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    BIOMARKER:

    MLL rearrangement

    i
    Other names: HTRX1, HTRX, MLL1A, Mixed Lineage Leukemia 1, Myeloid/Lymphoid Or Mixed-Lineage Leukemia Protein 1, CXXC7, MLL1, TRX1, Zinc Finger Protein HRX, Trithorax-Like Protein, ALL-1, Lysine (K)-Specific Methyltransferase 2A, CXXC-Type Zinc Finger Protein 7, Histone-Lysine N-Methyltransferase 2A, Myeloid/Lymphoid Or Mixed-Lineage Leukemia, Lysine Methyltransferase 2A, MLL, Myeloid/Lymphoid Or Mixed-Lineage Leukemia, KMT2A
    8d
    Digital PCR of CHIP and MR for MRD Monitoring After Allo-HSCT in AML (clinicaltrials.gov)
    P=N/A, N=100, Recruiting, Peking University People's Hospital
    New trial • Tumor mutational burden • Minimal residual disease
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    ABL1 (ABL proto-oncogene 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • NPM1 (Nucleophosmin 1) • JAK2 (Janus kinase 2) • RUNX1 (RUNX Family Transcription Factor 1) • SF3B1 (Splicing Factor 3b Subunit 1) • ASXL1 (ASXL Transcriptional Regulator 1) • KMT2A (Lysine Methyltransferase 2A) • TET2 (Tet Methylcytosine Dioxygenase 2) • SRSF2 (Serine and arginine rich splicing factor 2) • BCOR (BCL6 Corepressor) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • U2AF1 (U2 Small Nuclear RNA Auxiliary Factor 1) • STAG2 (Stromal Antigen 2) • NSD1 (Nuclear Receptor Binding SET Domain Protein 1) • HOXA9 (Homeobox A9) • NUP214 (Nucleoporin 214) • FUS (FUS RNA Binding Protein) • ZRSR2 (Zinc Finger CCCH-Type, RNA Binding Motif And Serine/Arginine Rich 2)
    |
    NPM1 mutation • MLL rearrangement
    26d
    Umbilical Cord Blood Transplantation Using a Myeloablative Preparative Regimen for Hematological Diseases (clinicaltrials.gov)
    P=N/A, N=200, Recruiting, Masonic Cancer Center, University of Minnesota | Trial completion date: Feb 2027 --> Feb 2028 | Trial primary completion date: Feb 2026 --> Feb 2027
    Trial completion date • Trial primary completion date
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    KMT2A (Lysine Methyltransferase 2A) • IKZF1 (IKAROS Family Zinc Finger 1)
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    MLL rearrangement
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    cyclophosphamide • fludarabine IV • cyclosporin A microemulsion
    1m
    The oncogenic role of ecotropic viral integration site 1 in hematological malignancies: mechanisms of activation and leukemogenesis. (PubMed, Front Immunol)
    Clinically, EVI1 overexpression is one of the most robust independent indicators of poor prognosis, associated with therapy resistance and reduced overall survival. This review provides a detailed discussion of the mechanisms underlying EVI1's activation, its complex molecular functions in hematopoietic transformation, and its profound clinical implications in hematological malignancies.
    Review • Journal
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    PTEN (Phosphatase and tensin homolog) • RUNX1 (RUNX Family Transcription Factor 1) • KMT2A (Lysine Methyltransferase 2A) • ETV6 (ETS Variant Transcription Factor 6) • MECOM (MDS1 And EVI1 Complex Locus) • GATA2 (GATA Binding Protein 2) • TGFB1 (Transforming Growth Factor Beta 1)
    |
    MLL rearrangement
    1m
    Recent Advances and Perspectives of Small Molecule Modulators Targeting DOT1L. (PubMed, J Med Chem)
    Modulators targeting DOT1L have been developed for more than a decade, and compounds such as competitive inhibitors, protein-protein interaction (PPI) inhibitors, and degraders block DOT1L's pathogenic functions through various pharmacological mechanisms. Challenges and opportunities are discussed in this perspective, aiming to provide valuable insights for the future design of DOT1L modulators.
    Review • Journal
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    KMT2A (Lysine Methyltransferase 2A) • HOXA9 (Homeobox A9) • DOT1L (DOT1 Like Histone Lysine Methyltransferase)
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    MLL rearrangement
    1m
    Overcoming Menin inhibitor resistance in AML cells with combinations including BET proteins and dual BRG1/BRM inhibitor. (PubMed, Blood)
    Compared to each drug alone, co-treatment with SNDX-5613 (revumenib) and FHD-286 or OTX015 and FHD-286 significantly reduced the in vivo AML burden and improved survival of the immune depleted mice, without inducing significant toxicity, in the xenograft models of MITR and MI-resistant PD MLL1-r AML cells. These findings highlight novel, targeted, drug combinations that overcome MI resistance in AML cells with MLL1-r or mtNPM1.
