Results 101 to 110 of about 68,946 (284)

Overcoming Bcr-Abl T315I mutation by combination of GNF-2 and ATP competitors in an Abl-independent mechanism

open access: yesBMC Cancer, 2012
Background Philadelphia positive leukemias are characterized by the presence of Bcr-Abl fusion protein which exhibits an abnormal kinase activity. Selective Abl kinase inhibitors have been successfully established for the treatment of Ph (+) leukemias ...
Khateb Mamduh   +7 more
doaj   +1 more source

Relation of common ABL kinase domain mutations with resistance to Tyrosine Kinase Inhibiters in patients with Chronic Myeloid Leukemia in Middle Euphrates of Iraq [PDF]

open access: yes, 2020
Background: Chronic myeloid leukemia (CML) is a hematopoietic stem cell disease, associated with a reciprocal translocation between chromosomes 9 and chromosome 22, lead to the formation of the BCRABL fusion gene (Philadelphia chromosome).
Musawi, Mohammed Sadeq Mahdi Al-
core  

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

Insights into the clinical, platelet and genetic landscape of inherited thrombocytopenia with malignancy risk

open access: yesBritish Journal of Haematology, EarlyView.
Inherited thrombocytopenia (IT) caused by germline variants in RUNX1, ETV6 or ANKRD26 carries a high risk of developing haematological malignancy. This study examined the clinical, platelet and molecular characteristics of 66 patients with these conditions, who carried 24 distinct genetic variants in the corresponding genes.
Ana Marín‐Quílez   +34 more
wiley   +1 more source

Environment-mediated drug resistance in Bcr/Abl-positive acute lymphoblastic leukemia [PDF]

open access: yesOncoImmunology, 2012
Although cure rates for acute lymphoblastic leukemia (ALL) have increased, development of resistance to drugs and patient relapse are common. The environment in which the leukemia cells are present during the drug treatment is known to provide significant survival benefit.
John Groffen   +8 more
openaire   +3 more sources

PF-114, a Novel Inhibitor of Bcr-Abl Chimeric Tyrosine Kinase, Attenuates Intracellular CrkL Phosphorylation and Kills Chronic Myeloid Leukemia Cells

open access: yesКлиническая онкогематология, 2016
Background & Aims. The chimeric tyrosine kinase Bcr-Abl triggers malignant transformation of myeloid cells via phosphorylation of a number of substrates including the CrkL adaptor protein.
ES Kolotova   +9 more
doaj   +1 more source

Transcriptional activation of the miR-17-92 cluster is involved in the growth-promoting effects of MYB in human Ph-positive leukemia cells. [PDF]

open access: yes, 2018
MicroRNAs, non-coding regulators of gene expression, are likely to function as important downstream effectors of many transcription factors including MYB. Optimal levels of MYB are required for transformation/maintenance of BCR-ABL-expressing cells.
Blandino, Giovanni   +15 more
core   +3 more sources

Association of HLA Class I and Class II genes with bcr-abl transcripts in leukemia patients with t(9;22) (q34;q11)

open access: yesBMC Cancer, 2004
Background Based on the site of breakpoint in t(9;22) (q34;q11), bcr-abl fusion in leukemia patients is associated with different types of transcript proteins.
Cano Pedro   +2 more
doaj   +1 more source

Oncogenic stress induced by acute hyper-activation of Bcr-Abl leads to cell death upon induction of excessive aerobic glycolysis. [PDF]

open access: yesPLoS ONE, 2011
In response to deregulated oncogene activation, mammalian cells activate disposal programs such as programmed cell death. To investigate the mechanisms behind this oncogenic stress response we used Bcr-Abl over-expressing cells cultivated in presence of ...
Michael A Dengler   +8 more
doaj   +1 more source

Inhibition of interleukin-1 signaling enhances elimination of tyrosine kinase inhibitor treated CML stem cells [PDF]

open access: yes, 2016
Treatment of chronic myelogenous leukemia (CML) with BCR-ABL tyrosine kinase inhibitors (TKI) fails to eliminate leukemia stem cells (LSC). Patients remain at risk for relapse, and additional approaches to deplete CML LSC are needed to enhance the ...
Agarwal, Puneet   +9 more
core   +1 more source

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