ArticleExperimental hematology2019
Acute myeloid leukemia driven by the CALM-AF10 fusion gene is dependent on BMI1.
Article in Experimental hematology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Genetic Variants of BMI1 (rs1042059 and rs11591377) and Their Potential Role in Leukemia Susceptibility: A Narrative Review.Health science reports · 2026Article
- PICALM::MLLT10 translocated leukemia.FEBS letters · 2026Review
- 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
- How CBX proteins regulate normal and leukemic blood cells.FEBS letters · 2024Review
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- Article
- The Crucial Roles of Bmi-1 in Cancer: Implications in Pathogenesis, Metastasis, Drug Resistance, and Targeted Therapies.International journal of molecular sciences · 2022Review
- The Systematic Analyses of RING Finger Gene Signature for Predicting the Prognosis of Patients with Hepatocellular Carcinoma.Journal of oncology · 2022Article
- Zebrafish models of acute leukemias: Current models and future directions.Wiley interdisciplinary reviews. Developmental biology · 2021Review
- A JAK/STAT-mediated inflammatory signaling cascade drives oncogenesis in AF10-rearranged AML.Blood · 2021Article
- Article
- Successful treatment of T/myeloid mixed-phenotype acute leukemia with the translocation (10;11)(p13;q14)Clinical case reports · 2021Article
- Genome-Wide DNA Methylation Profiles in Community Members Exposed to the World Trade Center Disaster.International journal of environmental research and public health · 2020Article
Corrections and comments
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Authors and funding
11 authors at 8 institutions in 3 countries.
Funding
Abstract
A subset of acute myeloid and lymphoid leukemia cases harbor a t(10;11)(p13;q14) translocation resulting in the CALM-AF10 fusion gene. Standard chemotherapeutic strategies are often ineffective in treating patients with CALM-AF10 fusions. Hence, there is an urgent need to identify molecular pathways dysregulated in CALM-AF10-positive leukemias which may lay the foundation for novel targeted therapies. Here we demonstrate that the Polycomb Repressive Complex 1 gene BMI1 is consistently overexpressed in adult and pediatric CALM-AF10-positive leukemias. We demonstrate that genetic Bmi1 depletion abrogates CALM-AF10-mediated transformation of murine hematopoietic stem and progenitor cells (HSPCs). Furthermore, CALM-AF10-positive murine and human AML cells are sensitive to the small-molecule BMI1 inhibitor PTC-209 as well as to PTC-596, a compound in clinical development that has been shown to result in downstream degradation of BMI1 protein. PTC-596 significantly prolongs survival of mice injected with a human CALM-AF10 cell line in a xenograft assay. In summary, these results validate BMI1 as a bona fide candidate for therapeutic targeting in AML with CALM-AF10 rearrangements.
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