TY - JOUR
T1 - Imatinib and chronic myeloid leukemia
T2 - validating the promise of molecularly targeted therapy.
AU - Druker, Brian J.
N1 - Copyright:
This record is sourced from MEDLINE/PubMed, a database of the U.S. National Library of Medicine
PY - 2002
Y1 - 2002
N2 - The Bcr-Abl tyrosine kinase inhibitor imatinib (Glivec, formerly STI571, Novartis Pharma AG, Basel, Switzerland) produces complete hematologic and cytogenetic responses in a substantial percentage of chronic myeloid leukemia patients. Imatinib is effective in chronic phase, accelerated phase and blast crisis, with lower response rates in patients with more advanced disease. Although responses have been durable in chronic phase patients, relapses have been common in blast crisis. Relapse has been associated with reactivation of Bcr-Abl kinase activity. The clinical development of imatinib illustrates the effectiveness of targeting molecular pathogenetic events. Hopefully, this example can be extended to other malignancies.
AB - The Bcr-Abl tyrosine kinase inhibitor imatinib (Glivec, formerly STI571, Novartis Pharma AG, Basel, Switzerland) produces complete hematologic and cytogenetic responses in a substantial percentage of chronic myeloid leukemia patients. Imatinib is effective in chronic phase, accelerated phase and blast crisis, with lower response rates in patients with more advanced disease. Although responses have been durable in chronic phase patients, relapses have been common in blast crisis. Relapse has been associated with reactivation of Bcr-Abl kinase activity. The clinical development of imatinib illustrates the effectiveness of targeting molecular pathogenetic events. Hopefully, this example can be extended to other malignancies.
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U2 - 10.1016/s0959-8049(02)80606-2
DO - 10.1016/s0959-8049(02)80606-2
M3 - Review article
C2 - 12528776
AN - SCOPUS:4243926785
SN - 0959-8049
VL - 38 Suppl 5
SP - S70-76
JO - European journal of cancer (Oxford, England : 1990)
JF - European journal of cancer (Oxford, England : 1990)
ER -