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PICALM::MLLT10 translocated leukemia.
John M Cullen1, Antonia C Nakatsugawa1, Natalie Barton1
1Department of Pediatrics, University of Vermont Larner College of Medicine, Burlington, USA.
FEBS Letters
|January 14, 2026
Summary
The PICALM::MLLT10 chromosomal translocation drives acute leukemia through epigenetic changes. Targeting this leukemia with venetoclax shows promising results, offering new hope for patients.
Area of Science:
- Hematology
- Oncology
- Molecular Biology
Background:
- The t(10;11)(p13;q14-21) translocation creates the CALM-AF10 fusion oncoprotein, a key driver in acute myeloid and T-lymphoblastic leukemia.
- This leukemia subtype is characterized by epigenetic dysregulation, including global hypomethylation leading to genomic instability and focal H3K79 hypermethylation driving proliferation.
Purpose of the Study:
- To provide an updated overview of the pathophysiology, clinical presentation, prognosis, and treatment of PICALM::MLLT10 acute leukemia.
- To highlight potential therapeutic targets based on a deeper biological understanding of the disease.
Main Methods:
- Review of existing literature and patient data.
- Analysis of the molecular mechanisms driving PICALM::MLLT10 leukemia, including epigenetic alterations and protein interactions.
- Evaluation of recent therapeutic interventions, such as venetoclax treatment.
Main Results:
- PICALM::MLLT10 leukemia exhibits distinct epigenetic features influencing genomic stability and gene expression.
- The translocation is associated with a poor prognosis and chemotherapy resistance.
- Recent studies show promising efficacy of venetoclax, a BCL2 inhibitor, in treating PICALM::MLLT10 acute leukemia.
Conclusions:
- PICALM::MLLT10 acute leukemia is an epigenetically driven malignancy with specific clinical and prognostic implications.
- Emerging therapeutic strategies, including targeted therapies like venetoclax, offer new treatment avenues for this challenging leukemia subtype.
