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    GENE:

    NUP214 (Nucleoporin 214)

    i
    Other names: 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
    9d
    CR109124: A Study of Bleximenib in Combination With Acute Myeloid Leukemia (AML) Directed Therapies (clinicaltrials.gov)
    P1, N=196, Active, not recruiting, Janssen Research & Development, LLC | Recruiting --> Active, not recruiting
    Enrollment closed
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    NPM1 (Nucleophosmin 1) • KMT2A (Lysine Methyltransferase 2A) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • NUP214 (Nucleoporin 214)
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    Venclexta (venetoclax) • cytarabine • azacitidine • daunorubicin • idarubicin hydrochloride • bleximenib (JNJ-6617)
    20d
    Identification of cellular hierarchy in paediatric acute myeloid leukaemia: The Japan Children's Cancer Group trial (JCCG AML-12). (PubMed, Br J Haematol)
    LSPC-Cycle, FLT3-ITD and NUP98::KDM5A were considered independent prognostic factors in multivariate analysis. Findings indicate the prognostic relevance of cellular hierarchy and the importance of integrating hierarchy-specific molecular profiles for improved risk stratification and treatment formulation.
    Journal
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    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) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • MECOM (MDS1 And EVI1 Complex Locus) • NSD1 (Nuclear Receptor Binding SET Domain Protein 1) • NUP214 (Nucleoporin 214) • CBFA2T3 (CBFA2/RUNX1 Partner Transcriptional Co-Repressor 3) • GATA1 (GATA Binding Protein 1) • GLIS2 (GLIS Family Zinc Finger 2) • KDM5A (Lysine Demethylase 5A) • MLLT3 (MLLT3 Super Elongation Complex Subunit)
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    FLT3-ITD mutation
    2ms
    Venetoclax Added to Fludarabine + Busulfan Prior to Transplant and to Maintenance Therapy for AML, MDS, and MDS/MPN (clinicaltrials.gov)
    P1, N=102, Active, not recruiting, Jacqueline Garcia, MD | Trial completion date: Feb 2026 --> Mar 2027 | Trial primary completion date: Dec 2025 --> May 2026
    Trial completion date • Trial primary completion date
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    KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • ABL1 (ABL proto-oncogene 1) • NRAS (Neuroblastoma RAS viral oncogene homolog) • BCR (BCR Activator Of RhoGEF And GTPase) • BCL2 (B-cell CLL/lymphoma 2) • NPM1 (Nucleophosmin 1) • NF1 (Neurofibromin 1) • RUNX1 (RUNX Family Transcription Factor 1) • SF3B1 (Splicing Factor 3b Subunit 1) • ASXL1 (ASXL Transcriptional Regulator 1) • KMT2A (Lysine Methyltransferase 2A) • PTPN11 (Protein Tyrosine Phosphatase Non-Receptor Type 11) • SRSF2 (Serine and arginine rich splicing factor 2) • BCOR (BCL6 Corepressor) • U2AF1 (U2 Small Nuclear RNA Auxiliary Factor 1) • STAG2 (Stromal Antigen 2) • MECOM (MDS1 And EVI1 Complex Locus) • NUP214 (Nucleoporin 214) • GATA2 (GATA Binding Protein 2) • DEK (DEK Proto-Oncogene) • RIT1 (Ras Like Without CAAX 1) • ZRSR2 (Zinc Finger CCCH-Type, RNA Binding Motif And Serine/Arginine Rich 2)
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    TP53 mutation • KRAS mutation • NRAS mutation • RUNX1 mutation • RAS mutation • ASXL1 mutation • CBL mutation • Chr del(5q)
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    Venclexta (venetoclax) • azacitidine • Inqovi (decitabine/cedazuridine) • fludarabine IV • busulfan
    2ms
    Pemigatinib After Chemotherapy for the Treatment of Newly Diagnosed Acute Myeloid Leukemia (clinicaltrials.gov)
    P1, N=32, Recruiting, OHSU Knight Cancer Institute | Trial completion date: Jun 2026 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Dec 2026
    Trial completion date • Trial primary completion date
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    TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • RUNX1 (RUNX Family Transcription Factor 1) • SF3B1 (Splicing Factor 3b Subunit 1) • ASXL1 (ASXL Transcriptional Regulator 1) • KMT2A (Lysine Methyltransferase 2A) • SRSF2 (Serine and arginine rich splicing factor 2) • BCOR (BCL6 Corepressor) • U2AF1 (U2 Small Nuclear RNA Auxiliary Factor 1) • STAG2 (Stromal Antigen 2) • MECOM (MDS1 And EVI1 Complex Locus) • NUP214 (Nucleoporin 214) • GATA2 (GATA Binding Protein 2) • MLLT3 (MLLT3 Super Elongation Complex Subunit) • CDKN1A (Cyclin-dependent kinase inhibitor 1A) • DEK (DEK Proto-Oncogene) • ZRSR2 (Zinc Finger CCCH-Type, RNA Binding Motif And Serine/Arginine Rich 2)
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    TP53 mutation • FLT3 mutation • RUNX1 mutation • ASXL1 mutation • EZH2 mutation • SRSF2 mutation • Chr del(5q)
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    cytarabine • Pemazyre (pemigatinib) • daunorubicin • Starasid (cytarabine ocfosfate)
    2ms
    Off-the-shelf NK Cells + SCT for Myeloid Malignancies (clinicaltrials.gov)
    P2, N=24, Completed, M.D. Anderson Cancer Center | Phase classification: P1/2 --> P2
    Phase classification
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    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) • GATA2 (GATA Binding Protein 2) • DEK (DEK Proto-Oncogene)
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    TP53 mutation • FLT3 mutation • RUNX1 mutation • ASXL1 mutation • Chr del(5q)
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    cyclophosphamide • melphalan • fludarabine IV • mesna • Neupogen (filgrastim)
    2ms
    Case Report: Genomic characterization of a rare skull-base plasmacytoma. (PubMed, Front Oncol)
    These findings provide novel insights into molecular landscape of SBP, highlighting potential for risk stratification and targeted therapy development. The case underscores the importance of comprehensive genomic profiling in rare skull-based tumors to enhance our understanding of their biology and to guide personalized clinical management.
