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

ABSTRACT: Comparison of a series of 6 CALM-AF10 positive T-ALL to a series of 17 CALM-AF10 negative T-ALL

ORGANISM(S): Homo sapiens

SUBMITTER: Eric DELABESSE

PROVIDER: E-GEOD-2117 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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CALM-AF10+ T-ALL expression profiles are characterized by overexpression of HOXA and BMI1 oncogenes.

Dik W A WA Brahim W W Braun C C Asnafi V V Dastugue N N Bernard O A OA van Dongen J J M JJ Langerak A W AW Macintyre E A EA Delabesse E E

Leukemia 20051101 11

The t(10;11)(p13;q14-21) is found in T-ALL and acute myeloid leukemia and fuses CALM (Clathrin-Assembly protein-like Lymphoid-Myeloid leukaemia gene) to AF10. In order to gain insight into the transcriptional consequences of this fusion, microarray-based comparison of CALM-AF10+ vs CALM-AF10- T-ALL was performed. This analysis showed upregulation of HOXA5, HOXA9, HOXA10 and BMI1 in the CALM-AF10+ cases. Microarray results were validated by quantitative RT-PCR on an independent group of T-ALL and ...[more]

PMID: 16107895

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

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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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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.

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RNA_seq Analysis of Murine Leukemias for Identifying Potential Leukemia Fusion Targets and JAK1 regulated genes

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Homo sapiens

Project description:CALM-AF10 T-ALL

| PRJNA91777 | ENA