Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1433-1452 |
| Number of pages | 20 |
| Journal | Expert Review of Anticancer Therapy |
| Volume | 13 |
| Issue number | 12 |
| DOIs | |
| State | Published - Nov 29 2013 |
| Externally published | Yes |
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Keywords
- Chronic myeloid leukemia
- Molecular response
- Suboptimal response
- Tyrosine kinase inhibition
ASJC Scopus subject areas
- Oncology
- Pharmacology (medical)
Cite this
Tyrosine kinase inhibition : A therapeutic target for the management of chronic-phase chronic myeloid leukemia. / Jabbour, Elias J.; Cortes, Jorge E.; Kantarjian, Hagop M.
In: Expert Review of Anticancer Therapy, Vol. 13, No. 12, 29.11.2013, p. 1433-1452.Research output: Contribution to journal › Review article
}
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.
PY - 2013/11/29
Y1 - 2013/11/29
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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UR - http://www.scopus.com/inward/citedby.url?scp=84888263504&partnerID=8YFLogxK
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 -