First-line treatment for chronic myeloid leukemia: dasatinib, nilotinib, or imatinib
G Wei, S Rafiyath, D Liu - Journal of hematology & oncology, 2010 - Springer
Imatinib, a tyrosine kinase inhibitor (TKI) of BCR-ABL, was the standard first-line therapy for
chronic myeloid leukemia (CML) for almost 10 years. Dasatinib and nilotinib, two newer …
chronic myeloid leukemia (CML) for almost 10 years. Dasatinib and nilotinib, two newer …
Targeting the BCR-ABL signaling pathway in therapy-resistant Philadelphia chromosome-positive leukemia
T O'Hare, MWN Deininger, CA Eide, T Clackson… - Clinical Cancer …, 2011 - AACR
Beginning with imatinib a decade ago, therapy based on targeted inhibition of the BCR-ABL
kinase has greatly improved the prognosis for chronic myeloid leukemia (CML) patients. The …
kinase has greatly improved the prognosis for chronic myeloid leukemia (CML) patients. The …
Therapeutic Options Against BCR-ABL1 T315I-Positive Chronic Myelogenous Leukemia
A Quintás-Cardama, J Cortes - Clinical Cancer Research, 2008 - AACR
Despite the efficacy of imatinib therapy in chronic myelogenous leukemia, the development
of resistance continues to challenge the treatment of this disease. Mutations within the …
of resistance continues to challenge the treatment of this disease. Mutations within the …
Practical advice for determining the role of BCR‐ABL mutations in guiding tyrosine kinase inhibitor therapy in patients with chronic myeloid leukemia
Data demonstrating the superiority of nilotinib over imatinib in the frontline treatment of
chronic myeloid leukemia (CML) and ongoing studies with dasatinib and bosutinib are …
chronic myeloid leukemia (CML) and ongoing studies with dasatinib and bosutinib are …
Novel dual Src/Abl inhibitors for hematologic and solid malignancies
S Schenone, C Brullo, F Musumeci… - Expert opinion on …, 2010 - Taylor & Francis
Importance of the field: c-Src and Bcr-Abl are two non-receptor or cytoplasmic tyrosine
kinases (TKs) that play important roles in the development of solid and hematological …
kinases (TKs) that play important roles in the development of solid and hematological …
Managing resistance in chronic myeloid leukemia
S Roychowdhury, M Talpaz - Blood reviews, 2011 - Elsevier
Chronic myeloid leukemia (CML) is a myeloproliferative disorder that affects 5000 new
patients per year in the United States. Prior to 10years ago, durable remission was rare and …
patients per year in the United States. Prior to 10years ago, durable remission was rare and …
Tyrosine kinase inhibitors: the first decade
M Agrawal, RJ Garg, J Cortes… - Current hematologic …, 2010 - Springer
The treatment of chronic myeloid leukemia (CML) drastically changed with the introduction
of imatinib mesylate, a Bcr-Abl1 tyrosine kinase inhibitor (TKI), in 1998. By directly targeting …
of imatinib mesylate, a Bcr-Abl1 tyrosine kinase inhibitor (TKI), in 1998. By directly targeting …
New Bcr-Abl inhibitors in chronic myeloid leukemia: keeping resistance in check
T O'Hare, CA Eide, MW Deininger - Expert opinion on …, 2008 - Taylor & Francis
Targeted therapy with the Abl kinase inhibitor imatinib has markedly improved the outlook
for patients with chronic myeloid leukemia (CML). Breakpoint cluster region (Bcr)-Abl …
for patients with chronic myeloid leukemia (CML). Breakpoint cluster region (Bcr)-Abl …
New insights into small‐molecule inhibitors of Bcr‐Abl
Chronic myelogenous leukemia (CML) is a myeloproliferative disease associated with a
defined genetic abnormality, the Bcr‐Abl fusion gene on the Philadelphia chromosome that …
defined genetic abnormality, the Bcr‐Abl fusion gene on the Philadelphia chromosome that …
Evolving treatment strategies for patients newly diagnosed with chronic myeloid leukemia: the role of second-generation BCR–ABL inhibitors as first-line therapy
PJ Shami, M Deininger - Leukemia, 2012 - nature.com
In patients with chronic myeloid leukemia (CML), disease in the initial chronic phase (CP)
and subsequent progression are driven by the oncogenic activity of the BCR–ABL fusion …
and subsequent progression are driven by the oncogenic activity of the BCR–ABL fusion …