Results 81 to 90 of about 402,161 (308)

Chronic myelomonocytic leukemia with ring sideroblasts/SF3B1 mutation presents with low monocyte count and resembles myelodysplastic syndromes with-RS/SF3B1 mutation in terms of phenotype and prognosis

open access: yesFrontiers in Oncology
IntroductionChronic myelomonocytic leukemia (CMML) and myelodysplastic syndromes (MDS) with ring sideroblasts (RS) or SF3B1 mutation (MDS-RS/SF3B1) differ in many clinical features, but share others, such as anemia.
Blanca Xicoy   +20 more
doaj   +1 more source

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

The miR-223 host non-coding transcript linc-223 induces IRF4 expression in acute myeloid leukemia by acting as a competing endogenous RNA [PDF]

open access: yes, 2016
Alterations in genetic programs required for terminal myeloid differentiation and aberrant proliferation characterize acute myeloid leukemia (AML) cells.
Bozzoni, Irene   +8 more
core   +2 more sources

SnapShot: Acute Myeloid Leukemia

open access: yesCancer Cell, 2012
20%-25% (28%-35%); High blast count; Poor prognosisespecially in cases with high mutant to WT allelic ratio5%-7% (10%-14%); Prognostic impact remains controversial10% (9%-14%); Enriched in CBF AML; Prognosis ...
Zeisig, Bernd B.   +3 more
openaire   +2 more sources

Aging Is a Key Driver for Adult Acute Myeloid Leukemia

open access: yesAging and Cancer, EarlyView.
Acute myeloid leukemia (AML) is a classical age‐related hematologic malignancy, and a key driver of AML is aging, which profoundly regulates intrinsic factors such as genomic instability, epigenetic reprogramming, and metabolic dysregulation, and alters bone marrow microenvironment.
Rong Yin, Haojian Zhang
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

Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance

open access: yesAging and Cancer, EarlyView.
NPM1 mutations drive acute myeloid leukemia by acting as neomorphic transcriptional regulators that cooperate with Menin–MLL and XPO1 to sustain HOX/MEIS1 expression and block differentiation. Targeting these mutant‐specific transcriptional dependencies provides a rational therapeutic strategy for NPM1‐mutated AML.
Yanan Jiang   +3 more
wiley   +1 more source

Molecular mechanisms in haematological malignancies [PDF]

open access: yes, 2009
Haematopoiesis requires the constant production of large numbers of peripheral blood cells. This process is under tight control of transcription factor networks as well as cytokines, growth factors and hormones.
Avellino, Roberto   +2 more
core  

Leukemia autopsies in Japan [PDF]

open access: yes, 1964
For the purpose to know whether the annual increase of leukemia incidence in Japan is due to some leukemogenic factors or due to the increased detection rate, the authors made some statistical survey of autopsy cases in which the diagnosis is reliable ...
Asakura, Hikaru   +10 more
core   +1 more source

Immune‐Driven Expression in Inclusion Body Myositis With T‐Cell Large Granular Lymphocytic Leukemia

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Objectives T‐cell large granular lymphocytic leukemia (T‐LGLL), reported in up to 58% of inclusion body myositis (IBM) patients, is a rare leukemia of cytotoxic or less commonly helper T cells. The range of myopathies in T‐LGLL and the impact of coexisting T‐LGLL in IBM are not well understood. Our objectives are to investigate the spectrum of
Pannathat Soontrapa   +10 more
wiley   +1 more source

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