|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
These results suggest that there is considerable overlap between the GM-CSF- and G-CSF-responsive AML-CFU subpopulations in most cases.
|
3495305 |
1987 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
These results indicate that G-CSF may be sufficient to provide a specific signal for induction of a transient proliferation in AML without induction of terminal differentiation.
|
2455572 |
1988 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Structure and expression of genes of GM-CSF and G-CSF in blast cells from patients with acute myeloblastic leukemia.
|
3257144 |
1988 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
We report: (i) that the respective position of the five genes is centromere - c-erbA-1 - G-CSF - c-erbB-2 - RAR alpha - MPO - telomere; (ii) that the breakpoints of the various AML subtypes are variably located between the centromere and c-erbB-2 in M1 and M2; (iii) that the breakpoints are consistently located between c-erbB-2 and RAR alpha/MPO in M3; and (iv) that the breakpoint on chromosome 17 in the 15;17 translocation is located on 17q21 and not on 17q11-12 as previously reported.
|
1701231 |
1990 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
This difference was reflected in the effectiveness of G-CSF to stimulate colony formation in acute myeloid leukemia blasts, while G-CSF did not stimulate colony formation of the blast cells from acute lymphoid leukemia.
|
1689609 |
1990 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Only in one patient a complex rearrangement of the G-CSF gene with possible amplification was noted indicating rarity of direct alterations of growth factor genes in acute myelogenous leukemia (AML).
|
2197515 |
1990 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
The in vitro growth response of bone marrow and blood cells to granulocyte/macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) was studied in 18 acute myeloid leukemia (AML) patients using semisolid and suspension cultures.
|
1690827 |
1990 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
As acute myeloblastic leukemia (AML) blasts can express and produce hematopoietic growth factors, the influence of TNF-alpha on the accumulation of mRNAs for c-myc, interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF), G-CSF, IL-6 and IL-1 beta was evaluated in fresh blasts from 13 patients with AML.
|
1961022 |
1991 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Incubation of blasts from three patients with AML in serum-free medium with TNF (10(3) U/ml), and subsequent binding studies using 125I-G-CSF reveal that TNF downregulates the numbers of G-CSF receptors by approximately 70%.
|
1705566 |
1991 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
No significant interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF) or granulocyte colony-stimulating factor (G-CSF), was detected in these patients demonstrating that a different pattern of growth factors secretion exist in AML and CML, where distinct molecular events are likely involved in the control of leukaemic proliferation.
|
1533785 |
1992 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
At high concentrations, DAB486-G-CSF is cytotoxic towards G-CSF-dependent OCI/AML1 cells, but not factor independent OCI/AML3 cells; colony formation by G-CSF-responsive leukemic blasts from a patient with acute myeloblastic leukemia (AML) was also inhibited.
|
7505148 |
1993 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Acute myeloblastic leukemia (ANLL-M2) with t(8;21)(q22;q22) variant expressing lymphoid but not myeloid surface antigens with a high number of G-CSF receptors.
|
8487587 |
1993 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
GCSF gene is expressed but not rearranged in a patient with isochromosome 17q positive acute nonlymphocytic leukemia.
|
7687196 |
1993 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
The G-CSF-combined pretransplant conditioning regimen for ABSCT may be effective in the treatment of high-risk AML by increasing the chemosensitivity of the residual leukemic cells.
|
7515302 |
1994 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Therapeutic
|
disease |
CTD_human |
In poor prognosis acute myeloid leukemia (AML), the combination of fludarabine with Ara-C and granulocyte colony-stimulating factor (G-CSF) has proven to be a highly effective regimen.
|
7528855 |
1994 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Abnormalities in the signal-transduction pathways for granulocyte colony-stimulating factor (G-CSF) may play a part in the progression to acute myeloid leukemia.
|
7542747 |
1995 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Acute myeloid leukemia (AML) blast cells frequently produce interleukin-6 (IL-6) and other cytokines such as colony-stimulating factors (CSF: G-CSF, M-CSF, and GM-CSF), tumor necrosis factor (TNF)-alpha, and IL-1.
|
8907269 |
1996 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Recently, point mutations in the gene of the granulocyte colony-stimulating factor (G-CSF) receptor have been reported in two patients with severe congenital neutropenia who developed acute myeloid leukemia (AML).
|
9116280 |
1997 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Intensive chemotherapy with idarubicin, cytosine arabinoside, and granulocyte colony-stimulating factor (G-CSF) in patients with secondary and therapy-related acute myelogenous leukemia. Club de Réflexion en Hématologie.
|
9001413 |
1997 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Randomized clinical study comparing aggressive chemotherapy with or without G-CSF support for high-risk myelodysplastic syndromes or secondary acute myeloid leukaemia evolving from MDS.
|
9722293 |
1998 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Despite this evidence for a hyperproliferative response to G-CSF, no cases of AML have been detected to date.
|
9691084 |
1998 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
These results explain the molecular basis for G-CSFR mutations in the pathogenesis of the dominant-negative phenotype and hypersensitivity to G-CSF in SCN/AML.
|
9885205 |
1999 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Expression of GIG-1 mRNA was elevated by treatment with G-CSF in normal bone marrow mononuclear cells, as well as in some cases of blast cells obtained from patients with acute myelogenous leukemia (AML) and CML.
|
9886253 |
1999 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Recently, studies of patients with SCN who subsequently developed acute myeloid leukemia (AML) revealed nonsense mutations in the cytoplasmic domain of the granulocyte colony-stimulating factor (G-CSF) receptor messenger RNA.
|
10372134 |
1999 |
|
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
G-CSF distinctly promoted the proliferation of leukaemic cells of t(16;21) AML, but did not enhance the expression of MPO and neutrophil differentiation of these cells.
|
10354136 |
1999 |