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    GENE:

    MLLT3 (MLLT3 Super Elongation Complex Subunit)

    i
    Other names: MLLT3, MLLT3 Super Elongation Complex Subunit, Myeloid/Lymphoid Or Mixed-Lineage Leukemia Translocated To Chromosome 3 Protein, ALL1-Fused Gene From Chromosome 9 Protein, YEATS Domain-Containing Protein 3, Protein AF-9, YEATS3, AF9, Myeloid/Lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog Drosophila); Translocated To 3, Myeloid/Lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog); Translocated To, 3, Myeloid/Lymphoid Or Mixed-Lineage Leukemia; Translocated To 3, Myeloid/Lymphoid Or Mixed-Lineage Leukemia; Translocated To 3
    11d
    Impact of Fusion Partners and Transplantation Benefit in Intensively Treated KMT2A-Rearranged Acute Myeloid Leukemia. (PubMed, Cancers (Basel))
    Our study revealed the heterogeneous outcomes of KMT2A-rearranged AML patients and clarified the impact of HSCT across different age groups.
    Journal
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    KMT2A (Lysine Methyltransferase 2A) • MLLT3 (MLLT3 Super Elongation Complex Subunit) • MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)
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    KMT2A rearrangement
    21d
    Identification of cellular hierarchy in paediatric acute myeloid leukaemia: The Japan Children's Cancer Group trial (JCCG AML-12). (PubMed, Br J Haematol)
    LSPC-Cycle, FLT3-ITD and NUP98::KDM5A were considered independent prognostic factors in multivariate analysis. Findings indicate the prognostic relevance of cellular hierarchy and the importance of integrating hierarchy-specific molecular profiles for improved risk stratification and treatment formulation.
    Journal
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    FLT3 (Fms-related tyrosine kinase 3) • NPM1 (Nucleophosmin 1) • RUNX1 (RUNX Family Transcription Factor 1) • KMT2A (Lysine Methyltransferase 2A) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • MECOM (MDS1 And EVI1 Complex Locus) • NSD1 (Nuclear Receptor Binding SET Domain Protein 1) • NUP214 (Nucleoporin 214) • CBFA2T3 (CBFA2/RUNX1 Partner Transcriptional Co-Repressor 3) • GATA1 (GATA Binding Protein 1) • GLIS2 (GLIS Family Zinc Finger 2) • KDM5A (Lysine Demethylase 5A) • MLLT3 (MLLT3 Super Elongation Complex Subunit)
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    FLT3-ITD mutation
    1m
    CSF1R marks a subset of foetal haematopoietic multipotent progenitor cells with acute myeloid leukaemia propagation properties. (PubMed, Leukemia)
    Finally, CSF1R inhibition on a KMT2A::MLLT3+ paediatric leukaemia cell line resulted in significant cell death, suggesting that CSF1R could be therapeutically targeted in these patients. Our findings suggest that KMT2A::MLLT3+ infant AML may originate from foetal liver CSF1R+ LMPPs, and that these patients may benefit from anti-CSF1R-CAR-T cell therapy.
    Journal • IO biomarker
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    KMT2A (Lysine Methyltransferase 2A) • CSF1R (Colony stimulating factor 1 receptor) • MLLT3 (MLLT3 Super Elongation Complex Subunit)
    2ms
    Targeting dysregulated epigenetic and transcription factor networks in KMT2A-rearranged AML using iPSC models. (PubMed, Blood Neoplasia)
    Treatment with the dual EZH1/2 inhibitor UNC1999 and 5-azacytidine reactivated these PRC2 target genes, specifically in AML-HSPCs, toward normal gene expression patterns. These findings suggest that targeting Polycomb repression offers a promising epigenetic strategy for improving outcomes in KMT2A-rearranged AML.
    Journal
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    EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • KMT2A (Lysine Methyltransferase 2A) • MLLT3 (MLLT3 Super Elongation Complex Subunit)
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    KMT2A rearrangement • MLL rearrangement
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    azacitidine • UNC1999
    2ms
    Development of a Multilayered Prognostic Model for Wilms' Tumor Based on Characteristic Lymphocyte Genes. (PubMed, Genet Res (Camb))
    Elevated immune cell infiltration and enhanced drug sensitivity characterized the high-risk group, exhibiting significant responsiveness to chemotherapy, targeted, and immunotherapy treatments (p < 0.05). The study developed an integrated LGCPN-WT model, significantly enhancing survival prediction accuracy and clinical utility for WT, thus supporting personalized treatment approaches.
