Results 11 to 20 of about 128,389 (322)

BCR-ABL affects STAT5A and STAT5B differentially. [PDF]

open access: yesPLoS ONE, 2014
Signal transducers and activators of transcription (STATs) are latent cytoplasmic transcription factors linking extracellular signals to target gene transcription. Hematopoietic cells express two highly conserved STAT5-isoforms (STAT5A/STAT5B), and STAT5
Michael Schaller-Schönitz   +9 more
doaj   +5 more sources

Novel lncRNA-IUR suppresses Bcr-Abl-induced tumorigenesis through regulation of STAT5-CD71 pathway

open access: yesMolecular Cancer, 2019
Background Long noncoding RNAs (lncRNAs), defined as the transcripts longer than 200 nt without protein-coding capacity, have been found to be aberrantly expressed in diverse human diseases including cancer.
Xuefei Wang   +9 more
doaj   +2 more sources

Cardiac arrhythmias of BCR-ABL inhibitors with or without triazole antifungal agents: A real-world pharmacovigilance study based on the food and drug administration adverse event reporting system database [PDF]

open access: yesSAGE Open Medicine
Objectives: Breakpoint Cluster Region (BCR)-Abelson tyrosine kinase (ABL) inhibitors are widely used in the treatment of blood cancers, particularly chronic myelogenous leukemia and are often combined with triazole antifungal agents to prevent fungal ...
Peitao Xie   +5 more
doaj   +2 more sources

New Inhibitors of Bcr-Abl Based on 2,6,9-Trisubstituted Purine Scaffold Elicit Cytotoxicity in Chronic Myeloid Leukemia-Derived Cell Lines Sensitive and Resistant to TKIs [PDF]

open access: yesPharmaceutics
Bcr-Abl is an oncoprotein with aberrant tyrosine kinase activity involved in the progression of chronic myeloid leukemia (CML) and has been targeted by inhibitors such as imatinib and nilotinib.
Thalia Delgado   +12 more
doaj   +2 more sources

Targeted disruption of the BCR-ABL fusion gene by Cas9/dual-sgRNA inhibits proliferation and induces apoptosis in chronic myeloid leukemia cells [PDF]

open access: yesActa Biochimica et Biophysica Sinica
The BCR-ABL fusion gene, formed by the fusion of the breakpoint cluster region protein (BCR) and the Abl Oncogene 1, Receptor Tyrosine Kinase (ABL) genes, encodes the BCR-ABL oncoprotein, which plays a crucial role in leukemogenesis.
Zeng Jianling   +9 more
doaj   +2 more sources

A Small Molecule Inhibitor, OGP46, Is Effective against Imatinib-Resistant BCR-ABL Mutations via the BCR-ABL/JAK-STAT Pathway

open access: yesMolecular Therapy - Oncolytics, 2020
Chronic myeloid leukemia (CML) is caused by the Philadelphia (Ph+) chromosome carrying the BCR-ABL oncogene, a constitutively active tyrosine kinase. The discovery of imatinib represents a major success story in the treatment against CML.
Luca Vincenzo Ballestra, Yu Ke, Xin Xu
exaly   +2 more sources

Multi-Lineage BCR-ABL Expression in Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia Is Associated With Improved Prognosis but No Specific Molecular Features

open access: yesFrontiers in Oncology, 2020
BackgroundRecently, various blood cell lineages expressing the BCR-ABL fusion gene in Philadelphia chromosome (Ph)-positive acute lymphoblastic leukemia (ALL) have been reported. However, the biological and clinical significance of these BCR-ABL lineages
Satoshi Nishiwaki   +2 more
exaly   +3 more sources

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

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   +2 more sources

Sphagneticola Trilobata (L.) Pruski (Asteraceae) Methanol Extract Induces Apoptosis in Leukemia Cells through Suppression of BCR/ABL

open access: yesPlants, 2021
We will study the effects of the methanol extract of Sphagneticola trilobata (L.) Pruski (Asteraceae) (MeST) on the growth of leukemia cells that may contain the BCR/ABL gene. This study also clarifies the mechanism of this effect on these cells.
Hoang Thanh Chi   +2 more
doaj   +1 more source

Home - About - Disclaimer - Privacy