ArticleLeukemia2005
CALM-AF10+ T-ALL expression profiles are characterized by overexpression of HOXA and BMI1 oncogenes.
Article in Leukemia, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.
- Identification of interconnected markers for T-cell acute lymphoblastic leukemia.BioMed research international · 2013Pooled it
- The prognosis of CALM-AF10-positive adult T-cell acute lymphoblastic leukemias depends on the stage of maturation arrest.Haematologica · 2013Trial
- Insertional oncogenesis in 4 patients after retrovirus-mediated gene therapy of SCID-X1.The Journal of clinical investigation · 2008Trial
- Beyond nuclear export: chromatin-bound XPO1/CRM1 as a transcriptional scaffold.International journal of hematology · 2026Review
- Article
- PICALM::MLLT10 translocated leukemia.FEBS letters · 2026Review
- CTCF Is Essential for the Development and Maintenance of CALM-AF10-Induced Leukemia.Cancer science · 2025Article
- 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
- Depletion of the RNA binding protein QKI and circular RNA dysregulation in T-cell acute lymphoblastic leukemia.Haematologica · 2025Article
- Targeting Menin in Acute Myeloid Leukemia: Therapeutic Advances and Future Directions.Cancers · 2024Review
- Article
- Acute myeloid leukemia with rare recurring translocations-an overview of the entities included in the international consensus classification.Annals of hematology · 2024Review
- TAL1 activation in T-cell acute lymphoblastic leukemia: a novel oncogenic 3' neo-enhancer.Haematologica · 2023Article
- Clinico-biological features of T-cell acute lymphoblastic leukemia with fusion proteins.Blood cancer journal · 2022Article
- Novel Diagnostic and Therapeutic Options forFrontiers in pharmacology · 2022Article
- Review
- Review
- CXCR4 Mediates Enhanced Cell Migration inFrontiers in oncology · 2021Article
- Blueprint of human thymopoiesis reveals molecular mechanisms of stage-specific TCR enhancer activation.The Journal of experimental medicine · 2020Article
- The SQSTM1-NUP214 fusion protein interacts with Crm1, activates Hoxa and Meis1 genes, and drives leukemogenesis in mice.PloS one · 2020Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 compared to mixed lineage leukemia-translocated acute leukemias (MLL-t AL). The overexpression of HOXA genes was associated with overexpression of its cofactor MEIS1 in CALM-AF10+ T-ALL, reaching levels of expression similar to those observed in MLL-t AL. Consequently, CALM-AF10+ T-ALL and MLL-t AL share a specific HOXA overexpression, indicating they activate common oncogenic pathways. In addition, BMI1, located close to AF10 breakpoint, was overexpressed only in CALM-AF10+ T-ALL and not in MLL-t AL. BMI1 controls cellular proliferation through suppression of the tumor suppressors encoded by the CDKN2A locus. This locus, often deleted in T-ALL, was conserved in CALM-AF10+ T-ALL. This suggests that decreased CDKN2A activity, as a result of BMI1 overexpression, contributes to leukemogenesis in CALM-AF10+ T-ALL. We propose to define a HOXA+ leukemia group composed of at least MLL-t, CALM-AF10 and HOXA-t AL, which may benefit from adapted management.
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