Targeted chemotherapy: Chronic myelogenous leukemia as a model

Nima Sharifi, Richard A. Steinman

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Many of the therapeutic agents used for cancer chemotherapy today are based on decades-old agents which are highly cytotoxic but are nonselective for cancer cells. The hallmark of chronic myelogenous leukemia (CML) is the Philadelphia chromosome translocation t(9;22), which results in the bcr-abl fusion gene. As an alteration that is nearly universal in CML cells, bcr-abl presents a therapeutic target that is unique to the pathological cells in CML patients. Advances in the understanding of the molecular mechanisms which sustain leukemic cells in CML have enabled the development of selective therapies for this disease. We review here the molecular pathogenesis and current treatment of CML. We also discuss the development of imatinib mesylate, a selective inhibitor of Bcr-Abl which has shown promise in clinical trials with CML. This recent advance in CML therapy represents a novel approach to rational design and development of new anticancer drugs.

Original languageEnglish (US)
Pages (from-to)219-232
Number of pages14
JournalJournal of Molecular Medicine
Volume80
Issue number4
DOIs
StatePublished - 2002

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Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Drug Therapy
abl Genes
Therapeutics
Philadelphia Chromosome
Antineoplastic Agents
Clinical Trials
Pharmaceutical Preparations
Neoplasms

Keywords

  • Chronic myelogenous leukemia
  • Drug development
  • Signal transduction
  • Tyrosine kinase inhibitors

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Targeted chemotherapy : Chronic myelogenous leukemia as a model. / Sharifi, Nima; Steinman, Richard A.

In: Journal of Molecular Medicine, Vol. 80, No. 4, 2002, p. 219-232.

Research output: Contribution to journalArticle

Sharifi, Nima ; Steinman, Richard A. / Targeted chemotherapy : Chronic myelogenous leukemia as a model. In: Journal of Molecular Medicine. 2002 ; Vol. 80, No. 4. pp. 219-232.
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