Results 111 to 120 of about 887,943 (333)

De novo UBE2A mutations are recurrently acquired during chronic myeloid leukemia progression and interfere with myeloid differentiation pathways

open access: yesHaematologica, 2019
Despite the advent of tyrosine kinase inhibitors, a proportion of chronic myeloid leukemia patients in chronic phase fail to respond to imatinib or to second-generation inhibitors and progress to blast crisis. Until now, improvements in the understanding
Vera Magistroni   +27 more
doaj   +1 more source

Metabolic gatekeeper function of B-lymphoid transcription factors. [PDF]

open access: yes, 2017
B-lymphoid transcription factors, such as PAX5 and IKZF1, are critical for early B-cell development, yet lesions of the genes encoding these transcription factors occur in over 80% of cases of pre-B-cell acute lymphoblastic leukaemia (ALL).
Borkhardt, Arndt   +26 more
core  

Detection of monosomy 7 in interphase cells of patients with myeloid disorders [PDF]

open access: yes, 1990
Six patients, five with acute myeloid leukemia (AML) and one with a myelodysplastic syndrome (MDS), were found to have monosomy 7 by conventional cytogenetics at diagnosis.
Cremer, Thomas   +5 more
core   +1 more source

Two‐way inhibition of PAX5 transcriptional activity by PAX5::CBFA2T3

open access: yesFEBS Open Bio, EarlyView.
PAX5::CBFA2T3 (PAX5‐C) is a fusion protein of the B‐cell transcription factor, PAX5, and is found in B‐cell ALL. We propose a putative model of two‐way inhibition of PAX5 transcriptional activity by PAX5‐C. There are two ways of repression by PAX5‐C: DNA‐binding‐dependent way and HDAC‐dependent way, with either being sufficient for the repression. HDAC
Reina Ueno   +12 more
wiley   +1 more source

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

FLT3 Length Mutations as Marker for Follow-Up Studies in Acute Myeloid Leukaemia [PDF]

open access: yes, 2004
Length mutations within the FLT3 gene (FLT3-LM) can be found in 23% of acute myeloid leukaemia (AML) and thus are the most frequent mutations in AML. FLT3-LM are highly correlated with AML with normal karyotype and other cytogenetic aberrations of the ...
Haferlach, Torsten   +4 more
core   +1 more source

Chronic Myeloid Leukemia in 2020

open access: yesHemaSphere, 2020
AbstractNew insights have emerged from maturing long‐term academic and commercial clinical trials regarding optimum management of chronic myeloid leukemia (CML). Velocity of response has unexpectedly proved less important than hitherto thought, does not predict survival, and is of unclear relevance for treatment‐free remission (TFR).
openaire   +3 more sources

Chronic myeloid leukemia in Asia

open access: yesInternational Journal of Hematology, 2008
Chronic myeloid leukemia (CML) in Asia has an incidence rather lower than in Western countries yet tends to afflict a younger population. As in the West, imatinib mesylate (IM, Glivec) has supplanted busulphan, hydroxyurea and interferon-alpha as first-line treatment.
Jootar, S   +9 more
openaire   +4 more sources

Statins induce monocytic differentiation in acute myeloid leukemia cells through the KLF4/DPYSL2A axis

open access: yesFEBS Open Bio, EarlyView.
Statins, identified via the Comparative Toxicogenomics Database, promote monocytic differentiation and apoptosis in non‐APL AML cells by upregulating DPYSL2A through a KLF4‐dependent pathway. Mevalonate supplementation reversed these effects, indicating involvement of the mevalonate pathway.
Mina Noura   +7 more
wiley   +1 more source

A unified model for Duchenne muscular dystrophy gene involvement in cancer: context‐dependent tumour suppression and oncogenicity

open access: yesFEBS Open Bio, EarlyView.
We propose a context‐dependent model where the Duchenne muscular dystrophy (DMD) gene acts as a tumour suppressor in aggressive tumours and as an oncogene in less aggressive ones. We propose this model as a unified framework to explain the opposing survival associations with DMD expression and to guide experimental exploration of the dual role of DMD ...
Lee Machado   +4 more
wiley   +1 more source

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