Results 1 to 10 of about 45,526 (248)

Pterostilbene downregulates BCR/ABL and induces apoptosis of T315I-mutated BCR/ABL-positive leukemic cells [PDF]

open access: yesScientific Reports, 2022
In this study, we examined the antileukemic effects of pterostilbene, a natural methylated polyphenol analog of resveratrol that is predominantly found in berries and nuts, using various human and murine leukemic cells, as well as bone marrow samples ...
Shohei Kawakami   +11 more
doaj   +5 more sources

EPS8 regulates proliferation, apoptosis and chemosensitivity in BCR-ABL positive cells via the BCR-ABL/PI3K/AKT/mTOR pathway. [PDF]

open access: hybridOncol Rep, 2018
Although the introduction of tyrosine kinase inhibitors greatly improved the survival of patients with chronic myeloid leukemia (CML), drug resistance remains a problem. Thus, mechanism-based novel therapeutic targets warrant exploration. Recently, epidermal growth factor receptor kinase substrate 8 (EPS8), which has been identified as an oncogene and ...
Huang R   +11 more
europepmc   +6 more sources

Allosteric inhibition enhances the efficacy of ABL kinase inhibitors to target unmutated BCR-ABL and BCR-ABL-T315I [PDF]

open access: yesBMC Cancer, 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.
Mian Afsar   +8 more
doaj   +3 more sources

p185BCR/ABL has a lower sensitivity than p210BCR/ABL to the allosteric inhibitor GNF-2 in Philadelphia chromosome-positive acute lymphatic leukemia [PDF]

open access: yesHaematologica, 2012
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. The p185BCR/ABL or the p210BCR/ABL fusion proteins are encoded as a result
Afsar A. Mian   +5 more
doaj   +4 more sources

Combination of bortezomib and mitotic inhibitors down-modulate Bcr-Abl and efficiently eliminates tyrosine-kinase inhibitor sensitive and resistant Bcr-Abl-positive leukemic cells. [PDF]

open access: yesPLoS ONE, 2013
Emergence of resistance to Tyrosine-Kinase Inhibitors (TKIs), such as imatinib, dasatinib and nilotinib, in Chronic Myelogenous Leukemia (CML) demands new therapeutic strategies.
Octavian Bucur   +7 more
doaj   +6 more sources

Differential effects of selective inhibitors targeting the PI3K/AKT/mTOR pathway in acute lymphoblastic leukemia. [PDF]

open access: yesPLoS ONE, 2013
PurposeAberrant PI3K/AKT/mTOR signaling has been linked to oncogenesis and therapy resistance in various malignancies including leukemias. In Philadelphia chromosome (Ph) positive leukemias, activation of PI3K by dysregulated BCR-ABL tyrosine kinase (TK)
Susanne Badura   +8 more
doaj   +11 more sources

Differential roles of STAT1 and STAT2 in the sensitivity of JAK2V617F- vs. BCR-ABL-positive cells to interferon alpha [PDF]

open access: yesJournal of Hematology & Oncology, 2019
Background Interferon alpha (IFNa) monotherapy is recommended as the standard therapy in polycythemia vera (PV) but not in chronic myeloid leukemia (CML). Here, we investigated the mechanisms of IFNa efficacy in JAK2V617F- vs.
Claudia Schubert   +11 more
doaj   +2 more sources

Case report: BCR-ABL-positive acute lymphoblastic leukemia with bone destruction: a treatment dilemma [PDF]

open access: yesFrontiers in Oncology
Although bone destruction and hypercalcemia without acute peripheral blast BCR-ABL-positive acute lymphoblastic leukemia (ALL) have been reported in children, they are rare in adults.
Shi Lijun   +6 more
doaj   +2 more sources

Co-Occurrence of Jak2-Positive Myelofibrosis and Bcr-Abl-Positive Chronic Myelogenous Leukaemia Treated with Combination of Tyrosine Kinase Inhibitors and Ruxolitinib. [PDF]

open access: goldMediterr J Hematol Infect Dis
Paciaroni K   +8 more
europepmc   +3 more sources

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   +1 more source

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