|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
(1) Generation of DCleu/DC: (a) "IFN-GIT" [containing granulocyte macrophage-colony stimulating factor (GM-CSF)+IFNα+ tumor necrosis factor (TNF)-α] produced DC successfully (≥10% DC, ≥5% DCleu/cells) from AML-MNC (WB) in 54 (56%), "MCM-Mimic" in 76 (75%), "Picibanil" in 83 (64%), and "Calcium-ionophore" in 42 (67%) of cases.
|
31090655 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
High expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor has been found in myelomonocytic or monocytic subtypes (M4/M5) of acute myeloid leukemia.
|
31115604 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The most popular mouse strains used in research, the NOG (NOD.Cg-Prkdc<sup>scid</sup> Il2rγ<sup>tm1Sug</sup>/Jic) and the NSG (NOD/SCID-IL2Rγ<sup>-/-</sup>, NOD.Cg-Prkdc<sup>scid</sup>Il2rγ<sup>tm1Wjl</sup>/SzJ) mouse, and their human-cytokine-producing (interleukin-3, granulocyte-macrophage colony-stimulating factor, and stem cell factor) counterparts (huNOG and NSGS), rely partly on a mutation in the DNA repair protein PRKDC, causing a severe combined immune deficiency (SCID) phenotype and rendering the mice less tolerant to DNA-damaging therapeutics, thereby limiting their usefulness in the investigation of novel acute myeloid leukemia (AML) therapeutics.
|
30125602 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Altogether, we discovered a novel molecular mechanism mediating the GM-CSF-induced reduction in leukemic potential of RE cells, and our findings support MYC inhibition as an effective strategy for reducing the leukemogenicity of t(8;21) AML.
|
27389055 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
To address this limitation, we here transplanted primary human AML with isolated nucleophosmin (NPM1) mutation and AML with inv(16) in mice in which human versions of genes encoding cytokines important for myelopoiesis (macrophage colony-stimulating factor [M-CSF], interleukin-3, granulocyte-macrophage colony-stimulating factor, and thrombopoietin) were knocked into their respective mouse loci.
|
27581357 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Individuals with WT1-positive acute myeloid leukemia (AML) in first (CR1) or second (CR2) remission or with higher-risk myelodysplastic syndrome (MDS) following at least 1 prior line of therapy were vaccinated with a mixture of peptides derived from the WT1 protein, with sargramostim injections before vaccination to amplify immunogenicity.
|
25802083 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
To learn more about the antigens that elicit antibodies during GVL reactions, we analyzed patients with advanced myelodysplasia (MDS) and acute myelogenous leukemia (AML) who received an autologous, granulocyte-macrophage colony-stimulating factor (GM-CSF)-secreting tumor cell vaccine early after allogeneic hematopoietic stem cell transplantation (HSCT).
|
25538258 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
The objective of this study was to generate a novel humanized chimeric protein with human DFF40 fused with GM-CSF for targeting acute myeloid leukemia (AML) cells. cDNA cloning of human DFF40 and GM-CSF was done and the chimeric gene GM-CSF-DFF40 was generated by overlap extension PCR.
|
23529188 |
2013 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
miR-590-5p, miR-219-5p, miR-15b and miR-628-5p are commonly regulated by IL-3, GM-CSF and G-CSF in acute myeloid leukemia.
|
22015065 |
2012 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
We identified such mutations using a Sleeping Beauty transposon, which caused rapid-onset AML in 80% of mice with Npm1c, associated with mutually exclusive integrations in Csf2, Flt3 or Rasgrp1 in 55 of 70 leukemias.
|
21441929 |
2011 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
CTD_human |
We identified such mutations using a Sleeping Beauty transposon, which caused rapid-onset AML in 80% of mice with Npm1c, associated with mutually exclusive integrations in Csf2, Flt3 or Rasgrp1 in 55 of 70 leukemias.
|
21441929 |
2011 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
In a first report, we have shown that priming with granulocyte-macrophage colony-stimulating factor (GM-CSF) may enhance complete remission (CR) rate and event-free survival (EFS) in younger adults with acute myeloid leukemia (AML).
|
20143449 |
2010 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
After lentiviral-mediated gene transfer of INPP5D into CD34(+) cells derived from AML patients (n=12) the granulocyte macrophage-colony stimulating factor (GM-CSF)-dependent proliferation was reduced in all samples analyzed (average 86%; range 72-93%).
|
19148132 |
2009 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Effect of priming with granulocyte-macrophage colony-stimulating factor in younger adults with newly diagnosed acute myeloid leukemia: a trial by the Acute Leukemia French Association (ALFA) Group.
|
17252021 |
2007 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Granulocyte-macrophage colony-stimulating factor (GM-CSF) induces antiapoptotic and proapoptotic signals in acute myeloid leukemia.
|
12663443 |
2003 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Phase I trial of a novel diphtheria toxin/granulocyte macrophage colony-stimulating factor fusion protein (DT388GMCSF) for refractory or relapsed acute myeloid leukemia.
|
12006512 |
2002 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
However, G-CSF, but not GM-CSF and IL-3, enhanced clonal growth in three cases of high risk patients with MDS (RAEB, RAEB-t, and MDS having progressed to acute myeloid leukemia (AML)) and one low risk patient (RA).
|
12012328 |
2002 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In some cases, endogenous GM-CSF expression by transduced AML cells induced phenotypic changes consistent with the maturation of leukemia blasts into antigen-presenting cells.
|
12200676 |
2002 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
LHGDN |
In vitro studies demonstrated that leptin increased AML blast release of interleukin (IL) 1beta, IL6, tumor necrosis factor (TNF) alpha and granulocyte-macrophage colony-stimulating factor (GM-CSF).
|
12031914 |
2002 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
CD40 was detected in blast cells from about 37% of AMLs, the highest frequency being documented in monocytic subtypes, and its expression was upregulated or de novo induced by treatment with interleukin (IL)-1alpha, IL-3, IL-4, granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon-gamma, and tumor necrosis factor-alpha.
|
12423681 |
2002 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Sera from 43 patients with AML were tested by bioassay and a specific enzymoimmunoassay (EIA) for anti-DT-GM antibodies.
|
11465948 |
2001 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
In AML cultures with GM-CSF and TNFalpha, coexpression of CD80 and either CD34 or an aberrant surface marker (CD56) was seen.
|
10720135 |
2000 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
We also found that GM-CSF induced the expression of RAR alpha in blood cells obtained from patients with acute myeloid leukemia.
|
10969805 |
2000 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Although adenoviruses can infect nondividing cells, we observed that a combination of growth factors (GM-CSF, IL-3, stem cell factor) was required for efficient transduction in order to maintain AML blast cell viability.
|
10435081 |
1999 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Under the same conditions of exposure, normal hematopoietic progenitors are relatively unaffected by DT388-GMCSF, suggesting its potential as a therapeutic agent in AML.
|
9657759 |
1998 |