Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA141749 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE27512: Identification of a Potently Oncogenic CALM-AF10 Minimal-Fusion Mutant (miRNA) GSE27513: Identification of a Potently Oncogenic CALM-AF10 Minimal-Fusion Mutant (mRNA) Refer to individual Series
2011-10-04 | E-GEOD-27514 | biostudies-arrayexpress
Project description:Identification of a Potently Oncogenic CALM-AF10 Minimal-Fusion Mutant (miRNA)
| PRJNA141867 | ENA
Project description:The t(10;11) p (13;q14) translocation, giving rise to CALM-AF10, is a recurring chromosomal translocation observed in several types of acute leukemias as well as in lymphoma. We have previously demonstrated that the expression of the human CALM/AF10 fusion gene in murine bone marrow stem and progenitor cells results in an aggressive acute myeloid leukemia in vivo. In this study, we have screened the various domains essential for CALM-AF10 function and leukemogenicity. Our study identifies a mutant of CALM-AF10 that greatly enhances the clonogenic potential of hematopoietic progenitors while retaining key characteristics of disease induced by the full length CALM-AF10 fusion.
2011-10-05 | GSE27513 | GEO
Project description:The t(10;11) p (13;q14) translocation, giving rise to CALM-AF10, is a recurring chromosomal translocation observed in several types of acute leukemias as well as in lymphoma. We have previously demonstrated that the expression of the human CALM/AF10 fusion gene in murine bone marrow stem and progenitor cells results in an aggressive acute myeloid leukemia in vivo. In this study, we have screened the various domains essential for CALM-AF10 function and leukemogenicity. Our study identifies a mutant of CALM-AF10 that greatly enhances the clonogenic potential of hematopoietic progenitors while retaining key characteristics of disease induced by the full length CALM-AF10 fusion.
2011-10-05 | GSE27512 | GEO
Project description:The t(10;11) p (13;q14) translocation, giving rise to CALM-AF10, is a recurring chromosomal translocation observed in several types of acute leukemias as well as in lymphoma. We have previously demonstrated that the expression of the human CALM/AF10 fusion gene in murine bone marrow stem and progenitor cells results in an aggressive acute myeloid leukemia in vivo. In this study, we have screened the various domains essential for CALM-AF10 function and leukemogenicity. Our study identifies a mutant of CALM-AF10 that greatly enhances the clonogenic potential of hematopoietic progenitors while retaining key characteristics of disease induced by the full length CALM-AF10 fusion. Global micro-RNA expression of bone marrow cells transduced with various constructs were compared. We used the empty vector, MIG, as a control and baseline. Four samples are tested with three biological replicates each.
2011-10-04 | E-GEOD-27512 | biostudies-arrayexpress
Project description:The t(10;11) p (13;q14) translocation, giving rise to CALM-AF10, is a recurring chromosomal translocation observed in several types of acute leukemias as well as in lymphoma. We have previously demonstrated that the expression of the human CALM/AF10 fusion gene in murine bone marrow stem and progenitor cells results in an aggressive acute myeloid leukemia in vivo. In this study, we have screened the various domains essential for CALM-AF10 function and leukemogenicity. Our study identifies a mutant of CALM-AF10 that greatly enhances the clonogenic potential of hematopoietic progenitors while retaining key characteristics of disease induced by the full length CALM-AF10 fusion. Global gene expression of bone marrow cells transduced with various constructs were compared. We used the empty vector, MIG, as a control and baseline. Four samples are tested with three biological replicates each.
2011-10-04 | E-GEOD-27513 | biostudies-arrayexpress
Project description:CALM (Clathrin Assembly Lymphoid Myeloid Leukemia)-AF10, a fusion gene frequently observed in acute myeloid leukemia (AML), is caused by the t(10;11)(q13;q14) translocation, and is associated with poor prognosis. In this study, we demonstrate that the CCCTC-binding factor (CTCF) is crucial for both the initiation and maintenance of CALM-AF10-induced AML (CALM-AF10 AML). To investigate the role of CTCF in CALM-AF10 AML, we used hematopoietic stem and progenitor cells (HSPCs) from conditional knockout (KO) mice and immortalized them by introducing the CALM-AF10 fusion gene to generate CALM-AF10 AML models. Our in vivo experiments revealed that CTCF deficiency significantly prolonged the survival of CALM-AF10 AML mice. Similarly, in vitro analyses showed that CTCF KO inhibited the colony-forming ability of CALM-AF10 AML cells and induced differentiation into macrophage-like cells. RNA sequencing (RNA-seq) of CTCF KO cells identified that the most downregulated gene was Transglutaminase 2 (TGM2). Chromatin immunoprecipitation followed by sequencing (ChIP-seq) showed that increase in levels of trimethylation of histone H3K27 as well as decrease in levels of trimethylation of histone H3K4 and acetylation of histone H3K27 were observed at the transcription start site (TSS) of the Tgm2 gene after CTCF KO. Knocking down (KD) TGM2 using small hairpin RNA (shRNA) in both CALM-AF10 AML cells and the human leukemic cell line U937, which expresses the CALM-AF10 fusion gene, resulted in reduced colony-forming ability and cell proliferation, alongside differentiation into macrophage-like cells. These results mirrored those observed with CTCF KO. Furthermore, treatment with GK921, a TGM2 inhibitor, yielded similar effects. Taken together, our findings suggest that CTCF regulates the expression of TGM2 by altering histone modifications at its TSS, thereby contributing to the maintenance of the undifferentiated state in CALM-AF10 AML. Given the efficacy of TGM2 inhibitors, such as GK921, against CALM-AF10 AML, TGM2 represents a promising therapeutic target for this leukemia subtype.
