TAL1 activation in T-cell acute lymphoblastic leukemia: a novel oncogenic 3’ neo-enhancer
Open accessAbstract
T-cell acute lymphocytic leukemia protein 1 (TAL1) is one of the most frequently deregulated oncogenes in T-cell acute lymphoblastic leukemia (T-ALL). Its deregulation can occur through diverse cis-alterations, including SIL-TAL1 microdeletions, translocations with T-cell Receptor loci, and more recently described upstream intergenic non-coding mutations. These mutations consist of recurrent focal microinsertions that create an oncogenic neo-enhancer accompanied by activating epigenetic marks. This observation laid the groundwork for an innovative paradigm concerning the activation of proto-oncogenes via genomic alterations of non-coding intergenic regions. However, for the majority of T-ALL expressing TAL1 (TAL1+), the deregulation mechanism remains 'unresolved'. We took advantage of H3K27ac and H3K4me3 chromatin immunoprecipitation sequencing data of eight cases of T-ALL, including five TAL1+ cases. We identified a putative novel oncogenic neo-enhancer downstream of TAL1 in an unresolved monoallelic TAL1+ case. A rare but recurrent somatic heterozygous microinsertion within this region creates a de novo binding site for MYB transcription factor. Here we demonstrate that this mutation leads to increased enhancer activity, gain of active epigenetic marks, and TAL1 activation via recruitment of MYB. These results highlight the diversity of non-coding mutations that can drive oncogene activation.
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Three groups of gain-of-function mutations affecting TAL1 in T-ALL-a cluster of 5′ neo-enhancer mutations upstream of TAL1 TSS, an intronic SNV and a 3′ neo-enhancer-converge on a common mechanism of upregulation of the TAL1 oncogene.
“We evaluated three groups of gain-of-function mutations affecting the TAL1 gene in T cell acute lymphoblastic leukaemia (T-ALL): a cluster of 5′ neo-enhancer mutations upstream of the TAL1 TSS6,33, an intronic single-nucleotide variant (SNV)34 and a 3′ neo-enhancer35.”
From Advancing regulatory variant effect prediction with AlphaGenome (2026) · cites this paper as [35]
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- Authors
- Smith, C., Goyal, A., Weichenhan, D., Allemand, E., Mayakonda, A., Toprak, U., Riedel, A., Balducci, E., Manojkumar, M., Pejkovska, A., Mücke, O., Sollier, E., Bakr, A., Breuer, K., Lutsik, P., Hermine, O., Spicuglia, S., Asnafi, V., Plass, C., & Touzart, A.
- Affiliations
- Hôpital Necker-Enfants Malades (FR)
- German Cancer Research Center (DE)
- Inserm (FR)
- Corresponding author
- Smith, Charlotte
- Goyal, Ashish
- Plass, Christoph
- Touzart, Aurore
- ORCID
- Venue
- Haematologica
- Published
- 2023-01-12
- Volume
- 108
- Issue
- 5
- Pages
- 1259-1271
- ISSN
- 0390-6078 (ISSN-L)
- 1592-8721
- PMC
- PMC10153542
- OpenAlex
- W4315752846
- Cited by
- 30
- References
- 40
- Citations by year
- 2026: 8 · 2025: 10 · 2024: 7 · 2023: 5
- FWCI
- 7.68
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Haematologica (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by-nc)
- Lirias (submittedVersion, cc-by-nc)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Deutsches Krebsforschungszentrum
- Institut des maladies génétiques Imagine
- Agence Nationale de la Recherche (ANR-21-CE17-0014, CE17-0014)
- Fondation pour la Recherche Médicale (FDT202012010638)
- Ligue Contre le Cancer
- Institut National Du Cancer (PLBIO_2018, PLBIO18)
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Acute Lymphoblastic Leukemia research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- TAL1, T-cell acute lymphoblastic leukemia, MYB binding site, non-coding mutations, H3K27ac, H3K4me3, enhancer activity, proto-oncogene activation, epigenetic modifications
- MeSH terms
- T-Cell Acute Lymphocytic Leukemia Protein 1, Enhancer Elements, Genetic, Humans, Mutation, T-Lymphocytes, Transcription Factors, Oncogene Proteins, Fusion, Basic Helix-Loop-Helix Proteins, Basic Helix-Loop-Helix Transcription Factors, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
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