TY - JOUR
T1 - Tyrosine kinase inhibition
T2 - A therapeutic target for the management of chronic-phase chronic myeloid leukemia
AU - Jabbour, Elias J.
AU - Cortes, Jorge E.
AU - Kantarjian, Hagop M.
N1 - Funding Information:
Medical writing support was provided by T Lonergan and J Ponting of Anthemis Consulting Ltd and was funded by Teva Pharmaceutical Industries, Frazer, PA, USA. Teva provided a single medical accuracy review of the final draft. The authors were not compensated and retained full editorial control over the content of the paper.
Funding Information:
Dr Jabbour has received honoraria from Bristol-Myers Squibb, Novar-tis, Pfizer, Ariad and Teva; Dr Cortes is a consultant for Ariad, Teva and Pfizer and has received grant support from Bristol-Myers Squibb, Novartis, Ariad, Teva and Pfizer; Dr Kantarjian has received research grants from Novartis, Bristol-Myers Squibb, Pfizer, Ariad and Chem-Genex and is an unpaid consultant to Novartis. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
PY - 2013
Y1 - 2013
N2 - Chronic myeloid leukemia (CML) is a hematologic neoplasm with a progressive, ultimately terminal, disease course. In most cases, CML arises owing to the aberrant formation of a chimeric gene for a constitutively active tyrosine kinase. Inhibition of the signaling activity of this kinase has proved to be a highly successful treatment target, transforming the prognosis of patients with CML. New tyrosine kinase inhibitors continue to improve the management of CML, offering alternative options for those resistant to or intolerant of standard tyrosine kinase inhibitors. Here we review the pathobiology of CML and explore emerging strategies to optimize the management of chronic-phase CML, particularly first-line treatment.
AB - Chronic myeloid leukemia (CML) is a hematologic neoplasm with a progressive, ultimately terminal, disease course. In most cases, CML arises owing to the aberrant formation of a chimeric gene for a constitutively active tyrosine kinase. Inhibition of the signaling activity of this kinase has proved to be a highly successful treatment target, transforming the prognosis of patients with CML. New tyrosine kinase inhibitors continue to improve the management of CML, offering alternative options for those resistant to or intolerant of standard tyrosine kinase inhibitors. Here we review the pathobiology of CML and explore emerging strategies to optimize the management of chronic-phase CML, particularly first-line treatment.
KW - Chronic myeloid leukemia
KW - Molecular response
KW - Suboptimal response
KW - Tyrosine kinase inhibition
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U2 - 10.1586/14737140.2013.859074
DO - 10.1586/14737140.2013.859074
M3 - Review article
C2 - 24236822
AN - SCOPUS:84888263504
VL - 13
SP - 1433
EP - 1452
JO - Expert Review of Anticancer Therapy
JF - Expert Review of Anticancer Therapy
SN - 1473-7140
IS - 12
ER -