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    BIOMARKER:

    DEK-NUP214 rearrangement

    i
    Other names: DEK, DEK Proto-Oncogene, DEK Oncogene, Protein DEK, NUP214, Nucleoporin 214, Nuclear Pore Complex Protein Nup214, CAN Protein, Putative Oncogene, Nucleoporin 214kDa, CAIN, Nucleoporin 214kD (CAIN), 214 KDa Nucleoporin, Nucleoporin Nup214, Protein CAN, IIAE9
    Entrez ID:
    8021; 7913
    Related biomarkers:
    Fusion
    Others
    Associations

    News

    Trials
    2ms
    Clinical features and long-term outcomes of pediatric patients with de novo acute myeloid leukemia in China with or without specific gene abnormalities: a cohort study of patients treated with BCH-AML 2005. (PubMed, Hematology)
    Not achieving complete remission after induction 2 was found to be an independent prognostic factor for OS and EFS. These findings indicate that genetic abnormalities could be considered stratification factors, predict patient outcomes, and imply the application of targeted therapy.
    Journal
    |
    FLT3 (Fms-related tyrosine kinase 3) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • RUNX1 (RUNX Family Transcription Factor 1) • KMT2A (Lysine Methyltransferase 2A) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • NUP214 (Nucleoporin 214) • CBFB (Core-Binding Factor Subunit Beta 2) • DEK (DEK Proto-Oncogene)
    |
    FLT3-ITD mutation • KIT mutation • KMT2A rearrangement • MLL rearrangement • DEK-NUP214 rearrangement
    12ms
    Iron-laden blasts in refractory acute myeloid leukemia. (PubMed, J Hematop)
    The granules were strongly positive for Perls' Prussian blue, consistent with hemosiderin deposits. This previously unreported finding is suggestive of siderophage activity by leukemic blasts, likely associated with monocytic differentiation.
    Journal
    |
    NUP214 (Nucleoporin 214) • DEK (DEK Proto-Oncogene)
    |
    DEK-NUP214 rearrangement
    over2years
    Molecular Classification and Overcoming Therapy Resistance for Acute Myeloid Leukemia with Adverse Genetic Factors. (PubMed, Int J Mol Sci)
    TP53 mutation is associated with particularly poor prognosis. Molecular-targeted therapies focusing on specific genomic abnormalities, such as FLT3, KMT2A, and TP53, have been developed and have demonstrated promising results.
    Review • Journal
    |
    TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • NPM1 (Nucleophosmin 1) • RUNX1 (RUNX Family Transcription Factor 1) • ASXL1 (ASXL Transcriptional Regulator 1) • KMT2A (Lysine Methyltransferase 2A) • MECOM (MDS1 And EVI1 Complex Locus) • NUP214 (Nucleoporin 214) • DEK (DEK Proto-Oncogene)
    |
    TP53 mutation • BCR-ABL1 fusion • FLT3 mutation • NPM1 mutation • ASXL1 mutation • KMT2A rearrangement • MLL rearrangement • DEK-NUP214 rearrangement