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    BIOMARKER:

    NUP98 rearrangement

    i
    Other names: NUP98, Nucleoporin 98 And 96 Precursor 2, Nuclear Pore Complex Protein Nup98-Nup96 2, Nucleoporin 98kDa, Nucleoporin 96, Nup98-Nup96, Nup98-96, NUP96, Nuclear Pore Complex Protein Nup98, GLFG-Repeat Containing Nucleoporin, NUP98/PHF23 Fusion 2 Protein, Nucleoporin 98kD, Nucleoporin 98, NUP196, ADIR2, ADAR2
    Entrez ID:
    4928
    Related biomarkers:
    Fusion
    Others
    1m
    Prognostic importance of NUP98-rearrangements in acute myeloid leukemia: A systematic review and meta-analysis. (PubMed, Caspian J Intern Med)
    NUP98 fusions could significantly impact the outcome of patients with AML. The use of these fusions as prognostic indicators in AML seems rational.
    Retrospective data • Review • Journal
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    FLT3 (Fms-related tyrosine kinase 3) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • NSD1 (Nuclear Receptor Binding SET Domain Protein 1) • KDM5A (Lysine Demethylase 5A)
    |
    NUP98-NSD1 fusion + FLT3-ITD mutation • NUP98 rearrangement
    2ms
    Rare Non-Cryptic NUP98 Rearrangements Associated With Myeloid Neoplasms and Their Poor Prognostic Impact. (PubMed, Ann Lab Med)
    Our study revealed the clinical and genetic characteristics of patients with myeloid neoplasms harboring rare and non-cryptic NUP98r. Given its association with poor prognosis, a comprehensive evaluation is crucial for identifying previously underdiagnosed NUP98r in patients with myeloid neoplasms.
    Journal
    |
    NUP98 (Nucleoporin 98 And 96 Precursor 2) • HOXA9 (Homeobox A9) • PRRX1 (Paired Related Homeobox 1) • DDX10 (DEAD-Box Helicase 10)
    |
    NUP98 rearrangement
    2ms
    Distinct FLT3 Pathways Gene Expression Profiles in Pediatric De Novo Acute Lymphoblastic and Myeloid Leukemia with FLT3 Mutations: Implications for Targeted Therapy. (PubMed, Int J Mol Sci)
    In summary, our study demonstrated that the forms and impacts of FLT3 mutations in ALL differed significantly from those in AML. The gene expression profiles of FLT3-related pathways may provide a rationale for using FLT3 inhibitors in AML rather than ALL when FLT3 mutations are present.
    Retrospective data • Journal • Gene Expression Profile
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    BRAF (B-raf proto-oncogene) • FLT3 (Fms-related tyrosine kinase 3) • HRAS (Harvey rat sarcoma viral oncogene homolog) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • MAP2K2 (Mitogen-activated protein kinase kinase 2) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • PIK3CB (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) • MAPK1 (Mitogen-activated protein kinase 1) • MAPK3 (Mitogen-Activated Protein Kinase 3) • PIK3R3 (Phosphoinositide-3-Kinase Regulatory Subunit 3)
    |
    FLT3 mutation • FLT3 wild-type • FLT3 expression • NUP98 rearrangement
    2ms
    Targeted gene sequencing and transcriptome sequencing reveal characteristics of NUP98 rearrangement in pediatric acute myeloid leukemia. (PubMed, Eur J Med Res)
    These investigations contribute to the understanding of the molecular characteristics, risk stratification, and prognostic evaluation of pediatric AML patients.
    Journal
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    FLT3 (Fms-related tyrosine kinase 3) • WT1 (WT1 Transcription Factor) • NUP98 (Nucleoporin 98 And 96 Precursor 2)
    |
    FLT3-ITD mutation • WT1 mutation • NUP93 mutation • NUP98 rearrangement
    6ms
    The landscape of NUP98 rearrangements clinical characteristics and treatment response from 1491 acute leukemia patients. (PubMed, Blood Cancer J)
    No abstract available
    Journal
    |
    NUP98 (Nucleoporin 98 And 96 Precursor 2)
    |
    NUP98 rearrangement
    12ms
    The future of HOXA-expressing leukemias: Menin inhibitor response and resistance. (PubMed, Curr Opin Hematol)
    Given the remarkable overall response rates, shedding light on treatment options for patients whose leukemias develop resistance to Menin inhibitors is an imminent clinical need. Studying the underlying mechanisms to inform clinical decision making, and to potentially prevent the development of resistance is of outmost importance.
