Results 141 to 150 of about 128,389 (322)

Detection of BCR-ABL kinase domain mutations in CD34+ cells from newly diagnosed chronic phase CML patients and their association with imatinib resistance [PDF]

open access: yes, 2011
BCR-ABL kinase domain (KD) mutations, the most common cause of imatinib resistance, are infrequently detected in newly diagnosed chronic-phase chronic myeloid leukemia (CP-CML) patients.
Aamer Aleem   +19 more
core   +1 more source

Deletions of the derivative chromosome 9 occur at the time of the Philadelphia translocation and provide a powerful and independent prognostic indicator in chronic myeloid leukemia [PDF]

open access: yes, 2001
Chronic myeloid leukemia (CML) is characterized by formation of the BCR-ABL fusion gene, usually as a consequence of the Philadelphia (Ph) translocation between chromosomes 9 and 22.
Bench, AJ   +11 more
core   +1 more source

PAK-dependent STAT5 serine phosphorylation is required for BCR-ABL-induced leukemogenesis

open access: yesLeukemia, 2013
The transcription factor STAT5 (signal transducer and activator of transcription 5) is frequently activated in hematological malignancies and represents an essential signaling node downstream of the BCR-ABL oncogene.
A. Berger   +16 more
semanticscholar   +1 more source

The deubiquitinase inhibitor WP1130 drives nuclear aggregation and reactivation of mutant p53 for selective cancer cell targeting

open access: yesThe FEBS Journal, Volume 292, Issue 11, Page 2823-2842, June 2025.
Targeting the stability of oncogenic mutant p53 (mutp53) presents a promising strategy for cancer therapy. This study identifies the deubiquitinases (DUBs) USP5 and USP9X as key regulators of mutp53 stability. The DUB inhibitor WP1130 selectively destabilized mutp53 by promoting its ubiquitination, nuclear aggregation, and degradation via the ...
Swapnil Oak   +6 more
wiley   +1 more source

ABL single nucleotide polymorphisms may masquerade as BCR-ABL mutations associated with resistance to tyrosine kinase inhibitors in patients with chronic myeloid leukemia

open access: yesHaematologica, 2008
The BCR-ABL K247R change is based on a rare single nucleotide polymorphism occurring likewise in healthy controls and non-hematologic cell types. Despite its juxtaposition to the P-loop, functional analysis showed no alteration compared to non-mutated ...
Thomas Ernst   +7 more
doaj   +1 more source

BCR-ABL gene rearrangement and expression of primitive hematopoietic progenitors in chronic myeloid leukemia [PDF]

open access: bronze, 1993
A Bedi   +6 more
openalex   +1 more source

Chronic myeloid leukemia cells require the bone morphogenic protein pathway for cell cycle progression and self-renewal [PDF]

open access: yes, 2018
Leukaemic stem cell (LSC) persistence remains a major obstacle to curing chronic myeloid leukaemia (CML). The bone morphogenic protein (BMP) pathway is deregulated in CML, with altered expression and response to the BMP ligands shown to impact on LSC ...
Busch, Caroline   +6 more
core   +2 more sources

Another tool in the BCR–ABL kit? [PDF]

open access: yesNature Reviews Cancer, 2011
This Cell paper shows that an interaction between the SH2 and kinase domains of BCR–ABL is necessary for kinase activation; inhibition of this interface prevents leukaemogenesis in mice and can restore sensitivity to tyrosine kinase inhibitors.
openaire   +3 more sources

Multi‐Omic Analysis of Glutamate Excitotoxicity in Primary Neuronal Cultures

open access: yesJournal of Neurochemistry, Volume 169, Issue 6, June 2025.
Our study on rat neuron cells found 250 μM glutamate to be toxic, causing neuron death. We identified genes in pathways linked to apoptosis, neuron plasticity, and cell signaling, along with proteins regulating the cell cycle and tumor proliferation.
Jennifer H. Nguyen   +13 more
wiley   +1 more source

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