BMC 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
A combined computational and experimental strategy identifies mutations conferring resistance to drugs targeting the BCR-ABL fusion protein [PDF]
Communications Biology, 2020 AbstractDrug resistance is of increasing concern, especially during the treatments of infectious diseases and cancer. To accelerate the drug discovery process in combating issues of drug resistance, here we developed a computational and experimental strategy to predict drug resistance mutations. Using BCR-ABL as a case study, we successfully recaptured
Jinxin Liu, Jianfeng Pei, Luhua Lai
openaire +2 more sources
Targeting the oligomerization of BCR/ABL by membrane permeable competitive peptides inhibits the proliferation of Philadelphia Chromosome positive leukemic cells [PDF]
, 2013 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.
Mahajna, Jamal +8 more
core +1 more source
Influence of BCR/ABL fusion proteins on the course of Ph leukemias.
Acta Biochimica Polonica, 2004 The hallmark of chronic myeloid leukemia (CML) and a subset of acute lymphoblastic leukemia (ALL) is the presence of the Philadelphia chromosome as a result of the t(9;22) translocation. This gene rearrangement results in the production of a novel oncoprotein, BCR/ABL, a constitutively active tyrosine kinase.
Gennady D, Telegeev +3 more
openaire +3 more sources
Allosteric inhibition enhances the efficacy of ABL kinase inhibitors to target unmutated BCR-ABL and BCR-ABL-T315I [PDF]
, 2012 Background: Chronic myelogenous leukemia (CML) and Philadelphia chromosome-positive (Ph+) acute lymphatic leukemia (Ph + ALL) are caused by the t(9;22), which fuses BCR to ABL resulting in deregulated ABL-tyrosine kinase activity.
Ruimi, Nili +18 more
core +2 more sources
Bcr/Abl Interferes with the Fanconi Anemia/BRCA Pathway: Implications in the Chromosomal Instability of Chronic Myeloid Leukemia Cells [PDF]
, 2010 Chronic myeloid leukemia (CML) is a malignant clonal disorder of the hematopoietic system caused by the expression of the BCR/ABL fusion oncogene. Although it is well known that CML cells are genetically unstable, the mechanisms accounting for this ...
Valeri, Antonio +71 more
core +2 more sources
Genetic fusions favor tumorigenesis through degron loss in oncogenes
Nature Communications, 2021 Chromosomal rearrangements can generate genetic fusions composed of two distinct gene sequences, many of which have been implicated in tumorigenesis and progression.
Jing Liu +7 more
doaj +1 more source
Light-Activating PROTACs in Cancer: Chemical Design, Challenges, and Applications
Applied Sciences, 2022 Nonselective cell damage remains a significant limitation of radiation therapies in cancer. Decades of successful integration of radiation therapies with other medicinal chemistry strategies significantly improved therapeutic benefits in cancer ...
Arvind Negi +2 more
doaj +1 more source
A dual origin for Bcr-Abl gene translocation/fusion as dynamics of synergism of the hematopoietic stem cell and hemangioblast in chronic myeloid leukemia [PDF]
, 2015 Contextual BCR-ABL tyrosine kinase over-activity determines in formulated fashion the emergence of proliferation and anti-apoptosis that arise largely as derived phenomena of otherwise homeostatic mechanisms of the c-ABL gene within hematopoietic ...
Agius, Lawrence M.
core +1 more source
Translational regulation of GPx-1 and GPx-4 by the mTOR pathway.
PLoS ONE, 2014 Glutathione peroxidase activity was previously determined to be elevated in lymphocytes obtained from patients treated with the Bcr-Abl kinase inhibitor imatinib mesylate.
Emily N Reinke +4 more
doaj +1 more source