Results 101 to 110 of about 60,584 (224)

Enhanced Bcr-Abl-specific antileukemic activity of arsenic trioxide through glutathione-depletion in imatinib-resistant cells

open access: yesHaematologica, 2007
The development of resistance to imatinib mesylate may partly depend on high Bcr-Abl-expression levels. Arsenic trioxide (ATO) has Bcr-Abl suppressing activity in vitro.
Heiko Konig   +8 more
doaj   +1 more source

Long-term follow-up of Philadelphia chromosome-positive (Ph+) chronic myeloid leukaemia (CML) in children and adolescents managed at a single institution over a 20-year period [PDF]

open access: yes, 2005
Chronic myeloid leukaemia (CML) is rare in childhood. In our Institution we managed 30 consecutive Ph+CML patients aged
DE CUIA MR   +7 more
core   +1 more source

Potential role of Notch signalling in CD34+ chronic myeloid leukaemia cells: cross-talk between Notch and BCR-ABL.

open access: yesPLoS ONE, 2015
Notch signalling is critical for haemopoietic stem cell (HSC) self-renewal and survival. The role of Notch signalling has been reported recently in chronic myeloid leukaemia (CML) - a stem cell disease characterized by BCR-ABL tyrosine kinase activation.
Abdullah Aljedai   +3 more
doaj   +1 more source

BCR-ABL induces the expression of Skp2 through the PI3K pathway to promote p27Kip1 degradation and proliferation of chronic myelogenous leukemia cells [PDF]

open access: yes, 2005
Chronic myelogenous leukemia (CML) is characterized by the expression of the BCR-ABL tyrosine kinase, which results in increased cell proliferation and inhibition of apoptosis.
Albero, M.P. (M. Pilar)   +11 more
core  

Targeting self-renewal pathways in myeloid malignancies [PDF]

open access: yes, 2013
A fundamental property of hematopoietic stem cells (HSCs) is the ability to self-renew. This is a complex process involving multiple signal transduction cascades which control the fine balance between self-renewal and differentiation through ...
Copland, M., Sands, W.A., Wheadon, H.
core   +2 more sources

Treatment of human pre-B acute lymphoblastic leukemia with the Aurora kinase inhibitor PHA-739358 (Danusertib)

open access: yesMolecular Cancer, 2012
Background Treatment of Philadelphia chromosome-positive acute lymphoblastic leukemias (Ph-positive ALL) with clinically approved inhibitors of the Bcr/Abl tyrosine kinase frequently results in the emergence of a leukemic clone carrying the T315I ...
Fei Fei   +5 more
doaj   +1 more source

Interactions of p62(dok) with p210(bcr-abl) and Bcr-Abl-associated proteins.

open access: yesThe Journal of biological chemistry, 1998
A 62-kDa Ras GTPase-activating protein (RasGAP)-associated protein is tyrosine-phosphorylated under a variety of circumstances including growth factor stimulation and in cells transformed by activated tyrosine kinases. A cDNA for p62(dok), reported to be the RasGAP-associated 62-kDa protein, was recently cloned from Abl-transformed cells. In this study,
A, Bhat   +4 more
openaire   +2 more sources

Targeting USP10–FAK pathway sensitizes BCR-ABL+ leukemia cells to tyrosine kinase inhibitors

open access: yesCell Investigation
BCR-ABL+ leukemia is driven by constitutive tyrosine kinase activity, and tyrosine kinase inhibitors (TKIs) are the standard therapy. However, resistance to TKIs remains a significant clinical challenge.
Kangjie Qiu   +8 more
doaj   +1 more source

Optimized Treatment Schedules for Chronic Myeloid Leukemia

open access: yes, 2016
Over the past decade, several targeted therapies (e.g. imatinib, dasatinib, nilotinib) have been developed to treat Chronic Myeloid Leukemia (CML). Despite an initial response to therapy, drug resistance remains a problem for some CML patients.
Dingli, David   +4 more
core   +3 more sources

Inhibition of BCR/ABL protein expression by miR-203 sensitizes for imatinib mesylate.

open access: yesPLoS ONE, 2013
Selective inhibition of BCR/ABL expression by RNA interference has been demonstrated as an effective strategy in CML treatment and a reversal to imatinib resistance.
Yajuan Li   +9 more
doaj   +1 more source

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