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Imatinib mesylate in the treatment of hematologic malignancies.

Abstract
The treatment of hematologic malignancies has been based for many years on chemotherapy and possibly, for the more aggressive forms, stem cell transplantation. In 2001, the signal transduction inhibitor 571 (STI571, imatinib mesylate) was reported to have striking effects in chronic myeloid leukaemia patients. Since then, imatinib became the first molecular-targeted agent approved for the treatment of human cancer and was later on demonstrated to be effective in other malignancies, such as Philadelphia positive acute lymphoid leukemia, hypereosinophilic syndromes, gastrointestinal stromal tumours and more recently, systemic mastocytosis and other myeloprolipherative disease-carrying platelet-derived growth factor receptor abnormalities. In this article, the authors review the evidence which led to imatinib approval in the treatment of several of the above mentioned diseases.
AuthorsPier Paolo Piccaluga, Michela Rondoni, Stefania Paolini, Gianantonio Rosti, Giovanni Martinelli, Michele Baccarani
JournalExpert opinion on biological therapy (Expert Opin Biol Ther) Vol. 7 Issue 10 Pg. 1597-611 (Oct 2007) ISSN: 1744-7682 [Electronic] England
PMID17916051 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Antineoplastic Agents
  • Benzamides
  • Oncogene Proteins, Fusion
  • Piperazines
  • Protein Kinase Inhibitors
  • Pyrimidines
  • mRNA Cleavage and Polyadenylation Factors
  • Imatinib Mesylate
  • FIP1L1-PDGFRA fusion protein, human
  • Receptor, Platelet-Derived Growth Factor alpha
  • Receptors, Platelet-Derived Growth Factor
  • Fusion Proteins, bcr-abl
Topics
  • Animals
  • Antineoplastic Agents (adverse effects, pharmacokinetics, pharmacology, therapeutic use)
  • Benzamides
  • Drug Interactions
  • Drug Resistance
  • Fusion Proteins, bcr-abl (genetics, metabolism)
  • Hematologic Neoplasms (drug therapy, enzymology, genetics, metabolism)
  • Humans
  • Hypereosinophilic Syndrome (drug therapy)
  • Imatinib Mesylate
  • Leukemia, Lymphoid (drug therapy, genetics)
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive (drug therapy)
  • Mastocytosis, Systemic (drug therapy)
  • Myeloproliferative Disorders (drug therapy, genetics, metabolism)
  • Oncogene Proteins, Fusion (genetics, metabolism)
  • Philadelphia Chromosome
  • Piperazines (adverse effects, pharmacokinetics, pharmacology, therapeutic use)
  • Protein Kinase Inhibitors (adverse effects, pharmacokinetics, pharmacology, therapeutic use)
  • Pyrimidines (adverse effects, pharmacokinetics, pharmacology, therapeutic use)
  • Receptor, Platelet-Derived Growth Factor alpha (genetics, metabolism)
  • Receptors, Platelet-Derived Growth Factor (genetics, metabolism)
  • Signal Transduction (drug effects)
  • Treatment Outcome
  • mRNA Cleavage and Polyadenylation Factors (genetics, metabolism)

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