    Journal
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    ARID1A (AT-rich interaction domain 1A) • KMT2D (Lysine Methyltransferase 2D) • PTPN11 (Protein Tyrosine Phosphatase Non-Receptor Type 11) • NUP214 (Nucleoporin 214) • BCL7A (BAF Chromatin Remodeling Complex Subunit BCL7A)
    3ms
    Efficacy of Venetoclax Based Regimen in Prevention Relapse of Consecutive MRD Positive AML Patients (clinicaltrials.gov)
    P2, N=20, Terminated, Institute of Hematology & Blood Diseases Hospital, China | N=40 --> 20 | Recruiting --> Terminated; The research center has conducted a more comprehensive study.
    Enrollment change • Trial termination • Minimal residual disease
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    NPM1 (Nucleophosmin 1) • RUNX1 (RUNX Family Transcription Factor 1) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • NUP214 (Nucleoporin 214) • DEK (DEK Proto-Oncogene)
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    NPM1 mutation
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    Venclexta (venetoclax) • azacitidine • daunorubicin
    3ms
    Pediatric T-Lymphoblastic Leukemia With Aberrant B-Cell Marker Expression: A Potential Role for Targeted Therapy. (PubMed, EJHaem)
    While the patient failed high-risk T-LBLL induction therapy, blinatumomab followed by decitabine and venetoclax induced a morphologic remission. This case illustrated the importance of integrating MFC analysis with NGS data to provide individualized patient treatment. The authors have confirmed clinical trial registration is not needed for this submission.
    Journal
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    NUP214 (Nucleoporin 214)
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    Venclexta (venetoclax) • Blincyto (blinatumomab) • decitabine
    3ms
    Genomic and transcriptomic characterization of acute myeloid leukaemia with IL3RA overexpression: Prognostic and therapeutic implications revisited. (PubMed, Br J Haematol)
    Pharmaco-transcriptomic analysis revealed that IL3RA-high AML exhibited selective sensitivity to venetoclax and sapanisertib, suggesting potential synergistic opportunities. In conclusion, IL3RA overexpression defines a clinically and biologically distinct subgroup of AML, with unique therapeutic vulnerabilities. Continued research efforts are warranted to integrate CD123-directed therapies into the upfront AML treatment paradigm.
    Journal
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    NPM1 (Nucleophosmin 1) • KMT2A (Lysine Methyltransferase 2A) • CD123 (Interleukin 3 Receptor Subunit Alpha) • NUP214 (Nucleoporin 214) • FUS (FUS RNA Binding Protein) • IL3RA (Interleukin 3 Receptor Subunit Alpha)
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    NPM1 mutation
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    Venclexta (venetoclax) • sapanisertib (CB-228)
    3ms
    Characterization of Acute Myeloid Leukemia Patients with DEK-NUP214 Fusion Gene Positive (PubMed, Zhongguo Shi Yan Xue Ye Xue Za Zhi)
    DEK-NUP214 fusion gene positive AML is a type of acute leukemia subtype with high risk and poor prognosis. Allo-HSCT treatment at the early stage of disease remission is the most effective way to improve the prognosis of patients.
    Journal
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    FLT3 (Fms-related tyrosine kinase 3) • NUP214 (Nucleoporin 214) • DEK (DEK Proto-Oncogene)
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    FLT3-ITD mutation
    3ms
    Decoding the genetic complexity in a pediatric case of B-ALL through long-read genomic sequencing and RNA sequencing. (PubMed, Cancer Genet)
    Notably, the presence of NUP214::ABL1 identified a clinically actionable target, supporting the use of tyrosine kinase inhibitors (TKIs) such as imatinib. This case underscores the critical role of integrated sequencing approaches in identifying cryptic genetic alterations in B-ALL for precise classification of oncogenic drivers and for targeted therapeutic strategies to improve patient outcomes.
    Journal
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    ABL1 (ABL proto-oncogene 1) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) • TSC1 (TSC complex subunit 1) • NUP214 (Nucleoporin 214) • TRB (T Cell Receptor Beta Locus)
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    CDKN2A deletion • ABL1 fusion
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    imatinib
    3ms
    Allogeneic transplantation in adverse-risk acute myeloid leukemia: Challenges, strategies, and future directions. (PubMed, Chin J Cancer Res)
    Allogeneic hematopoietic stem cell transplantation (allo-HSCT) remains the cornerstone of consolidation for eligible patients; however, due to high relapse rates, regimen-related toxicity, and variable responses across genetic subtypes, optimal transplant timing, conditioning regimens (e.g., busulfan- or melphalan-based protocols), and bridging strategies require further refinement. Meanwhile, post-transplant maintenance therapies, such as hypomethylating agents or targeted drugs, are one emerging area under investigation for relapse prevention. In this perspective, we review the latest advances in allo-HSCT strategies for adverse-risk AML and highlight the importance of molecularly-guided approaches to improve outcomes in these aggressive subtypes.
    Journal
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    TP53 (Tumor protein P53) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • NUP214 (Nucleoporin 214) • FUS (FUS RNA Binding Protein)
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    TP53 mutation
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    melphalan • busulfan