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Genome-wide H3K27acetylation ChIP-seq in CALM-AF10 On and Off AML cells

ABSTRACT: We report calling of super-enhancers in CALM-AF10 mouse AML cells where the fusion is either on (DMSO) or turned off (using Doxycycline).

ORGANISM(S): Mus musculus

PROVIDER: GSE164182 | GEO | 2021/01/05

REPOSITORIES: GEO

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CALM-AF10 T-ALL

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

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CRISPR Screening for CALM-AF10 interactome and transcriptional targets

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.

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Identification of a Potently Oncogenic CALM-AF10 Minimal-Fusion Mutant (mRNA)

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.

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Identification of a Potently Oncogenic CALM-AF10 Minimal-Fusion Mutant (miRNA)

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Expression Profiling of a CALM/AF10 leukemia mouse model

Project description:Expression profiling of three cell populations of a CALM/AF10 leukemia mouse model Keywords: expression profiling

2006-07-20 | GSE5030 | GEO

Identification of a Potently Oncogenic CALM-AF10 Minimal-Fusion Mutant (miRNA)

2011-10-04 | E-GEOD-27512 | biostudies-arrayexpress

Identification of a Potently Oncogenic CALM-AF10 Minimal-Fusion Mutant (mRNA)

2011-10-04 | E-GEOD-27513 | biostudies-arrayexpress

Identification of a Potently Oncogenic CALM-AF10 Minimal-Fusion Mutant

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

Transcription profiling of human CALM-AF10 positive and negative T-ALL samples

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

Tissue and differentiation stage specific expression of CALM/AF10 is required for leukemogenesis

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

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