Results 121 to 130 of about 838,442 (361)

m6A‐Mediated Glycolysis by IL‐37 Drives T Cell Metabolic Reprogramming to Regulate Colitis

open access: yesAdvanced Science, EarlyView.
This study identifies an IL‐37/SIGIRR‐METTL14 regulatory axis that suppresses global m6A modification in CD4+ T cells. IL‐37 signaling, mediated through SIGIRR, inhibits IRAK4 and JNK phosphorylation, leading to downregulation of the methyltransferase METTL14.
Xiaoyan Wang   +26 more
wiley   +1 more source

Phenotypical differences and thrombosis rates in secondary erythrocytosis versus polycythemia vera

open access: yesBlood Cancer Journal, 2021
Eliane Nguyen   +8 more
doaj   +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

No evidence that FLT3 status should be considered as an indicator for transplantation in acute myeloid leukemia (AML): an analysis of 1135 patients, excluding acute promyelocytic leukemia, from the UK MRC AML 10 and 12 trials

open access: yes, 2005
Fetal liver tyrosine kinase 3 (FLT3) internal tandem duplications (ITDs) are powerful adverse prognostic indicators for relapse in acute myelold leukemia (AML) but the most efficacious therapy for FLT3/ ITD+ patients is currently unknown.
Wheatley, Keith   +14 more
core   +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 ...
Kern, Wolfgang   +4 more
core   +1 more source

T Cell Exhaustion in Cancer Immunotherapy: Heterogeneity, Mechanisms, and Therapeutic Opportunities

open access: yesAdvanced Science, EarlyView.
T cell exhaustion limits immunotherapy efficacy. This article delineates its progression from stem‐like to terminally exhausted states, governed by persistent antigen, transcription factors, epigenetics, and metabolism. It maps the exhaustion landscape in the TME and proposes integrated reversal strategies, providing a translational roadmap to overcome
Yang Yu   +7 more
wiley   +1 more source

Evaluation of gene expression signatures predictive of cytogenetic and molecular subtypes of pediatric acute myeloid leukemia

open access: yesHaematologica, 2011
Background Pediatric acute myeloid leukemia is a heterogeneous disease characterized by non-random genetic aberrations related to outcome. The genetic subtype is currently detected by different diagnostic procedures which differ in success rate and/or ...
Brian V. Balgobind   +19 more
doaj   +1 more source

Unravelling the mechanisms of resistance to imatinib mesylate in chronic myeloid leukemia: a proteomic approach

open access: yes, 2010
Imatinib mesylate is a potent inhibitor of the Bcr-Abl tyrosine kinase, an oncoprotein that plays a key role in the development of chronic myeloid leukemia. Consequently, imatinib is used as front-line therapy for this disease.
Colavita, Irene
core  

adaptive capabilities of the pi3k/akt/mtor pathway in acute myeloid leukemia revealed by the use of selective inhibitors

open access: yes, 2013
Because of its aberrant activation, the PI3K/AKT/mTOR signaling pathway represents a pharmacological target in blast cells from patients with acute myelogenous leukemia (AML).
Bertacchini, Jessika <1980>
core   +1 more source

Clonal karyotype evolution involving ring chromosome 1 with myelodysplastic syndrome subtype RAEB-t progressing into acute leukemia [PDF]

open access: yes, 2006
s Karyotypic evolution is a well-known phenomenon in patients with malignant hernatological disorders during disease progression. We describe a 50-year-old male patient who had originally presented with pancytopenia in October 1992.
Wunderlich, Bettina   +18 more
core   +1 more source

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