    Journal
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    NPM1 (Nucleophosmin 1) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4) • CREBBP (CREB binding protein) • HOXA9 (Homeobox A9) • MEIS1 (Meis Homeobox 1) • BRD4 (Bromodomain Containing 4) • SMARCA2 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily A, Member 2)
    |
    NPM1 mutation • MLL rearrangement • MLL mutation
    |
    Revuforj (revumenib) • birabresib (OTX015) • camibirstat (FHD-286)
    2ms
    Comparative analysis of long-term efficacy between the CCCG-ALL-2015 and CCLG-ALL-2008 protocols in adolescents with acute lymphoblastic leukemia (PubMed, Zhonghua Xue Ye Xue Za Zhi)
    By incorporating MRD-guided dynamic risk stratification and optimized drug regimens, the CCCG-ALL-2015 protocol significantly improved the quality of induction remission, reduced adverse events, and improved the long-term survival in adolescents (aged 10-18 years) with ALL. The MRD status at the end of induction therapy is a critical prognostic indicator and provides important guidance for individualized therapy.
    Clinical • Retrospective data • Journal
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    KMT2A (Lysine Methyltransferase 2A)
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    MLL rearrangement
    2ms
    Matrine enhances RLS3-induced ferroptosis at non-toxic doses in acute myeloid leukemia cells with MLL rearrangement. (PubMed, Am J Cancer Res)
    In addition, the combination of MAT and RSL3 can dramatically reduce the population of bone marrow CD45+ cells in AML xenograft mouse. In conclusion, MAT can synergistically promote non-toxic-dose RSL3 induced ferroptosis by modulating the p53 pathway in AML with MLL translocation, which may potentially enable the clinical application of ferroptosis inducers in further.
    Journal
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    KMT2A (Lysine Methyltransferase 2A) • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • GPX4 (Glutathione Peroxidase 4) • SLC7A11 (Solute Carrier Family 7 Member 11)
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    MLL rearrangement
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    RSL3
    2ms
    Analysis of factors influencing the prognosis of pediatric acute myeloid leukemia based on minimal residual disease with different detection methods (PubMed, Zhonghua Yi Xue Za Zhi)
    The 3-year overall survival rates and event-free survival (EFS) rates were 80.7% and 69.4%, respectively. Multivariate Cox regression analysis revealed that gene MLL rearrangement (excluding MLL-AF9) (HR=3.071, 95%CI: 1.024-9.205) and positive molecular MRD after Induction Course Ⅱ therapy (HR=5.571, 95%CI: 1.244-24.957) were risk factors for EFS in pediatric AML patients.
    Retrospective data • Journal • Minimal residual disease
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    KMT2A (Lysine Methyltransferase 2A)
    |
    MLL rearrangement
    2ms
    Menin Inhibition in Acute Myeloid Leukemia: Pathobiology, Progress and Promise. (PubMed, Biomedicines)
    We evaluate the latest data on various menin inhibitors-both as monotherapy and in combinations-emphasizing their efficacy and safety profiles. As new evidence continues to accumulate with recent drug approvals and ongoing randomized, phase 3 studies, menin inhibitors are rapidly becoming a component of the AML treatment paradigm for relapsed/refractory and likely newly diagnosed disease.
    Review • Journal
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    NPM1 (Nucleophosmin 1) • KMT2A (Lysine Methyltransferase 2A) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • HOXA9 (Homeobox A9) • MEIS1 (Meis Homeobox 1)
    |
    NPM1 mutation • MLL rearrangement
    3ms
    Cord Blood Transplant in Children and Young Adults With Blood Cancers and Non-malignant Disorders (clinicaltrials.gov)
    P2, N=31, Recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Dec 2026
    Trial completion date • Trial primary completion date
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    KMT2A (Lysine Methyltransferase 2A)
    |
    MLL rearrangement
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    clofarabine • fludarabine IV • busulfan • cyclosporin A microemulsion
    3ms
    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
    |
    azacitidine • UNC1999
    4ms
    CD19-CAR_Lenti T Cells in Pediatric Patients Affected by Relapsed/Refractory CD19+ ALL and DLBCL or PML (clinicaltrials.gov)
    P1/2, N=32, Active, not recruiting, Bambino Gesù Hospital and Research Institute | Recruiting --> Active, not recruiting | Trial primary completion date: Mar 2025 --> Mar 2027
    Enrollment closed • Trial primary completion date
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    TP53 (Tumor protein P53) • CD19 (CD19 Molecule) • TCF3 (Transcription Factor 3) • PBX1 (PBX Homeobox 1)
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    MLL rearrangement
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    cyclophosphamide • CD19-CAR_Lenti T cells