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TranscriptomicsGfi1 as a new predictive and therapeutical target of MDS/AML
MDS is characterized by a disturbed function of the myeloid lineage of the hematopoietic system that may transform to AML, a malignant disease of the myeloid compartment. Epigenetic and genetic aberrations contribute to the initiation and progression of MDS/AML. GFI1 is a transcriptional repressor, ...
ORGANISM(S): Mus musculus 
2016-07-31 | E-GEOD-72489 | biostudies-arrayexpress
TranscriptomicsEffect of loss of Gfi1b on hematopietic stem cells
Using Gfi1b conditional mice, deletion of gfi1b in the hematopietic system was induced by injecting MxCre tg Gfi1bfl/fl mice with pIpC. 30 days after injection, Cd150 pos, Cd 48 neg, Lin neg Sca and c-kit pos stem cells were sortrted from Gfi1bfl/fl and Mxcre tg Gfi1bfl/fl mice and analysed. We used...
ORGANISM(S): Mus musculus 
2010-09-03 | E-GEOD-20655 | biostudies-arrayexpress
GenomicsThe Growth factor independence 1 (GFI1) 36N variant predisposes to Acute Myeloid Leukemia (AML) by inducing epigenetic changes at the Hoxa9 locus
GFI136N is a coding Single Nucleotide Polymorphism (SNP) in the gene GFI1 that increases the risk for Acute myeloid leukemia (AML) by 60%. It is present in 3-5% of Caucasians and has a prevalence of 12% among AML patients. We generated knockin mice expressing either the human GFI136N variant or the ...
ORGANISM(S): Mus musculus 
2012-12-04 | E-GEOD-31657 | biostudies-arrayexpress
TranscriptomicsExpression data from bone marrow derived granulocyte monocyte precursors (GMPs) from wt -, Gfi1 knock-out -, human-Gfi1-SNP36N knock in and human wt-Gfi1 knock in mice
The incidence of cancer is not only influenced by exposure to environmental factors such as toxic substances and chemotherapy, but is also a result of individual predispositions. Single Nucleotide Polymorphisms (SNPs) represent one such individual predisposition to cancer1. Gfi136N is a SNP in the c...
ORGANISM(S): Mus musculus 
2012-11-22 | E-GEOD-25551 | biostudies-arrayexpress
TranscriptomicsGrowth factor independence 1 (Gfi1) as a new target for leukemia therapy
Using (conditional) Gfi1 knock-out mice we show that ablation of the transcriptional repressor Gfi1 cures mice from lymphoid leukemia and reduces the expansion of primary human T-ALL xenografts in mice. We find that Gfi1 alters the p53 dependent transcriptional activation of a substantial subset of ...
ORGANISM(S): Mus musculus 
2012-10-03 | E-GEOD-32910 | biostudies-arrayexpress
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