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    GENE:

    NPM1 (Nucleophosmin 1)

    i
    Other names: Nucleophosmin (Nucleolar Phosphoprotein B23, Numatrin), Testicular Tissue Protein Li 128, Nucleolar Protein NO38, Numatrin, NPM1, Nucleophosmin 1, Nucleophosmin/Nucleoplasmin Family, Member 1, Nucleolar Phosphoprotein B23
    1d
    Mutation-specific NPM1 immunohistochemistry is a sensitive method for detecting residual disease in mid- and postinduction bone marrows: comparison of NPM1 immunohistochemistry, NPM1 real-time polymerase chain reaction, and flow cytometric studies. (PubMed, Am J Clin Pathol)
    Mutation-specific NPM1 IHC is a valuable tool for a rapid assessment of residual morphologic and molecular disease in mid- and postinduction NPM1mut AML.
    Clinical • Journal • Polymerase Chain Reaction
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    KIT (KIT proto-oncogene, receptor tyrosine kinase) • NPM1 (Nucleophosmin 1) • CD34 (CD34 molecule)
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    NPM1 mutation • KIT expression
    1d
    Fine particulate matter and tobacco product exposure exacerbates metabolic syndrome-related colon cancer via regulating oxidative stress and tumor-associated macrophage interactions. (PubMed, Cancer Metab)
    Our results provided new insights into the mechanisms of intestinal cancer progresses by paracrine IR-PD-L1 signaling, which is aided by the deregulation of oxidative stress and macrophage communication brought on by smoking carcinogen-induced the metabolic syndrome.
    Journal • PD(L)-1 Biomarker • IO biomarker
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    NPM1 (Nucleophosmin 1) • IGF2 (Insulin-like growth factor 2) • IR (Insulin receptor) • SLC2A1 (Solute Carrier Family 2 Member 1)
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    PD-L1 expression
    2d
    Optimization of Analytical Performances and Routine Laboratory Implementation of NPM1 Mutation Detection by Digital PCR in the Diagnosis and Monitoring of NPM1-Mutated Acute Myeloid Leukemias. (PubMed, Int J Lab Hematol)
    The approach enabled early relapse prediction in selected patients and improved molecular follow-up, even for rare NPM1 mutations not covered by standard qPCR panels. It simplifies laboratory routine and improves MRD assessment, according to current ELN guidelines and the growing need for personalized molecular monitoring in AML.
    Journal
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    NPM1 (Nucleophosmin 1)
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    NPM1 mutation
    2d
    Shogaol triggers apoptosis and ferroptosis in Ewing sarcoma by targeting the polo-like kinase 1/nucleophosmin 1 axis. (PubMed, Free Radic Biol Med)
    Key findings were validated by CETSA, isothermal dose-response fingerprinting, co-immunoprecipitation, and ubiquitination assays. These results demonstrate that shogaol exerts dual cytotoxic effects through the PLK1/NPM1 axis, presenting a potential natural therapeutic approach for Ewing sarcoma.
    Journal • IO biomarker
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    BCL2 (B-cell CLL/lymphoma 2) • NPM1 (Nucleophosmin 1) • SLC3A2 (Solute Carrier Family 3 Member 2) • PLK1 (Polo Like Kinase 1) • BAX (BCL2-associated X protein) • GPX4 (Glutathione Peroxidase 4) • TRIM28 (Tripartite Motif Containing 28)
    3d
    Stearoyl-CoA Desaturase-1 Drives Tumor Growth by Interacting With Histone Deacetylase-2 and Deacetylating Nucleophosmin-1. (PubMed, MedComm (2020))
    Notably, we observed that knockdown of SCD1 in vitro or its pharmacological inhibition in vivo enhances cancer cell sensitivity to HDAC inhibitors. Our findings underscore the role of SCD1 in reshaping the cellular acetylome and suggest that targeting SCD1 could sensitize cancer cells to HDAC inhibitors, highlighting a promising therapeutic strategy.
    Journal
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    NPM1 (Nucleophosmin 1) • HDAC2 (Histone deacetylase 2) • PLIN2 (Perilipin) • SCD (Stearoyl-CoA Desaturase)
    3d
    Dissecting PCD-driven molecular landscapes in AML: a multi-omic framework for prognostication and therapeutic targeting. (PubMed, Clin Exp Med)
    As an exploratory analysis, subtype-specific therapeutic vulnerabilities were revealed: Subtype A displays predicted sensitivity to immune checkpoint inhibitors (anti-PD-1) and tipifarnib, whereas Subtype B responds better to cytarabine/doxorubicin. Crucially, experimental validation confirmed significant upregulation of key model genes (HIP1, SQLE, VNN1) in AML patient samples and cell lines (P < 0.05), reinforcing the model's biological relevance. These findings establish PCD dysregulation as a central axis of AML heterogeneity, providing a framework for precision risk stratification and hypothesis-generating immunophenotype-guided therapy.
