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    GENE:

    RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1)

    i
    Other names: RUNX1T1, RUNX1 Partner Transcriptional Co-Repressor 1, ZMYND2, MTG8, CDR, ETO, Core-Binding Factor Runt Domain Alpha Subunit 2; Translocated To 1; Cyclin D-Related, Runt Related Transcription Factor 1; Translocated To 1 (Cyclin D Related), Zinc Finger MYND Domain-Containing Protein, RUNX1 Translocation Partner, Eight Twenty One Protein, Protein CBFA2T1, CBFA2T1, AML1T1, Acute Myelogenous Leukemia 1 Translocation 1 Cyclin-D Related, Myeloid Translocation Gene On 8q22, Cyclin-D-Related Protein, Protein MTG8, Protein ETO, AML1-MTG8, RUNX1T1
    4d
    Decoding the molecular drivers of TP53-mutant acute myeloid leukaemia: Clinical implications and prognostic insights. (PubMed, Br J Haematol)
    Better responses were observed in patients treated with the venetoclax in combination with hypomethylating agent (VEN + HMA) regimen compared to those receiving the '3 + 7' regimens (composite complete remission [CRc], 53.8% vs. 30.2%; p = 0.018)...In conclusion, molecular factors matter in influencing the prognosis of TP53-mutant AML patients. Among them, TP53 mutation sites merit particular attention.
    Journal
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    TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • RUNX1 (RUNX Family Transcription Factor 1) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • CEBPA (CCAAT Enhancer Binding Protein Alpha)
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    TP53 mutation • FLT3-ITD mutation • RUNX1 mutation • RUNX1-RUNX1T1 fusion
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    Venclexta (venetoclax)
    9d
    Gene Expression Profiling Provides an Improved Characterization of CD79B-Mutated Diffuse Large B-Cell Lymphomas. (PubMed, J Pers Med)
    TP53 mutation showed an association with poorer overall survival in a secondary analysis, consistent with prior reports, while survival by CD79B/MYD88 mutation status and the differentially expressed genes showed no significant differences in this cohort. In conclusion, the current study identified novel up-regulated genes in CD79B-mutated DLBCLs beyond NF-κB pathway signaling, which may contribute to a better definition of potential therapeutic targets and further improves the characterization of this distinct and aggressive DLBCL subgroup.
    Journal
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    TP53 (Tumor protein P53) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • RUNX1 (RUNX Family Transcription Factor 1) • CD79B (CD79b Molecule) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • STAT3 (Signal Transducer And Activator Of Transcription 3) • CARD11 (Caspase Recruitment Domain Family Member 11) • IL10 (Interleukin 10) • CD14 (CD14 Molecule) • PIM1 (Pim-1 Proto-Oncogene) • BCL2A1 (BCL2 Related Protein A1) • GZMB (Granzyme B) • IL7 (Interleukin 7) • RASGRF1 (Ras Protein Specific Guanine Nucleotide Releasing Factor 1) • AFDN (Afadin, Adherens Junction Formation Factor) • HSP90AB1 (Heat Shock Protein 90 Alpha Family Class B Member 1) • WNT11 (Wnt Family Member 11)
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    TP53 mutation
    9d
    Unveiling the Genetic Mosaic of Pediatric AML: Insights from Southwest China. (PubMed, Curr Oncol)
    This study delineated the genetic landscape of pAML in Southwest China and explored the prognostic value of gene fusions and mutations in early and long-term outcomes. These findings provide a foundation for understanding the genetic heterogeneity of pAML and offer evidence for the development of precision medicine approaches.
    Journal
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    KRAS (KRAS proto-oncogene GTPase) • FLT3 (Fms-related tyrosine kinase 3) • NRAS (Neuroblastoma RAS viral oncogene homolog) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • RUNX1 (RUNX Family Transcription Factor 1) • KMT2A (Lysine Methyltransferase 2A) • PTPN11 (Protein Tyrosine Phosphatase Non-Receptor Type 11) • WT1 (WT1 Transcription Factor) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • CEBPA (CCAAT Enhancer Binding Protein Alpha)
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    FLT3-ITD mutation • KIT mutation • KMT2A rearrangement
    11d
    RUNX1T1-HDAC Reprogramming of the HOX Code Signaling Drives a Targetable Pan-Cancer Lineage Plasticity. (PubMed, bioRxiv)
    Finally, pharmacologic HDAC inhibition selectively suppressed the growth of plastic cells, revealing a novel therapeutic vulnerability. These findings establish ectopic RUNX1T1 as a pan-cancer biomarker and critical mediator of lineage plasticity and identify the RUNX1T1-HDAC complex as a druggable target.
