Results 51 to 60 of about 30,839 (241)

BCR-ABL1 tyrosine kinase sustained MECOM expression in chronic myeloid leukaemia [PDF]

open access: yes, 2012
MECOM oncogene expression correlates with chronic myeloid leukaemia (CML) progression. Here we show that the knockdown of MECOM (E) and MECOM (ME) isoforms reduces cell division at low cell density, inhibits colony-forming cells by 34% and moderately ...
Alzuherri   +53 more
core   +1 more source

Adoptive Immunotherapy in Chimeras with Donor Lymphocytes [PDF]

open access: yes, 2003
Allogeneic stem cell transplantation has a well-defined indication in the treatment of hematological malignancies. The beneficial immune effect of allogeneic marrow transplantation has long been known, but only recently have methods been developed to ...
Chen, Xiao   +8 more
core   +1 more source

Celecoxib inhibits proliferation and survival of chronic myelogeous leukemia (CML) cells via AMPK-dependent regulation of β-catenin and mTORC1/2. [PDF]

open access: yes, 2016
CML is effectively treated with tyrosine kinase inhibitors (TKIs). However, the efficacy of these drugs is confined to the chronic phase of the disease and development of resistance to TKIs remains a pressing issue.
Calabretta, Bruno   +10 more
core   +2 more sources

Combination therapy of BCR-ABL-positive B cell acute lymphoblastic leukemia by tyrosine kinase inhibitor dasatinib and c-JUN N-terminal kinase inhibition

open access: yesJournal of Hematology & Oncology, 2020
Background The Philadelphia chromosome (Ph), which leads to the creation and expression of the fusion gene product BCR-ABL, underlines the pathogenesis of chronic myelogenous leukemia (CML) and a fraction of adult and pediatric acute B-lymphoblastic ...
Xin-hua Xiao   +9 more
semanticscholar   +1 more source

Brazilian chronic myeloid leukemia working group recommendations for discontinuation of tyrosine kinase inhibitors in chronic myeloid leukemia in clinical practice

open access: yesHematology, Transfusion and Cell Therapy, 2022
Introduction: Treatment-free remission (TFR) is a new goal of chronic myeloid leukemia (CML) therapy. TFR is feasible when the patient has achieved a deep and stable molecular response and met the criteria required to ensure its success.
Carla Boquimpani   +8 more
doaj  

Targeting quiescent leukemic stem cells using second generation autophagy inhibitors [PDF]

open access: yes, 2019
In chronic myeloid leukemia (CML), tyrosine kinase inhibitor (TKI) treatment induces autophagy that promotes survival and TKI-resistance in leukemic stem cells (LSCs).
A Hamilton   +42 more
core   +2 more sources

The antiproliferative activity of kinase inhibitors in chronic myeloid leukemia cells is mediated by FOXO transcription factors [PDF]

open access: yes, 2014
Chronic myeloid leukemia (CML) is initiated and maintained by the tyrosine kinase BCR-ABL which activates a number of signal transduction pathways, including PI3K/AKT signaling and consequently inactivates FOXO transcription factors.
Bhatia   +38 more
core   +2 more sources

Excellent outcomes of 2G-TKI therapy after imatinib failure in chronic phase CML patients [PDF]

open access: yes, 2018
open25noSecond-generation tyrosine kinase inhibitors (2G-TKIs) dasatinib and nilotinib produced historical rates of about 50% complete cytogenetic response (CCyR) and about 40% major molecular response (MMR) in chronic myeloid leukaemia (CML) patients ...

core   +1 more source

Factors associated with achievement and durability of cytogenetic response in patients with chronic myeloid leukemia treated with imatinib [PDF]

open access: yesVojnosanitetski Pregled, 2011
Background/Aim. Imatinib mesylate, a selective Bcr-Abl tyrosine kinase inhibitor, has revolutionized the treatment of Bcr-Abl positive chronic myeloid leukemia and become the standard of care for this disease.
Ćojbašić Irena   +1 more
doaj   +1 more source

BCR-ABL residues interacting with ponatinib are critical to preserve the tumorigenic potential of the oncoprotein [PDF]

open access: yes, 2013
Patients with chronic myeloid leukemia in whom tyrosine kinase inhibitors (TKIs) fail often present mutations in the BCR-ABL catalytic domain. We noticed a lack of substitutions involving 4 amino acids (E286, M318, I360, and D381) that form hydrogen ...
Alessandro Pandini   +11 more
core   +1 more source

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