    Journal • PD(L)-1 Biomarker • IO biomarker
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    FLT3 (Fms-related tyrosine kinase 3) • NPM1 (Nucleophosmin 1) • DNMT3A (DNA methyltransferase 1) • HAVCR2 (Hepatitis A Virus Cellular Receptor 2) • HIP1 (Huntingtin Interacting Protein 1)
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    NPM1 mutation
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    cytarabine • doxorubicin hydrochloride • Zarnestra (tipifarnib)
    6d
    FH-WT1-E50 TCR T Cells With Azacitidine for the Treatment of Minimal Residual Disease Positive Acute Myeloid Leukemia (clinicaltrials.gov)
    P1, N=9, Not yet recruiting, Fred Hutchinson Cancer Center
    New P1 trial • Minimal residual disease
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    FLT3 (Fms-related tyrosine kinase 3) • NPM1 (Nucleophosmin 1) • WT1 (WT1 Transcription Factor)
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    FLT3-ITD mutation • NPM1 mutation
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    azacitidine
    6d
    Menin Inhibition in Acute Myeloid Leukemia: Rewiring Leukemic Transcriptional Networks. (PubMed, Int J Mol Sci)
    Clinical activity observed with menin inhibitors provides translational validation of this dependency and establishes menin inhibition as a differentiation-based therapeutic strategy. In this review, we examine the molecular basis of menin-dependent transcriptional regulation in AML and its implications for therapeutic targeting with menin inhibitors and resistance to therapy.
    Review • Journal
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    NPM1 (Nucleophosmin 1) • KMT2A (Lysine Methyltransferase 2A)
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    NPM1 mutation
    6d
    Integrated proteogenomic and metabolomic profiling of acute myeloid leukemias to identify molecular subtypes and associated therapy targets. (PubMed, Nat Cancer)
    To nominate therapeutic targets across subtypes, we developed a multiomic machine-learning approach and validated MTA1 as a contributor to panobinostat resistance. Altogether our findings underscore the complex nature of AML and provide a clinically and translationally informed unified view that reveals coalescent phenotypes across multiomic layers.
    Journal • Metabolomic study
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    NPM1 (Nucleophosmin 1) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • FOXC1 (Forkhead Box C1)
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    NPM1 mutation
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    Farydak (panobinostat)
    7d
    NCI-2017-02296: Testing Olaparib in Patients With Advanced or Metastatic (Cancer That Has Spread) Bladder Cancer and Other Genitourinary Tumors With DNA-Repair Genetic Changes (clinicaltrials.gov)
    P2, N=60, Active, not recruiting, National Cancer Institute (NCI) | Suspended --> Active, not recruiting
    Enrollment closed • Tumor mutational burden
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    TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • ABL1 (ABL proto-oncogene 1) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • STK11 (Serine/threonine kinase 11) • NPM1 (Nucleophosmin 1) • POLE (DNA Polymerase Epsilon) • CCND1 (Cyclin D1) • BAP1 (BRCA1 Associated Protein 1) • MLH1 (MutL homolog 1) • MSH6 (MutS homolog 6) • MSH2 (MutS Homolog 2) • ATRX (ATRX Chromatin Remodeler) • CHEK2 (Checkpoint kinase 2) • SMARCB1 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily B, Member 1) • RAD51 (RAD51 Homolog A) • FANCA (FA Complementation Group A) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • POLD1 (DNA Polymerase Delta 1) • CHEK1 (Checkpoint kinase 1) • BARD1 (BRCA1 Associated RING Domain 1) • FANCL (FA Complementation Group L) • BRD4 (Bromodomain Containing 4) • DOT1L (DOT1 Like Histone Lysine Methyltransferase) • FANCE (FA Complementation Group E) • FANCG (FA Complementation Group G) • IKBKE (Inhibitor Of Nuclear Factor Kappa B Kinase Subunit Epsilon) • FANCC (FA Complementation Group C)
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    PALB2 mutation • BRIP1 mutation
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    FoundationOne® CDx
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    Lynparza (olaparib)
    7d
    The All-Oral Combination of Revumenib, Decitabine and Venetoclax for Relapsed or Refractory Acute Myeloid Leukemia (SAVE). (PubMed, J Clin Oncol)
    This combination was associated with high response rates and durable remissions, with an acceptable safety, in heavily pretreated patients with AML harboring alterations susceptible to menin inhibition.
    Journal • IO biomarker
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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
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    Venclexta (venetoclax) • Revuforj (revumenib) • Inqovi (decitabine/cedazuridine)
    7d
    Targeting SMC3 deacetylation synergizes with XPO1 inhibition to reprogram the epigenetic landscape and suppress NPM1-mutated acute myeloid leukemia. (PubMed, Nat Commun)
    The combined treatment effectively eliminates NPM1-mutated AML cell lines and primary human AML cells in vitro and in vivo. This study reveals an ESCO2 deficiency-induced aberrant epigenetic landscape via SMC3 hypoacetylation and identifies a potential therapeutic strategy for NPM1-mutated AML.
    Journal • IO biomarker
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    NPM1 (Nucleophosmin 1) • ESCO2 (Establishment Of Sister Chromatid Cohesion N-Acetyltransferase 2)
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    NPM1 mutation