    Journal
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    NPM1 (Nucleophosmin 1) • KMT2A (Lysine Methyltransferase 2A) • NUP98 (Nucleoporin 98 And 96 Precursor 2)
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    NPM1 mutation • KMT2A rearrangement • MLL rearrangement • NUP98 rearrangement
    1year
    Integrated Methylation and Transcriptional Landscape and Evolution of Pediatric AML (ASH 2023)
    Since pediatric AML is associated with a low mutational burden, understanding leukemia-specific transcriptional and epigenetic alterations is of utmost importance. Our study demonstrates the translational promise offered by deep functional genomic characterization of pediatric AML and we believe that further interrogation may provide additional novel insights into leukemia initiation, relapse prediction, and novel treatment approaches.
    Clinical • Tumor mutational burden
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    TMB (Tumor Mutational Burden) • FLT3 (Fms-related tyrosine kinase 3) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • DNMT3A (DNA methyltransferase 1) • RUNX1 (RUNX Family Transcription Factor 1) • KMT2A (Lysine Methyltransferase 2A) • WT1 (WT1 Transcription Factor) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • CD34 (CD34 molecule) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • NSD1 (Nuclear Receptor Binding SET Domain Protein 1) • KDM5A (Lysine Demethylase 5A)
    |
    TMB-L • KMT2A rearrangement • MLL rearrangement • CEBPA mutation • MLL fusion • NUP98 rearrangement
    1year
    Clinical Characteristics, Genetic Profile and Prognosis of Adult Acute Myeloid Leukemia with NUP98 Rearrangement (ASH 2023)
    Nineteen patients were treated with standard dose of "7+3" induction therapy, and 2 with hypomethylating agents (HMA) plus venetoclax (VEN)... Adult AML with NUP98 rearrangement may combine with a set of partner fusion genes and mutations, with NUP98::NSD1 and FLT3-ITD as the most common combination. Both IC an LIT can induce CR, and FLT3i will benefit those with FLT3 mutations, also prevention of fatal bleeding should be paid attention to. After achieving CR with whatever method and whatever MRD status, allo-HSCT is the key to long-term survival.
    Clinical
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    FLT3 (Fms-related tyrosine kinase 3) • WT1 (WT1 Transcription Factor) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • NSD1 (Nuclear Receptor Binding SET Domain Protein 1) • HOXA9 (Homeobox A9) • HOXA11 (Homeobox A11)
    |
    FLT3-ITD mutation • FLT3 mutation • NUP98 rearrangement
    |
    Venclexta (venetoclax)
    1year
    Combination of Liposomal Mitoxantrone, Venetoclax, Homoharringtonine, and Olverembatinib (HQP1351) (MVHO) in Pediatric Patients with Refractory or Relapsed Acute Myeloid Leukemia (AML): Case Series (ASH 2023)
    Prophylactic oral levofloxacin and posaconazole were administered from day 8 through whole myelosuppression period of every cycles. MVHO therapy was effective and reasonably well tolerated in pediatric patients with refractory or relapsed AML, suggesting that it may comprise a suitable first-line treatment option for pediatric AML patients.
    Clinical
    |
    NUP98 (Nucleoporin 98 And 96 Precursor 2) • FUS (FUS RNA Binding Protein) • CBFA2T3 (CBFA2/RUNX1 Partner Transcriptional Co-Repressor 3) • GLIS2 (GLIS Family Zinc Finger 2)
    |
    NUP98 rearrangement
    |
    Venclexta (venetoclax) • Nailike (olverembatinib) • Synribo (omacetaxine mepesuccinate) • Duoenda (mitoxantrone liposomal) • Noxafil (posaconazole)
    1year
    Treatment of Molecular Relapses in Pediatric AML Saves Toxicities Prior to Hematopoietic Stem Cell Transplantation (HSCT) - Results of AMoRe2017 Trial (ASH 2023)
    A promising approach is the use of Azacitidine (Aza) for treatment of molecular relapse which we evaluated within the clinical trial "AMoRe2017"...Conversely, the relatively slow-acting mechanism of epigenetic therapy seems to be ineffective in highly proliferative subgroups of AML with KMT2A-rearrangements or FLT3-ITD. Further studies are mandatory to define treatment options for molecular relapses of non-favorable pediatric AML and to confirm potential improvement of outcome post-HSCT.
    Clinical
    |
    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) • NSD1 (Nuclear Receptor Binding SET Domain Protein 1) • MLLT3 (MLLT3 Super Elongation Complex Subunit) • SEPTIN6 (Septin 6) • MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)
    |
    KMT2A rearrangement • MLL rearrangement • NUP98 rearrangement
    |
    azacitidine