    Journal • Pan tumor
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    RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1)
    14d
    Case Report: CD19 CAR-T therapy induces dual remission in AML-M2b patient with CNS-PTLD and relapse. (PubMed, Front Immunol)
    This case demonstrates the efficacy and feasibility of CD19 CAR-T therapy for concomitant post-transplant AML-M2b relapse and CNS-PTLD, leveraging their shared CD19 expression. It provides clinical evidence that targeting a shared antigen with a single CAR-T product can effectively treat heterogeneous malignancies, offering a promising new strategy for such complex cases.
    Journal • IO biomarker
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    CD19 (CD19 Molecule) • RUNX1 (RUNX Family Transcription Factor 1) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1)
    1m
    Resolving intra-tumor heterogeneity and clonal evolution of core-binding factor acute myeloid leukemia patients with single-cell resolution. (PubMed, Exp Hematol Oncol)
    We identified remaining tumor clones in 6 patients with complete remission samples indicating incomplete eradication of the tumor clones. Here, we show that identifying the order of mutation acquisition can provide valuable insights into evolutionary history, offering a framework to improve drug selection in the era of targeted therapies.
    Journal
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    RUNX1 (RUNX Family Transcription Factor 1) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1)
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    CBFB-MYH11 fusion
    1m
    The characteristics and prognostic analysis of therapy-related acute myeloid leukemia patients in China. (PubMed, Sci China Life Sci)
    We developed a prognostic scoring system including clinical and molecular profiles termed NTCTH (NPM1 (HR=0.16), TP53 (HR=3.45), CBF t-AML (HR=0.09), first course intensive induction Therapy regime (HR=0.24), and allo-HSCT (HR=0.36)) in patients who performed NGS. Our study first demonstrated prognostic factors of t-AML in large samples from multiple centers in China and found that NPM1 and CBF t-AML were associated with superior OS, and TP53 was associated with inferior OS.
    Journal
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    TP53 (Tumor protein P53) • NPM1 (Nucleophosmin 1) • RUNX1 (RUNX Family Transcription Factor 1) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • CBFB (Core-Binding Factor Subunit Beta 2)
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    TP53 mutation • NPM1 mutation
    1m
    Rare case of PLAG1::RUNX1 fusion mimicking classical t(8;21): the value of optical genome mapping in acute myeloid leukemia. (PubMed, Mol Cytogenet)
    PLAG1 is a rare translocation partner of RUNX1 in AML, mistaken for classical t(8;21) on conventional karyotyping. The rare reported cases of PLAG1::RUNX1 suggest a distinctly poor prognosis, highlighting the importance of accurate diagnosis and the role of OGM in our practice.
    Journal
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    RUNX1 (RUNX Family Transcription Factor 1) • SF3B1 (Splicing Factor 3b Subunit 1) • ASXL1 (ASXL Transcriptional Regulator 1) • KMT2A (Lysine Methyltransferase 2A) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • PHF6 (PHD Finger Protein 6) • PLAG1 (PLAG1 Zinc Finger)
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    RUNX1-RUNX1T1 fusion
    2ms
    Acute Myeloid Leukemia With RUNX1::RUNX1T1 Fusion Transformed From JAK2V617F-Mutated Polycythemia Vera: A Case Report. (PubMed, Cureus)
    An 87-year-old Japanese man was diagnosed with PV 22 years earlier and had been treated with hydroxyurea and aspirin. Leukemic evolution from MPNs often involves morphological changes in addition to genetic and chromosomal abnormalities. Therefore, during the follow-up of MPN, it is important to focus on changes in the blood cell morphology.
    Journal
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    RUNX1 (RUNX Family Transcription Factor 1) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • CD34 (CD34 molecule) • MPO (Myeloperoxidase)
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    RUNX1-RUNX1T1 fusion
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    hydroxyurea • aspirin
    2ms
    Pediatric Severe Eosinophilia: Etiological Spectrum, Diagnostic Algorithm, and Case-Based Insights From a Tertiary Care Center. (PubMed, Int J Lab Hematol)
    A structured, laboratory-driven algorithm beginning with blood counts, smear, and parasitic testing, and escalating to early bone marrow with cytogenetic/molecular studies for high-risk phenotypes, enabled timely identification of clonal HE while conserving resources in reactive cases. This LMIC-adapted pathway highlights laboratory turnaround time as a critical determinant of outcomes and provides a practical framework for pediatric HE evaluation.
    Journal
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    RUNX1 (RUNX Family Transcription Factor 1) • PDGFRB (Platelet Derived Growth Factor Receptor Beta) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1)
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    imatinib