Suppression of USP7 induces BCR-ABL degradation and chronic myelogenous leukemia cell apoptosis
Cell Death and Disease, 2021 Chronic myelogenous leukemia (CML) is a clonal malignancy of hematopoietic stem cells featured with the fusion protein kinase BCR-ABL. To elicit the mechanism underlying BCR-ABL stability, we perform a screen against a panel of deubiquitinating enzymes ...
Shuoyi Jiang +9 more
doaj +1 more source
Cholesterol esterification inhibition and imatinib treatment synergistically inhibit growth of BCR-ABL mutation-independent resistant chronic myelogenous leukemia [PDF]
, 2017 Since the advent of tyrosine kinase inhibitors (TKIs) such as imatinib, nilotinib, and dasatinib, chronic myelogenous leukemia (CML) prognosis has improved greatly. However, ~30-40% of patients develop resistance to imatinib therapy.
Bandyopadhyay, Shovik +6 more
core +10 more sources
Molecular Pathways: BCR-ABL [PDF]
Clinical Cancer Research, 2012 Abstract Aberrant tyrosine kinase activity plays a critical role in many hematologic disorders, including chronic myeloid leukemia characterized by the constitutive activity of BCR-ABL. ABL therefore represents a crucial target for new therapeutic strategies.
CILLONI, Daniela, SAGLIO, Giuseppe
openaire +3 more sources
The functional interplay between the t(9;22)-associated fusion proteins BCR/ABL and ABL/BCR in Philadelphia chromosome-positive acute lymphatic leukemia. [PDF]
PLoS Genetics, 2015 The hallmark of Philadelphia chromosome positive (Ph(+)) leukemia is the BCR/ABL kinase, which is successfully targeted by selective ATP competitors. However, inhibition of BCR/ABL alone is unable to eradicate Ph(+) leukemia.
Anahita Rafiei +8 more
doaj +1 more source
Target Inhibition of CBP Induced Cell Senescence in BCR-ABL- T315I Mutant Chronic Myeloid Leukemia
Frontiers in Oncology, 2021 The treatment of chronic myeloid leukemia (CML) with BCR-ABL tyrosine kinase inhibitors (TKIs), such as imatinib, has yielded clinical success. However, the direct targeting of BCR-ABL does not eradicate CML cells expressing mutant BCR-ABL, especially ...
Ke Yang +10 more
doaj +1 more source
Allosteric inhibition of BCR-ABL [PDF]
Cell Cycle, 2010 Impaired regulation of kinase activity can lead to a variety of diseases, including cancer. Inhibition of kinase activity has, therefore, been considered an attractive anti-cancer therapeutic strategy. The success of targeted therapy with kinase inhibitors has been well documented with BCR-ABL, where imatinib specifically inhibits kinase activity with ...
Sreenath V. Sharma +2 more
openaire +3 more sources
A Nimbolide-Based Kinase Degrader Preferentially Degrades Oncogenic BCR-ABL
bioRxiv, 2020 Targeted protein degradation (TPD) and proteolysis-targeting chimeras (PROTACs) have arisen as powerful therapeutic modalities for degrading specific protein targets in a proteasome-dependent manner.
Bingqi Tong +12 more
semanticscholar +1 more source
Interactions of CBL with BCR-ABL and CRKL in BCR-ABL-transformed Myeloid Cells [PDF]
Journal of Biological Chemistry, 1997 The Philadelphia chromosome, detected in virtually all cases of chronic myelogenous leukemia (CML), is formed by a reciprocal translocation between chromosomes 9 and 22 that fuses BCR-encoded sequences upstream of exon 2 of c-ABL. The BCR-ABL fusion creates a gene whose protein product, p210BCR-ABL, has been implicated as the cause of the disease ...
Tsukasa Oda +5 more
openaire +3 more sources
Small interfering RNA against BCR-ABL transcripts sensitize mutated T315I cells to nilotinib
Haematologica, 2010 Background Selective inhibition of the BCR-ABL tyrosine kinase by RNA interference has been demonstrated in leukemic cells. We, therefore, evaluated specific BCR-ABL small interfering RNA silencing in BCR-ABL-positive cell lines, including those ...
Michael Koldehoff +3 more
doaj +1 more source
p185(BCR/ABL) has a lower sensitivity than p210(BCR/ABL) to the allosteric inhibitor GNF-2 in Philadelphia chromosome-positive acute lymphatic leukemia [PDF]
, 2011 Background: The t(9;22) translocation leads to the formation of the chimeric breakpoint cluster region/c-abl oncogene 1 (BCR/ABL) fusion gene on der22, the Philadelphia chromosome.
Mahajna, Jamal +5 more
core +2 more sources