Results 71 to 80 of about 29,567 (180)

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

Identification of novel posttranscriptional targets of the BCR/ABL oncoprotein by ribonomics: requirement of E2F3 for BCR/ABL leukemogenesis

open access: yesBlood, 2008
Several RNA binding proteins (RBPs) have been implicated in the progression of chronic myelogenous leukemia (CML) from the indolent chronic phase to the aggressively fatal blast crisis. In the latter phase, expression and function of specific RBPs are aberrantly regulated at transcriptional or posttranslational levels by the constitutive kinase ...
Eiring AM   +12 more
openaire   +5 more sources

Anaphylactic transfusion reaction to group B platelets related to alpha‐gal syndrome: A case report

open access: yesTransfusion, Volume 66, Issue 8, Page 1690-1693, August 2026.
Abstract Background Alpha‐gal syndrome (AGS), a distinct form of IgE‐mediated hypersensitivity to the carbohydrate galactose‐α‐1,3‐galactose (α‐Gal), typically occurs after repeated tick bites and leads to allergic reactions after ingestion of mammalian meat.
Oscar Andre Hinojosa   +2 more
wiley   +1 more source

Role of STAT3 in transformation and drug resistance in CML

open access: yesFrontiers in Oncology, 2012
Chronic Myeloid Leukemia (CML) is initially driven by the bcr-abl fusion oncoprotein. The identification of bcr-abl led to the discovery and rapid translation into the clinic of bcr-abl kinase inhibitors.
Rajesh R Nair   +2 more
doaj   +1 more source

Interaction of Abl Tyrosine Kinases with SOCS3 Impairs Its Suppressor Function in Tumorigenesis

open access: yesNeoplasia: An International Journal for Oncology Research, 2018
Suppressor of cytokine signaling 3 (SOCS3) is involved in Bcr-Abl–induced tumorigenesis. However, how SOCS3 interacts with Bcr-Abl and is regulated by Abl kinases remains largely unknown.
Riyue Feng   +8 more
doaj   +1 more source

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

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

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

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

Targeting HSPA8 to repress GPX4 and induce ferroptosis in BCR-ABL positive leukemia

open access: yesBiomedical Technology
BCR-ABL positive (BCR-ABL+) leukemia is driven by constitutive activation of tyrosine kinase activity, with tyrosine kinase inhibitors (TKIs) serving as the standard treatment. However, resistance to TKIs remains a significant clinical challenge. In this
Shuxin Zhong   +12 more
doaj   +1 more source

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