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Characterization of leukemia progression in the Cbfb-MYH11 knockin mice by single cell RNA sequencing

ABSTRACT: Characterization of leukemia progression in the Cbfb-MYH11 knockin mice by single cell RNA sequencing

PROVIDER: PRJNA906630 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22452600.fastq.gz	Fastqsanger.gz
	SRR22452601.fastq.gz	Fastqsanger.gz
	SRR22452602.fastq.gz	Fastqsanger.gz
	SRR22452579.fastq.gz	Fastqsanger.gz
	SRR22452580.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

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

2010-03-31 | GSE19194 | GEO

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

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

| PRJNA535600 | ENA

CHD7 deficiency delays leukemogenesis in mice induced by CBFB-MYH11

Project description:CHD7 interacts with CBFb-SMMHC through RUNX1 and modulates their gene expression regulation and is important for CBFB-MYH11 leukemogenesis in the mouse model.

2018-08-08 | GSE102388 | 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

Characterization of leukemia progression in the Cbfb-MYH11 knockin mice by single cell RNA sequencing

Project description:We used single cell RNA-sequencing to investigate the expression changes during the progression of leukemia in a conditional knock-in mouse model.

2023-07-03 | GSE219043 | GEO

inv(16)/t(16;16) acute myeloid leukemia with non-type A CBFB-MYH11 fusions associate with distinct clinical and genetic features and lack KIT mutations

Project description:The inv(16)(p13q22)/t(16;16)(p13;q22) in acute myeloid leukemia results in multiple CBFB-MYH11 fusion transcripts, with type A being most frequent. The biologic and prognostic implications of different fusions are unclear. We analyzed CBFB-MYH11 fusion types in 208 inv(16)/t(16;16) patients with de novo disease, and compared clinical and cytogenetic features and KIT mutation status between type A (n=182; 87%) and non-type A (n=26; 13%) patients. We derived a fusion-type-associated gene- global expression profile. Gene Ontology analysis of the differentially expressed genes revealed - among others - an enrichment of up-regulated genes involved in activation of caspase activity, cell differentiation and cell cycle control in non-type A patients.

2013-01-23 | E-MTAB-1356 | biostudies-arrayexpress

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

Project description:Inversion of chromosome 16 (inv(16)) generates a fusion gene CBFB-MYH11, which is a driver mutation for acute myeloid leukemia (AML). Gene expression profiling suggests that Gata2, a hematopoietic transcription factor, is a top upregulated gene in preleukemic Cbfb-MYH11 knockin mice and is expressed in human inv(16) AML. On the other hand, we have also identified recurrent monoallelic deletions of GATA2 in relapsed human CBF-AML patients. To clarify the role of Gata2 in leukemogenesis by Cbfb-MYH11, we generated conditional Cbfb-MYH11 knockin mice with Gata2 heterozygous knockout. Gata2 heterozygous knockout reduced abnormal myeloid progenitors, which are capable of inducing leukemia in the Cbfb-MYH11 mice. Consequently, Cbfb-MYH11 mice with Gata2 heterozygous knockout developed leukemia with longer latencies than those with intact Gata2. Interestingly, leukemic cells with Gata2 heterozygous knockout gained higher number of mutations and showed more aggressive phenotype in both primary and transplanted mice. Moreover, leukemic cells with Gata2 heterozygous knockout showed higher repopulating capacity in competitive transplantation experiments. In summary, reduction of Gata2 activity affects mutational dynamics of leukemia with delayed leukemia onset in Cbfb-MYH11 knockin mice, but paradoxically results in a more aggressive leukemia phenotype, which may be correlated with leukemia relapse or poor prognosis in human patients.

| S-EPMC7056539 | biostudies-literature

Gene expression differences between leukemic cells from Mx1-Cre, Cbfb+/56M and Chd7f/f, Mx1-Cre, Cbfb+/56M mice by microarray

Project description:Results showed that Chd7 deficiency delay Cbfb-MYH11 induced leukemia, to explore the mechanism, We also performed microarray analysis on c-Kit+ leukemic cells to determine gene expression differences between Mx1-Cre, Cbfb+/56M and Chd7f/f, Mx1-Cre, Cbfb+/56M leukemic cells.

2018-02-14 | GSE103367 | GEO

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