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AML patient granulocyte macrophage progenitor (GMP) cells

ABSTRACT: AML patient GMPs or CMPs were FACS sorted as described in Supplementary Information (Reckzeh, K et al. 2020) TET2 deficiency cooperates with CBFB-MYH11 to induce acute myeloid leukemia and represents an early leukemogenic event. Reckzeh, K et al

ORGANISM(S): Homo sapiens

PROVIDER: GSE161391 | GEO | 2022/03/28

REPOSITORIES: GEO

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Mouse inv(16):TET2ko granulocyte macrophage progenitor (GMP) cells

Project description:inv(16)/Tet2-/- GMPs (Lin- Sca1- ckit+ CD41- FcgR+ CD150-) were FACS sorted as described in Supplementary Information (Reckzeh, K et al 2020) TET2 deficiency cooperates with CBFB-MYH11 to induce acute myeloid leukemia and represents an early leukemogenic event. Reckzeh, K et al.

2022-03-28 | GSE161390 | GEO

AML patient granulocyte macrophage progenitor (GMP) cells [human]

Project description:AML patient GMPs or CMPs were FACS sorted as described in material and methods from supplementary data (Estruch M et al 2020)

2020-11-09 | GSE150159 | GEO

WT and inv(16)/KITD816Y granulocyte macrophage progenitor (GMP) cells [mouse]

Project description:WT GMPs (Lin- IL7R- Sca1- ckit+ FcgRhiCD34+) and inv(16)/KITD816Y GMPs (Lin- Sca1- ckit+ CD41- FcgR+ CD150-) were FACS sorted as described in material and methods from supplementary data (Estruch M et al 2020)

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Identification of STAT5 target genes in human CB HSC, CMP, GMP and MEP

Project description:CB CD34+ cells were isolated by Miltenyi miniMACS column. Cells were prestimulated in HPGM with 100 ng/ml KITL, FLT#L and TPO for 48 hrs. Cells were transduced with control MiNR1 or STAT5A-ER in three rounds over 48 hrs. Hematopoietic stem cells (HSCs), common myeloid progenitors (CMPs), granulocyte/macrophage progenitors (GMPs), and megakaryocyte/erythroid progenitors (MEPs) were sorted (for details see Blood 2011, Fatrai et al). cells were stimulated with 100 ng/ml 4OHT for 24 hrs after which RNA was isolated for Illumina beadhchiop arrays HT12 v3 CB CD34+ cells were isolated by Miltenyi miniMACS column. Cells were prestimulated in HPGM with 100 ng/ml KITL, FLT#L and TPO for 48 hrs. Cells were transduced with control MiNR1 or STAT5A-ER in three rounds over 48 hrs. Hematopoietic stem cells (HSCs), common myeloid progenitors (CMPs), granulocyte/macrophage progenitors (GMPs), and megakaryocyte/erythroid progenitors (MEPs) were sorted (for details see Blood 2011, Fatrai et al). cells were stimulated with 100 ng/ml 4OHT for 24 hrs after which RNA was isolated for Illumina beadhchiop arrays HT12 v3

2011-01-22 | E-GEOD-26775 | biostudies-arrayexpress

Identification of STAT5 target genes in human CB HSC, CMP, GMP and MEP

2011-01-22 | GSE26775 | GEO

Cbfb/Runx1-repression independent blockage of differentiation and accumulation of Csf2rb expressing cells by Cbfb-MYH11

Project description:It is known that CBFB-MYH11, the fusion gene generated by inversion of chromosome 16 in human acute myeloid leukemia, is causative for oncogenic transformation. However, the mechanism by which CBFB-MYH11 initiates leukemogenesis is not clear. Previously published reports showed that CBFB-MYH11 dominantly inhibits RUNX1 and CBFB, and such inhibition has been suggested as the mechanism for leukemogenesis. However, knockin mice expressing Cbfb-MYH11 (Cbfb+/MYH11) showed defects in primitive hematopoiesis not seen in Cbfb null (Cbfb-/-) embryos indicating that Cbfb-MYH11 has repression independent activities as well. To identify gene expression changes associated with this novel activity, we compared the gene expression profile in the blood cells of Cbfb+/MYH11 and Cbfb-/- embryonic day 12.5 (E12.5) embryos with that of their wildtype littermates. Cbfb-MYH11 chimeras were mated to C57/Bl6 females to generate Cbfb+/MYH11 (Cbfb+/MYH11) and Cbfb+/+ (WT) embryos. Cbfb+/- x Cbfb+/- matings were used to generate Cbfb+/+ (Cbfb+/+) and Cbfb-/- (Cbfb-/-) embryos. Blood from 8-10 E12.5 embryos of the same genotype was pooled, and RNA was isolated, labeled, and hybridized to Affymetrix Genechip mouse microarray (430 2.0) chips. 4 chips were used for both the Cbfb+/MYH11 and littermate control samples. 3 chips were used for the Cbfb-/- samples and littermate control samples.

2010-04-12 | E-GEOD-19194 | biostudies-arrayexpress

Cbfb/Runx1-repression independent blockage of differentiation and accumulation of Csf2rb expressing cells by Cbfb-MYH11

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2021-02-04 | GSE166065 | GEO

Expression data from wild type, CBFB-MYH11-overexpressing, DNMT3A knockdown and RUNX1 knockdown K562 cells

Project description:We searched for genes which are mutated in a manner that is linked with gene mutations involved in DNA de/methylation in AML. We found that recurrent CBFB-MYH11 fusions, which result in the expression of fusion protein comprising core-binding factor β (CBFB) and myosin heavy chain 11 (MYH11), occur mutually exclusively with DNMT3A mutations. The CBFB-MYH11 fusion tumors show DNA hypomethylation patterns similar to cancers with loss-of-function mutation of DNMT3A. Expression of CBFB-MYH11 fusion protein or inhibition of DNMT3A similarly impairs the methylation and expression of target genes of Runt related transcription factor 1 (RUNX1), a functional partner of CBFB. We demonstrate that RUNX1 directly interacts with DNMT3A and that CBFB-MYH11 fusion protein sequesters RUNX1 in the cytoplasm, thereby preventing RUNX1 from interacting with and recruiting DNMT3A to its target genes. Our results identify a novel regulation of DNA methylation and provide a molecular basis how CBFB-MYH11 fusion contributes to leukemogenesis.

2021-04-13 | GSE169682 | GEO

Gata2 deficiency delays leukemogenesis while contributes to aggressive leukemia phenotype in Cbfb-MYH11 knockin mice

Project description:To clarify the role of Gata2 in the development of Cbfb-MYH11 induced leukemia, we generated conditional Cbfb-MYH11 knockin mice with Gata2 heterozygous knockout. Leukemic cells with Gata2 heterozygous knockout gained higher number of genetic mutations and showed more aggressive phenotype in both primary and transplanted recipient mice. We compared gene expression profilings between Gata2+/+ and Gata2+/f leukemic cells with Cbfb-MYH11.

2019-04-26 | GSE130343 | GEO

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