    Journal • IO biomarker
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    MLLT3 (MLLT3 Super Elongation Complex Subunit) • KLRC1 (Killer Cell Lectin Like Receptor C1) • SIGLEC5 (Sialic Acid Binding Ig Like Lectin 5)
    2ms
    Pemigatinib After Chemotherapy for the Treatment of Newly Diagnosed Acute Myeloid Leukemia (clinicaltrials.gov)
    P1, N=32, Recruiting, OHSU Knight Cancer Institute | Trial completion date: Jun 2026 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Dec 2026
    Trial completion date • Trial primary completion date
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    TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • RUNX1 (RUNX Family Transcription Factor 1) • SF3B1 (Splicing Factor 3b Subunit 1) • ASXL1 (ASXL Transcriptional Regulator 1) • KMT2A (Lysine Methyltransferase 2A) • SRSF2 (Serine and arginine rich splicing factor 2) • BCOR (BCL6 Corepressor) • U2AF1 (U2 Small Nuclear RNA Auxiliary Factor 1) • STAG2 (Stromal Antigen 2) • MECOM (MDS1 And EVI1 Complex Locus) • NUP214 (Nucleoporin 214) • GATA2 (GATA Binding Protein 2) • MLLT3 (MLLT3 Super Elongation Complex Subunit) • CDKN1A (Cyclin-dependent kinase inhibitor 1A) • DEK (DEK Proto-Oncogene) • ZRSR2 (Zinc Finger CCCH-Type, RNA Binding Motif And Serine/Arginine Rich 2)
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    TP53 mutation • FLT3 mutation • RUNX1 mutation • ASXL1 mutation • EZH2 mutation • SRSF2 mutation • Chr del(5q)
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    cytarabine • Pemazyre (pemigatinib) • daunorubicin • Starasid (cytarabine ocfosfate)
    2ms
    Thrombopoietin increases susceptibility for EVI1 + KMT2A-MLLT3-driven AML expressing stem cell genes linked to poor outcome. (PubMed, Nat Commun)
    Knockdown experiments show exclusive MECOM-dependency of human EVI1high KMT2A-rearranged OCI-AML4 cells while reduction of IL12Rβ2 also impairs clonogenic growth of EVI1low MOLM-13, THP-1 or HL-60 AML cells. Collectively, we show that exogenous factors like TPO can increase the susceptibility for iKMT2A-MLLT3-driven HSC-originating Evi1+ AML expressing stem cell genes linked to transformation maintenance of cell lines, and poor disease outcome of patients.
    Journal
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    KMT2A (Lysine Methyltransferase 2A) • MECOM (MDS1 And EVI1 Complex Locus) • INPP4B (Inositol polyphosphate-4-phosphatase type II B) • MLLT3 (MLLT3 Super Elongation Complex Subunit)
    4ms
    Retraction Note: miR-564 inhibited metastasis and proliferation of prostate cancer by targeting MLLT3. (PubMed, Eur Rev Med Pharmacol Sci)
    The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/13723.
    Journal
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    MLLT3 (MLLT3 Super Elongation Complex Subunit)
    4ms
    KMT2A alterations in acute myeloid leukemia: a proposed genetic risk model and transplantation outcomes. (PubMed, Exp Hematol Oncol)
    Allogeneic hematopoietic cell transplantation significantly improved survival, with 3-year OS rates of 75.2% in transplant recipients versus 22.5% in non-transplanted patients (P < 0.001), particularly in high-risk groups and when performed in first complete remission. These findings support the use of molecularly guided, risk-adapted therapy in KMT2A-altered AML.
    Journal
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    KMT2A (Lysine Methyltransferase 2A) • MLLT3 (MLLT3 Super Elongation Complex Subunit)
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    RAS mutation • KMT2A rearrangement • MLL mutation
    5ms
    Detection of leukemia gene fusions on DNA-level through targeted Next-Generation Sequencing. (PubMed, PLoS One)
    This study confirms the feasibility of employing tNGS methods to concurrently identify gene mutations and fusions (including IGH and MYC rearrangements) at the DNA level in adults with leukemia.
    Journal • Next-generation sequencing
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    MYC (V-myc avian myelocytomatosis viral oncogene homolog) • KMT2A (Lysine Methyltransferase 2A) • MLLT3 (MLLT3 Super Elongation Complex Subunit)
    5ms
    Dual Targeting of IKKβ and NR4A1 for AML Therapy. (PubMed, bioRxiv)
    Our results reveal a potentially novel strategy to treat intractable and aggressive AMLs in the clinic. IKKβ and NR4A1 are clinically relevant mediators of AML pathogenesis.A novel celastrol-based PROTAC can effectively degrade both IKKβ and NR4A1 to disrupt AML pathogenesis.
    Journal
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    KMT2A (Lysine Methyltransferase 2A) • CRBN (Cereblon) • MLLT3 (MLLT3 Super Elongation Complex Subunit) • NR4A1 (Nuclear Receptor Subfamily 4 Group A Member 1)