Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA91777 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:Comparison of a series of 6 CALM-AF10 positive T-ALL to a series of 17 CALM-AF10 negative T-ALL Keywords: ordered
2005-07-01 | GSE2117 | GEO
Project description:We performed pooled CRISPR screens to determine the whether the CALM-AF10 target genes and protein interactors identified by RNA-Seq and proteomics methods are functional dependencies for CALM-AF10-driven AML. We constructed a pooled CRISPR library of CALM-AF10 mouse target genes and interactors, and used it to transduce CALM-AF10 mouse AMLs. The cells were sampled at "Day 0" and kept in culture to determine in vitro dependencies at day 12. For in vivo screens, the input cell pool from day 0 was injected in mice and mice where sacrificed upon signs of AML disease, and the AML cells were harvested.
2021-01-05 | GSE164183 | GEO
Project description:Comparison of a series of 6 CALM-AF10 positive T-ALL to a series of 17 CALM-AF10 negative T-ALL
2007-08-30 | E-GEOD-2117 | 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 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:The translocation t(10,11)(p13;q14) resulting in the formation of the CALM/AF10 fusion gene is involved in various hematological malignancies including acute myeloid leukemia, T-cell acute lymphoblastic leukemia, and malignant lymphoma and is usually associated with poor prognosis. We established a knock-in mouse model allowing tissue-specific CALM/AF10 expression from the Rosa26 locus using a loxP-STOP-loxP cassette to study leukemic transformation by the CALM/AF10 fusion protein during hematopoiesis. vav-Cre induced pan-hematopoietic expression of the CALM/AF10 fusion gene led to acute leukemia with a median latency of 12 months. Leukemias were either myeloid or had myeloid feature and showed expression of the B cell marker B220. Gene expression profiling of leukemic bone marrow cells revealed the overexpression of Hoxa cluster genes and the Hox co-factor Meis1. The long latency to leukemia development suggested that additional, collaborative genetic lesions are required. We identified an average of 2 to 3 additional mutations per leukemia using whole-exome sequencing. When CALM/AF10 was expressed in the B lymphoid compartment using mb1-Cre or CD19-Cre inducer lines no leukemia development was observed. Our results indicate that CALM/AF10 needs to be expressed from the stem or early progenitor cell stage onward to permit the acquisition of additional mutations required for leukemic transformation.
2017-06-19 | GSE58853 | GEO
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:Purpose: The goals of this study are to compare transcriptomes after shutting off the CALM-AF10, MLL-AF10 and MLL-AF9 fusion proteins in mouse AML cells. Furthermore, we also perform transcriptomic experiments to assess the changes in transcripts upon JAK1 deletion in mouse CALM-AF10 AML. Methods: Mouse AMLs cells grown in Mouse leukemia medium (see below) were treated with DMSO (Tet-On) or 4ug/ul Doxycycline (Tet-Off) and RNA was isolated to perform RNA-seq. RNA for CALM-AF10, MLL-AF10 was poly-A selected and MLL-AF9, total RNA was used to make RNAseq libraries using the NEB RNAseq lbrary prep kit. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays Results: Using an optimized data analysis workflow, we mapped about 20 million sequence reads per sample to the mouse genome (build mm9) and 60 million reads for MLL-AF9 data. Data analysis with BWA and TopHat workflows revealed genes that are significantly changed after shutting off the fusions or after deleting Jak1 in CALM-AF10 Jak1 floxed cells using the Cre recombinase. Conclusions:
2021-01-05 | GSE164181 | GEO