Results 51 to 60 of about 128,389 (322)

Protein Kinase CK2: A Targetable BCR-ABL Partner in Philadelphia Positive Leukemias

open access: yesAdvances in Hematology, 2015
BCR-ABL-mediated leukemias, either Chronic Myeloid Leukemia (CML) or Philadelphia positive Acute Lymphoblastic Leukemia (ALL), are the paradigm of targeted molecular therapy of cancer due to the impressive clinical responses obtained with BCR-ABL ...
Alessandro Morotti   +6 more
doaj   +1 more source

circCRKL, a circRNA derived from CRKL, regulates BCR-ABL via sponging miR-877-5p to promote chronic myeloid leukemia cell proliferation

open access: yesJournal of Translational Medicine, 2022
Background The BCR-ABL fusion protein is the key factor that results in the occurrence of chronic myeloid leukemia (CML). Imatinib (IM) is a targeted inhibitor of BCR-ABL to achieve complete remission.
Jianming Wang   +5 more
doaj   +1 more source

Systems-pharmacology dissection of a drug synergy in imatinib-resistant CML [PDF]

open access: yes, 2012
Occurrence of the BCR-ABL[superscript T315I] gatekeeper mutation is among the most pressing challenges in the therapy of chronic myeloid leukemia (CML). Several BCR-ABL inhibitors have multiple targets and pleiotropic effects that could be exploited for ...
A Quintás-Cardama   +58 more
core   +1 more source

Targeting BCR-ABL+ stem/progenitor cells and BCR-ABL-T315I mutant cells by effective inhibition of the BCR-ABL-Tyr177-GRB2 complex

open access: yesOncotarget, 2017
Treatment of BCR-ABL+ human leukemia has been significantly improved by ABL tyrosine kinase inhibitors (TKIs), but they are not curative for most patients and relapses are frequently associated with BCR-ABL mutations, warranting new targets for improved treatments.
Kun Meng   +5 more
openaire   +4 more sources

Targeting the Allosteric Site of Oncoprotein BCR-ABL as an Alternative Strategy for Effective Target Protein Degradation.

open access: yesACS Medicinal Chemistry Letters, 2017
Protein degradation technology based on hybrid small molecules is an emerging drug modality that has significant potential in drug discovery and as a unique method of post-translational protein knockdown in the field of chemical biology.
K. Shimokawa   +9 more
semanticscholar   +1 more source

Combination therapy of BCR-ABL-positive B cell acute lymphoblastic leukemia by tyrosine kinase inhibitor dasatinib and c-JUN N-terminal kinase inhibition

open access: yesJournal of Hematology & Oncology, 2020
Background The Philadelphia chromosome (Ph), which leads to the creation and expression of the fusion gene product BCR-ABL, underlines the pathogenesis of chronic myelogenous leukemia (CML) and a fraction of adult and pediatric acute B-lymphoblastic ...
Xinhua Xiao   +9 more
doaj   +1 more source

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

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

Interactions of p62 with p210 and Bcr-Abl-associated Proteins [PDF]

open access: yesJournal 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,
Kara Johnson   +4 more
openaire   +3 more sources

Pharmacological difference between degrader and inhibitor against oncogenic BCR-ABL kinase

open access: yesScientific Reports, 2018
Chronic myelogenous leukemia (CML) is characterized by the oncogenic fusion protein, BCR-ABL protein kinase, against which clinically useful inhibitors have been developed. An alternative approach to treat CML is to degrade the BCR-ABL protein. Recently,
N. Shibata   +10 more
semanticscholar   +1 more source

Knockdown of insulin receptor substrate 1 reduces proliferation and downregulates Akt/mTOR and MAPK pathways in K562 cells [PDF]

open access: yes, 2011
BCR-ABL kinase activates downstream signaling pathways, including the PI3K-Akt/mTOR and the MAPK pathway. IRS1 has been previously described as constitutively phosphorylated and associated with BCR-ABL in K562 cells, suggesting that IRS1 has role in the ...
Costa, Fernando Ferreira   +5 more
core   +1 more source

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