2025-12-03 | GSE281045 | GEO
Project description:CALM (Clathrin Assembly Lymphoid Myeloid Leukemia)-AF10, a fusion gene frequently observed in acute myeloid leukemia (AML), is caused by the t(10;11)(q13;q14) translocation, and is associated with poor prognosis. In this study, we demonstrate that the CCCTC-binding factor (CTCF) is crucial for both the initiation and maintenance of CALM-AF10-induced AML (CALM-AF10 AML). To investigate the role of CTCF in CALM-AF10 AML, we used hematopoietic stem and progenitor cells (HSPCs) from conditional knockout (KO) mice and immortalized them by introducing the CALM-AF10 fusion gene to generate CALM-AF10 AML models. Our in vivo experiments revealed that CTCF deficiency significantly prolonged the survival of CALM-AF10 AML mice. Similarly, in vitro analyses showed that CTCF KO inhibited the colony-forming ability of CALM-AF10 AML cells and induced differentiation into macrophage-like cells. RNA sequencing (RNA-seq) of CTCF KO cells identified that the most downregulated gene was Transglutaminase 2 (TGM2). Chromatin immunoprecipitation followed by sequencing (ChIP-seq) showed that increase in levels of trimethylation of histone H3K27 as well as decrease in levels of trimethylation of histone H3K4 and acetylation of histone H3K27 were observed at the transcription start site (TSS) of the Tgm2 gene after CTCF KO. Knocking down (KD) TGM2 using small hairpin RNA (shRNA) in both CALM-AF10 AML cells and the human leukemic cell line U937, which expresses the CALM-AF10 fusion gene, resulted in reduced colony-forming ability and cell proliferation, alongside differentiation into macrophage-like cells. These results mirrored those observed with CTCF KO. Furthermore, treatment with GK921, a TGM2 inhibitor, yielded similar effects. Taken together, our findings suggest that CTCF regulates the expression of TGM2 by altering histone modifications at its TSS, thereby contributing to the maintenance of the undifferentiated state in CALM-AF10 AML. Given the efficacy of TGM2 inhibitors, such as GK921, against CALM-AF10 AML, TGM2 represents a promising therapeutic target for this leukemia subtype.
2025-12-03 | GSE281044 | GEO
Project description:CALM (Clathrin Assembly Lymphoid Myeloid Leukemia)-AF10, a fusion gene frequently observed in acute myeloid leukemia (AML), is caused by the t(10;11)(q13;q14) translocation, and is associated with poor prognosis. In this study, we demonstrate that the CCCTC-binding factor (CTCF) is crucial for both the initiation and maintenance of CALM-AF10-induced AML (CALM-AF10 AML). To investigate the role of CTCF in CALM-AF10 AML, we used hematopoietic stem and progenitor cells (HSPCs) from conditional knockout (KO) mice and immortalized them by introducing the CALM-AF10 fusion gene to generate CALM-AF10 AML models. Our in vivo experiments revealed that CTCF deficiency significantly prolonged the survival of CALM-AF10 AML mice. Similarly, in vitro analyses showed that CTCF KO inhibited the colony-forming ability of CALM-AF10 AML cells and induced differentiation into macrophage-like cells. RNA sequencing (RNA-seq) of CTCF KO cells identified that the most downregulated gene was Transglutaminase 2 (TGM2). Chromatin immunoprecipitation followed by sequencing (ChIP-seq) showed that increase in levels of trimethylation of histone H3K27 as well as decrease in levels of trimethylation of histone H3K4 and acetylation of histone H3K27 were observed at the transcription start site (TSS) of the Tgm2 gene after CTCF KO. Knocking down (KD) TGM2 using small hairpin RNA (shRNA) in both CALM-AF10 AML cells and the human leukemic cell line U937, which expresses the CALM-AF10 fusion gene, resulted in reduced colony-forming ability and cell proliferation, alongside differentiation into macrophage-like cells. These results mirrored those observed with CTCF KO. Furthermore, treatment with GK921, a TGM2 inhibitor, yielded similar effects. Taken together, our findings suggest that CTCF regulates the expression of TGM2 by altering histone modifications at its TSS, thereby contributing to the maintenance of the undifferentiated state in CALM-AF10 AML. Given the efficacy of TGM2 inhibitors, such as GK921, against CALM-AF10 AML, TGM2 represents a promising therapeutic target for this leukemia subtype.
2025-12-03 | GSE281043 | GEO