Intrinsic structural disorder confers cellular viability on oncogenic fusion proteins. [PDF]
PLoS Computational Biology, 2009 Chromosomal translocations, which often generate chimeric proteins by fusing segments of two distinct genes, represent the single major genetic aberration leading to cancer.
Hedi Hegyi, László Buday, Peter Tompa
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Does thyroid dysfunction happen in CML patients receiving Imatinib for treatment? [PDF]
Reviews in Clinical Medicine, 2015 Chronic myelogenous leukemia is a myeloproliferative disorder presenting with anemia, elevated blood granulocytosis and the presence of immature granulocytes, basophilia, frequently thrombocytosis and spleen enlargement.
Hossein Rahimi +2 more
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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
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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.
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Epigenetic dysregulation in chronic myeloid leukaemia: A myriad of mechanisms and therapeutic options [PDF]
, 2018 The onset of global epigenetic changes in chromatin that drive tumor proliferation and heterogeneity is a hallmark of many forms cancer. Identifying the epigenetic mechanisms that govern these changes and developing therapeutic approaches to modulate ...
Koschmieder, Steffen, Vetrie, David
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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
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Activation of tyrosine kinases by mutation of the gatekeeper threonine. [PDF]
, 2008 Protein kinases targeted by small-molecule inhibitors develop resistance through mutation of the gatekeeper threonine residue of the active site. Here we show that the gatekeeper mutation in the cellular forms of c-ABL, c-SRC, platelet-derived growth ...
Azam, Mohammad +4 more
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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
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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
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Detection of derivative 9 deletion by BCR-ABL fluorescence in-situ hybridization signal pattern to evaluate treatment response in CML patients [PDF]
Archive of Oncology, 2009 Background: To evaluate prognostic effect of submicroscopic deletions involving breakage and fusion points of the derivative chromosome 9 and 22 in chronic myeloid leukemia in untreated patients and their follow up samples to correlate with disease ...
Bakshi Sonal R. +8 more
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