Results 31 to 40 of about 205,035 (295)

Improvement of platelet dysfunction in chronic myelogenous leukemia following treatment with imatinib: a case report

open access: yesJournal of Medical Case Reports, 2011
Introduction In patients with chronic myeloid leukemia, tyrosine kinase inhibitors suppress the BCR-ABL+ clone and often induce complete molecular remissions.
Scheid Christoph   +5 more
doaj   +1 more source

A Case of Chronic Myeloid Leukemia Presenting with Osteoid Osteoma: A Diagnostic Dilemma

open access: yesAsian Pacific Journal of Cancer Care, 2021
Chronic myeloid leukemia is a hematological malignancy resulting from a clonal proliferation of hematopoietic stem cells of the myeloid series. It is developed by chromosomal translocation.
Mannavi Suman   +4 more
doaj   +1 more source

Inhibition of interleukin-1 signaling enhances elimination of tyrosine kinase inhibitor treated CML stem cells [PDF]

open access: yes, 2016
Treatment of chronic myelogenous leukemia (CML) with BCR-ABL tyrosine kinase inhibitors (TKI) fails to eliminate leukemia stem cells (LSC). Patients remain at risk for relapse, and additional approaches to deplete CML LSC are needed to enhance the ...
Agarwal, Puneet   +9 more
core   +1 more source

Comparative analysis of blood lymphocytes of patients with acute and chronic myeloid leukemia by surface and intracellular α1-acid glycoprotein and fibronectin

open access: yesБіологічні студії, 2014
The exposition of α1-acid glycoprotein and fibronectin on the surface and inside the lymphocytes of healthy donors and hematological patients with acute and chronic myeloid leukemia were studied.
G. S. Маslak
doaj   +1 more source

Dipeptidylpeptidase IV (CD26) defines leukemic stem cells (LSC) in chronic myeloid leukemia [PDF]

open access: yes, 2014
Chronic myeloid leukemia (CML) is a stem cell (SC) neoplasm characterized by the BCR/ABL1 oncogene. Although mechanisms of BCR/ABL1-induced transformation are well-defined, little is known about effector-molecules contributing to malignant expansion and ...
Bilban, Martin   +15 more
core   +1 more source

Bone marrow mesenchymal stromal cells non-selectively protect chronic myeloid leukemia cells from imatinib-induced apoptosis via the CXCR4/CXCL12 axis

open access: yesHaematologica, 2010
Background Residual chronic myeloid leukemia disease following imatinib treatment has been attributed to the presence of quiescent leukemic stem cells intrinsically resistant to imatinib.
Fabrizio Vianello   +10 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]

open access: yes, 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

Reciprocal t(9;22) ABL/BCR fusion proteins: leukemogenic potential and effects on B cell commitment [PDF]

open access: yes, 2009
Background: t(9;22) is a balanced translocation, and the chromosome 22 breakpoints (Philadelphia chromosome – Ph+) determine formation of different fusion genes that are associated with either Ph+ acute lymphatic leukemia (Ph+ ALL) or chronic myeloid ...
Henschler, Reinhard   +4 more
core   +9 more sources

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]

open access: yes, 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

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

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