M3 - Review article

C2 - 11454136

AN - SCOPUS:0035724240

SN - 0954-6820

VL - 250

SP - 3

EP - 9

JO - Journal of Internal Medicine

JF - Journal of Internal Medicine

IS - 1

ER -

Chronic myelogenous leukaemia - New therapeutic principles

Abstract

UN SDGs

Keywords

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