Results 41 to 50 of about 44,642 (305)

Bacterial translocation in acute lymphocytic leukemia

open access: yesPLOS ONE, 2019
Bloodstream infection (BSI) is the major cause of mortality in acute lymphocytic leukemia (ALL). Causative pathogens in BSI originate from the gut microbiota due to an increase in intestinal permeability, a process known as bacterial translocation (BT).
Yajing Song, Peter Gyarmati
openaire   +5 more sources

Association between maternal breastfeeding and risk of systemic neoplasms of offspring

open access: yesItalian Journal of Pediatrics, 2022
Background Breastfeeding might prevent childhood cancer by stimulating the immune system. Methods The following databases, including PubMed, Embase, and Cochrane Library, were searched from inception to January 10, 2021. Results In dose-dependent manner,
Qin-Qin Gong   +4 more
doaj   +1 more source

Comprehensive omics‐based classification system in adult patients with B‐cell acute lymphoblastic leukemia

open access: yesMolecular Oncology, EarlyView.
The COMBAT classification system, developed through multi‐omics integration, stratifies adult patients with B‐cell acute lymphoblastic leukemia(B‐ALL) into three molecular subtypes with distinct surface antigen patterns, immune landscape, methylation patterns, biological pathways and prognosis.
Yang Song   +11 more
wiley   +1 more source

Diagnosis of large granular lymphocytic leukemia in a patient previously treated for acute myeloblastic leukemia

open access: yesHematology Reports, 2013
Large granular lymphocytic (LGL) leukemia is a lymphoproliferative disease characterized by the clonal expansion of cytotoxic T or natural killer cells.
Sinem Civriz Bozdag   +7 more
doaj   +1 more source

Preserved cellular immunity in smoldering acute leukemia [PDF]

open access: yes, 1976
"Smoldering acute leukemia", a variant of acute myelogenous leukemia, has been recognized with frequent incidence in recent years. This is chracterized by benign clinical course, poor physical findings, leukopenia and mild anemia in the ...
Toki, Hironobu
core   +1 more source

PYCR1 inhibition in bone marrow stromal cells enhances bortezomib sensitivity in multiple myeloma cells by altering their metabolism

open access: yesMolecular Oncology, EarlyView.
This study investigated how PYCR1 inhibition in bone marrow stromal cells (BMSCs) indirectly affects multiple myeloma (MM) cell metabolism and viability. Culturing MM cells in conditioned medium from PYCR1‐silenced BMSCs impaired oxidative phosphorylation and increased sensitivity to bortezomib.
Inge Oudaert   +13 more
wiley   +1 more source

Predictors of response and rational combinations for the novel MCL‐1 inhibitor MIK665 in acute myeloid leukemia

open access: yesMolecular Oncology, EarlyView.
This study characterizes the responses of primary acute myeloid leukemia (AML) patient samples to the MCL‐1 inhibitor MIK665. The results revealed that monocytic differentiation is associated with MIK665 sensitivity. Conversely, elevated ABCB1 expression is a potential biomarker of resistance to the treatment, which can be overcome by the combination ...
Joseph Saad   +17 more
wiley   +1 more source

Biological aspects of mTOR in leukemia [PDF]

open access: yes, 2018
The mammalian target of rapamycin (mTOR) is a central processor of intra-and extracellular signals, regulating many fundamental cellular processes such as metabolism, growth, proliferation, and survival.
Bianchi, Mp   +5 more
core   +1 more source

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

The IFNγ‐CIITA‐MHC II axis modulates melanoma cell susceptibility to NK‐cell‐mediated cytotoxicity

open access: yesMolecular Oncology, EarlyView.
Natural killer (NK) cells play a central role in anti‐melanoma immunity. However, melanoma cells adapt during co‐culture by upregulating CIITA and MHC II in response to interferon gamma (IFNγ), thereby evading NK‐cell lysis. Blocking IFNγ signaling or treatment with dimethyl fumarate/simvastatin counteracts this immune escape and maintains NK‐cell ...
Lena C. M. Krause   +6 more
wiley   +1 more source

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