ArticleLeukemia2011
The clathrin-binding domain of CALM and the OM-LZ domain of AF10 are sufficient to induce acute myeloid leukemia in mice.
Article in Leukemia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Evolution of distinct subclones in a CALM-AF10-driven AML murine model results in leukemias with different phenotypes.Blood neoplasia · 2026Article
- PICALM::MLLT10 translocated leukemia.FEBS letters · 2026Review
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- Observation of PICALM::MLLT10-rearrangement and coincidental EZH2 mutations in a patient with acute myeloid leukemia: A case report and review of the literature.BJC reports · 2025Article
- Monocytic Differentiation of Human Acute Myeloid Leukemia Cells: A Proteomic and Phosphoproteomic Comparison of FAB-M4/M5 Patients with and without Nucleophosmin 1 Mutations.International journal of molecular sciences · 2024Article
- Challenging our understanding of B-cell lymphomagenesis and risk: Paediatric high-grade B-cell lymphoma, not otherwise specified with a DDX3X::MLLT10 fusion and an IGH deletion.Pediatric blood & cancer · 2024Article
- MOZ/ENL complex is a recruiting factor of leukemic AF10 fusion proteins.Nature communications · 2023Article
- Childhood acute myeloid leukemia with 5q deletion and HNRNPH1-MLLT10 fusion: the first case report.Blood advances · 2022Article
- Targeting the histone H3 lysine 79 methyltransferase DOT1L in MLL-rearranged leukemias.Journal of hematology & oncology · 2022Review
- Clinico-biological features of T-cell acute lymphoblastic leukemia with fusion proteins.Blood cancer journal · 2022Article
- The role of the PZP domain of AF10 in acute leukemia driven by AF10 translocations.Nature communications · 2021Article
- Specific patterns of H3K79 methylation influence genetic interaction of oncogenes in AML.Blood advances · 2020Article
- Article
- Acute myeloid leukemia driven by the CALM-AF10 fusion gene is dependent on BMI1.Experimental hematology · 2019Article
- Article
- The upstreams and downstreams of H3K79 methylation by DOT1L.Chromosoma · 2016Review
- The target cell of transformation is distinct from the leukemia stem cell in murine CALM/AF10 leukemia models.Leukemia · 2016Article
- Article
- Nuclear export signal within CALM is necessary for CALM-AF10-induced leukemia.Cancer science · 2014Article
- A CALM-derived nuclear export signal is essential for CALM-AF10-mediated leukemogenesis.Blood · 2013Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
The t(10;11)(p13-14;q14-21) translocation, giving rise to the CALM-AF10 fusion gene, is a recurrent chromosomal rearrangement observed in patients with poor prognosis acute myeloid leukemia (AML). Although splicing of the CALM-AF10 fusion transcripts has been described in AML patients, the contribution of different CALM and AF10 domains to in vivo leukemogenesis remains to be defined. We therefore performed detailed structure-function studies of the CALM-AF10 fusion protein. We demonstrate that fusion of the C-terminal 248 amino acids of CALM, which include the clathrin-binding domain, to the octapeptide motif-leucine-zipper (OM-LZ) domain of AF10 generated a fusion protein (termed CALM-AF10 minimal fusion (MF)), with strikingly enhanced transformation capabilities in colony assays, providing an efficient system for the expeditious assessment of CALM-AF10-mediated transformation. Leukemias induced by the CALM-AF10 (MF) mutant recapitulated multiple aspects of full-length CALM-AF10-induced leukemia, including aberrant Hoxa cluster upregulation, a characteristic molecular lesion of CALM-AF10 leukemias. In summary, this study indicates that collaboration of the clathrin-binding and the OM-LZ domains of CALM-AF10 is sufficient to induce AML. These findings further suggest that future approaches to antagonize CALM-AF10-induced transformation should incorporate strategies, which aim at blocking these key domains.
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