leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, critical molecules such as C-X-C motif chemokine 12 (CXCL12), interleukin (IL)-8, colony-stimulating factor 3 (CSF3), and leukaemia inhibitory factor (LIF), were expressed at similar levels in BM-A and in primary human BM mesenchymal stromal cells (BM-MSC), whereas IL-3 was higher in BM-A.
|
28574591 |
2018 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Immunological effects of vaccines combined with granulocyte colony-stimulating factor on a murine WEHI-3 leukemia model.
|
28454398 |
2017 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We show here for the first time that LPXN is a fusion partner of ETV6 and present evidence indicating that ETV6-LPXN plays a crucial role in leukemia progression through enhancing the response to G-CSF and CXCL12.
|
26542893 |
2016 |
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
These findings raised the questions how CSF3R mutations affect CSF3 responses of myeloid progenitors, how they contribute to the pre-leukemic state of SCN, and which additional events are responsible for progression to leukemia.
|
26637693 |
2015 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Long-term treatment with G-CSF, especially at high doses, augments the spontaneous risk of leukemia in patients with congenital neutropenia.
|
21595885 |
2011 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Hematopoietic stem cell transplantation remains the only currently available treatment for refractory cases to G-CSF and patients who have transformed into leukemia.
|
20165869 |
2010 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We evaluated the safety and efficacy of donor lymphocyte infusion (DLI) with granulocyte colony-stimulating factor priming and short-term immunosuppressive agents for prophylaxis of relapse in patients with advanced leukemia after human leukocyte antigen (HLA)-mismatched T cell-replete hematopoietic stem cell transplantation (HCT).
|
18204965 |
2008 |
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
One possible pathomechanism causing leukemia is that clones of cells harboring acquired CSF3R mutations have a growth advantage over wild type cells in vivo during granulocyte-colony stimulating factor treatment due to activation of STAT5 and ss-catenin, both known to be involved in leukemogenesis.
|
18536571 |
2008 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Point mutations in the gene for the granulocyte colony-stimulating factor (G-CSF) receptor CSF3R have been implicated in the progression of severe congenital neutropenia (CN) to leukemia.
|
16985178 |
2007 |
leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Granulocyte colony-stimulating factor and its receptor in normal myeloid cell development, leukemia and related blood cell disorders.
|
17127321 |
2007 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study reveals that cases showing remission after treatment with G-CSF mostly had leukemia with AML1/ETO rearrangement.
|
16791271 |
2006 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Owing to their particular susceptibility to infections, patients with severe congenital neutropenia had the strongest exposure to G-CSF; the risk of leukemia increased with the degree of G-CSF exposure in this subgroup.
|
15642668 |
2005 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In addition to the ability of G-CSF to stimulate the maturation and function of granulocytes, experimental and clinical evidence suggests that induction of leukemia cell differentiation may also be possible.
|
15203865 |
2004 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Finally, in the PLZF-RARalpha acute promyelocytic leukemia transgenic model, G-CSF deficiency suppressed leukemia development.
|
15223604 |
2004 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
G-CSF-primed haploidentical marrow transplantation without ex vivo T cell depletion: an excellent alternative for high-risk leukemia.
|
12476277 |
2002 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We compared transduction of autologous B-cell lines and granulocyte colony-stimulating factor-mobilized peripheral CD34(+) cells from these patients using an MFGS retrovirus vector containing the gamma(c) gene IL2RG pseudotyped with amphotropic, gibbon ape leukemia virus, or RD114 envelopes.
|
12070011 |
2002 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Optimization of gene transfer into primitive human hematopoietic cells of granulocyte-colony stimulating factor-mobilized peripheral blood using low-dose cytokines and comparison of a gibbon ape leukemia virus versus an RD114-pseudotyped retroviral vector.
|
12162814 |
2002 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We studied nine patients affected by chronic myeloid leukemia (CML Ph+ and bcr-abl positive) and treated with alpha-interferon (alpha-INF) in order to: first, to evaluate the feasibility of a mobilization of peripheral blood stem cells induced by granulocyte-colony-stimulating factor (G-CSF) and the contamination by Ph+ cells and second, to quantify the amount of bcr-abl leukemia associated transcript by a quantitative assay during mobilization procedures, and post mobilization follow-up.
|
10975389 |
2000 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Spontaneous remission of granulocyte colony-stimulating factor-associated leukemia in a child with severe congenital neutropenia.
|
11071667 |
2000 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The presence of G-CSF receptors was demonstrated in 4/14 (29%) patients, two with ALL, one with CLL, and one with CML-LBC, and was associated with stimulation of leukemia clonogenic cell growth by G-CSF.
|
10803934 |
2000 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Nevertheless, DAB486-G-CSF may be included with the increasing number of other toxin-hormone fusion proteins whose toxicity is directed towards specific receptor-bearing cells, and may represent a novel approach towards the study and treatment of leukemia.
|
7505148 |
1993 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
This property of G-CSF has led to suggestions that its absence is responsible for lack of differentiation of leukemic cells and that the therapeutic administration of G-CSF could reverse this defect and result in a cure for leukemia.
|
2448221 |
1988 |