Bcr-Abl inhibition as a modality of CML therapeutics

Elisabeth Buchdunger, Alex Matter, Brian Druker

Research output: Contribution to journalArticle

91 Citations (Scopus)
Original languageEnglish (US)
JournalBiochimica et Biophysica Acta - Reviews on Cancer
Volume1551
Issue number1
DOIs
StatePublished - Aug 31 2001

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Piperazines
bcr-abl Fusion Proteins
Cultured Tumor Cells
Combined Modality Therapy
Pyrimidines
Molecular Models
Hydroxyurea
Hematopoietic Stem Cell Transplantation
Enzyme Inhibitors
Structure-Activity Relationship
Protein Kinase Inhibitors
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Drug Resistance
Interferon-alpha
Cell Division
Antineoplastic Agents
Binding Sites
Clinical Trials
Therapeutics
Imatinib Mesylate

Keywords

  • Bcr-Abl
  • Chronic myelogenous leukemia
  • STI571
  • Tyrosine kinase inhibitor

ASJC Scopus subject areas

  • Oncology
  • Cancer Research
  • Biophysics

Cite this

Bcr-Abl inhibition as a modality of CML therapeutics. / Buchdunger, Elisabeth; Matter, Alex; Druker, Brian.

In: Biochimica et Biophysica Acta - Reviews on Cancer, Vol. 1551, No. 1, 31.08.2001.

Research output: Contribution to journalArticle

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