Results 61 to 70 of about 128,389 (322)
Induction of autophagy by Imatinib sequesters Bcr‐Abl in autophagosomes and down‐regulates Bcr‐Abl protein [PDF]
Chronic Myeloid Leukemia (CML) is a disease of hematopoietic stem cells which harbor the chimeric gene Bcr‐Abl. Expression levels of this constitutively active tyrosine kinase are critical for response to tyrosine kinase inhibitor treatment and also disease progression, yet the regulation of protein stability is poorly understood.
Elzinga, Baukje M.+5 more
openaire +3 more sources
TRIM24 and TRIM28 are androgen receptor (AR) coregulators which exhibit increased expression with cancer progression. Both TRIM24 and TRIM28 combine to influence the response of castrate‐resistant prostate cancer (CRPC) cells to AR inhibitors by mediating AR signalling, regulation of MYC and upregulating VEGF to promote angiogenesis. Castrate‐resistant
Damien A. Leach+8 more
wiley +1 more source
Background The bcr-abl fusion gene is the pathological origin of chronic myeloid leukemia (CML) and plays a critical role in the resistance of imatinib. Thus, bcr-abl disruption-based novel therapeutic strategy may warrant exploration.
Ningshu Huang+8 more
doaj +1 more source
Targeting the oligomerization of BCR/ABL by membrane permeable competitive peptides inhibits the proliferation of Philadelphia Chromosome positive leukemic cells [PDF]
The BCR/ABL fusion protein is the hallmark of Philadelphia Chromosome positive (Ph+) leukemia. The constitutive activation of the ABL-kinase in BCR/ABL cells induces the leukemic phenotype.
Beißert, Tim+8 more
core
Regulation of hTERT by BCR-ABL at multiple levels in K562 cells
Background The cytogenetic characteristic of Chronic Myeloid Leukemia (CML) is the formation of the Philadelphia chromosome gene product, BCR-ABL. Given that BCR-ABL is the specific target of Gleevec in CML treatment, we investigated the regulation of ...
Chai Juin Hsien+5 more
doaj +1 more source
Evaluation of Morpholino Antisense Oligos’ Role on BCR-ABL Gene Silencing in the K562 Cell Line [PDF]
Objective: Chronic myeloid leukemia (CML) develops when a hematopoietic stem cellacquires the BCR/ABL fusion gene. This causes these transformed hematopoietic cellsto have a greater than normal proliferation rate.
Bahman Delalat+6 more
doaj
Genetic requirement for Ras in the transformation of fibroblasts and hematopoietic cells by the Bcr-Abl oncogene. [PDF]
To determine the functional importance of Ras in transformation by Abl oncogenes, we used a genetic approach to measure the effect of impaired Ras activity on the ability of Bcr-Abl or v-Abl to transform cells.
McLaughlin, J, Sawyers, CL, Witte, ON
core
This study analyzes 148 patients (66 women and 82 men) with chronic myeloid leukemia treated with tyrosine kinase inhibitors, focusing on cardiovascular adverse events. The risk assessment, performed using the HFA/ICOS score, reveals sex‐specific differences: venous thrombosis is more common in women, while arterial thrombosis predominates in men.
Cristina Madaudo+10 more
wiley +1 more source
Treatment with imatinib is very effective in Bcr-Abl positive leukemia. However, development of resistance to this drug is a common phenomenon in late stage disease.
Rama Krishna Kancha+5 more
doaj +1 more source
Critical role for Gab2 in transformation by BCR/ABL [PDF]
The BCR/ABL oncogene causes chronic myelogenous leukemia (CML) in humans and a CML-like disease, as well as lymphoid leukemia, in mice. p210 BCR/ABL is an activated tyrosine kinase that phosphorylates itself and several cellular signaling proteins. The autophosphorylation site tyrosine 177 binds the adaptor Grb2 and helps determine the lineage and ...
Sattler, M+12 more
openaire +4 more sources