Results 41 to 50 of about 541,695 (230)

Acute Myeloid Leukemia in Adults [PDF]

open access: yes, 2018
AML is a malignancy of hematopoietic immature precursors (myeloblasts) that accumulate in the BM at the expense of their normal counterparts.
Charles Craddock   +5 more
openaire   +2 more sources

Acute Myeloid Leukemia: Is It T Time? [PDF]

open access: yesCancers, 2021
Acute myeloid leukemia (AML) is a heterogeneous disease driven by impaired differentiation of hematopoietic primitive cells toward myeloid lineages (monocytes, granulocytes, red blood cells, platelets), leading to expansion and accumulation of “stem” and/or “progenitor”-like or differentiated leukemic cells in the bone marrow and blood. AML progression
Meriem Ben Ben Khoud   +4 more
openaire   +3 more sources

Targeting PI3Kδ and PI3Kγ signalling disrupts human AML survival and bone marrow stromal cell mediated protection [PDF]

open access: yes, 2016
Phosphoinositide-3-kinase (PI3K) is an enzyme group, known to regulate key survival pathways in acute myeloid leukaemia (AML). It generates phosphatidylinositol-3,4,5-triphosphate, which provides a membrane docking site for protein kinaseB activation ...
Alves   +37 more
core   +1 more source

One Stone, Two Birds: N6-Methyladenosine RNA Modification in Leukemia Stem Cells and the Tumor Immune Microenvironment in Acute Myeloid Leukemia

open access: yesFrontiers in Immunology, 2022
Acute myeloid leukemia is the most common acute leukemia in adults, with accumulation of abundant blasts and impairment of hematogenic function. Despite great advances in diagnosis and therapy, the overall survival of patients with acute myeloid leukemia
Xianfeng Ouyang   +2 more
doaj   +1 more source

Acute Myeloid Leukemia: Is That All There Is? [PDF]

open access: yesCureus, 2018
Acute myeloid leukemia (AML) is characterized by the clonal proliferation of malignant myeloid blast cells in the marrow along with impaired normal hematopoiesis. With an almost stagnant approach for the management of patients with AML in the last three decades, the main purpose of this paper is to increase our understanding of recent scientific ...
Aneeqa Saif   +4 more
openaire   +3 more sources

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

Pharmacological inhibition of dihydroorotate dehydrogenase induces apoptosis and differentiation in acute myeloid leukemia cells

open access: yesHaematologica, 2018
Acute myeloid leukemia is a disorder characterized by abnormal differentiation of myeloid cells and a clonal proliferation derived from primitive hematopoietic stem cells.
Dang Wu   +13 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

Acute Myeloid Leukemia and Acute Promyelocytic Leukemia

open access: yesHematology, 2003
AbstractThe therapeutic approach to the patient with acute myeloid leukemia (AML) currently evolves toward new frontiers. This is particularly apparent from the entree of high-throughput diagnostic technologies and the identification of prognostic and therapeutic targets, the introduction of therapies in genetically defined subgroups of AML, as well as
Martin S. Tallman   +2 more
openaire   +3 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

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