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GENE:

NUP98 (Nucleoporin 98 And 96 Precursor 2)

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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
10d
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
22d
Optical genome mapping detects cryptic high-risk and targetable abnormalities in adult AML. (PubMed, Br J Haematol)
Survival analyses suggested a trend towards poorer outcomes in patients reclassified as adverse, though the small sample limits definitive conclusions. In low-complexity AML, OGM provides substantial incremental diagnostic value, detecting cryptic high-risk and targetable abnormalities, supporting its use as a complementary tool.
Journal
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KMT2A (Lysine Methyltransferase 2A) • NUP98 (Nucleoporin 98 And 96 Precursor 2)
27d
Menin Inhibition in Acute Myeloid Leukemia: Pathobiology, Progress and Promise. (PubMed, Biomedicines)
We evaluate the latest data on various menin inhibitors-both as monotherapy and in combinations-emphasizing their efficacy and safety profiles. As new evidence continues to accumulate with recent drug approvals and ongoing randomized, phase 3 studies, menin inhibitors are rapidly becoming a component of the AML treatment paradigm for relapsed/refractory and likely newly diagnosed disease.
Review • Journal
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NPM1 (Nucleophosmin 1) • KMT2A (Lysine Methyltransferase 2A) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • HOXA9 (Homeobox A9) • MEIS1 (Meis Homeobox 1)
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NPM1 mutation • MLL rearrangement
29d
Acute Leukemia with BCL11B Rearrangements: Genetic Landscape, BCL11B Expression, and Therapeutic Response. (PubMed, Hum Pathol)
Clinically, newly diagnosed patients, most treated with venetoclax based regimens, achieved high remission rates. Our data delineate the structural diversity of BCL11B rearrangements identified by OGM and show that BCL11B activation cannot be reliably inferred from partner gene identity alone. BCL11B immunohistochemistry as a practical surrogate for assessing BCL11B activation is recommended in routine practice.
Journal
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CCDC6 (Coiled-Coil Domain Containing 6) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • ARID1B (AT-Rich Interaction Domain 1B) • CDK6 (Cyclin-dependent kinase 6) • TNFAIP3 (TNF Alpha Induced Protein 3) • LMO2 (LIM Domain Only 2) • BCL11B (BAF Chromatin Remodeling Complex Subunit BCL11B) • GAPDH (Glyceraldehyde-3-Phosphate Dehydrogenase) • TLX1 (T Cell Leukemia Homeobox 1)
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Venclexta (venetoclax)
1m
Identification of cryptic KMT2A-PTD and other novel fusion genes by transcriptome sequencing alters molecular risk stratification in AML-NK. (PubMed, J Mol Med (Berl))
Fusion-based ELN 2022 reclassified most intermediate-risk patients. RNA-seq enhances prognostic assessment in AML-NK.
Journal
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NPM1 (Nucleophosmin 1) • KMT2A (Lysine Methyltransferase 2A) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • NSD1 (Nuclear Receptor Binding SET Domain Protein 1) • HOXA9 (Homeobox A9) • LATS2 (Large Tumor Suppressor Kinase 2)
1m
A Study of Revumenib and Mezigdomide in People With Leukemia (clinicaltrials.gov)
P1/2, N=52, Recruiting, Memorial Sloan Kettering Cancer Center
New P1/2 trial
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NPM1 (Nucleophosmin 1) • KMT2A (Lysine Methyltransferase 2A) • NUP98 (Nucleoporin 98 And 96 Precursor 2)
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MSK-IMPACT
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Revuforj (revumenib) • mezigdomide (CC-92480)
2ms
Condensatopathies as a mechanistic framework for disease and integrated theranostic intervention. (PubMed, Theranostics)
Furthermore, we review how emerging technologies like optogenetics and cryo-ET are decoding these mechanisms. Finally, we propose an integrated "See-and-Treat" theranostic paradigm, utilizing the unique material properties of condensates to design specific diagnostic probes and "molecular scalpels" for precision intervention.
Review • Journal
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NUP98 (Nucleoporin 98 And 96 Precursor 2) • TARDBP (TAR DNA Binding Protein)
2ms
Dual targeting of AMRC12 and Malassezia globosa disrupts MYC liquid condensates-driven nuclear pore complex biogenesis in neuroblastoma. (PubMed, Theranostics)
High ARMC12, MYC, NUP62, NUP93, or NUP98 levels served as markers of unfavorable patient outcomes in clinical cohorts. These findings collectively demonstrate that dual targeting of AMRC12 and Malassezia globosa disrupts MYC liquid condensates-driven NPC biogenesis during NB progression.
Journal
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NUP98 (Nucleoporin 98 And 96 Precursor 2) • NUP62 (Nucleoporin 62) • NUP93 (Nucleoporin 93)
2ms
NUP98 rearrangements in adult AML patients: evaluation of clinical implications and identification of novel fusion partners. (PubMed, Leukemia)
Allogeneic hematopoietic stem cell transplantation was associated with better survival, underscoring its significance. These findings reveal the genetic and clinical heterogeneity of NUP98-rearranged AML in adults and support its classification as a distinct entity, highlighting the need for fusion partner-specific therapeutic strategies.
Journal
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FLT3 (Fms-related tyrosine kinase 3) • NPM1 (Nucleophosmin 1) • TET2 (Tet Methylcytosine Dioxygenase 2) • WT1 (WT1 Transcription Factor) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • NSD1 (Nuclear Receptor Binding SET Domain Protein 1) • HOXA9 (Homeobox A9) • MEOX2 (Mesenchyme Homeobox 2)
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FLT3-ITD mutation • NPM1 mutation • TET2 mutation
2ms
Optical genome mapping as a high-resolution tool for uncovering cytogenetic complex and cryptic alterations in a cohort of patients with MDS and AML. (PubMed, NPJ Precis Oncol)
The identified abnormalities have shown significant and potential clinical implications. Additionally, the discovery of novel alterations could offer insights into previously unknown pathogenic mechanisms, enhancing our understanding of AML and MDS pathogenesis.
Journal
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KMT2A (Lysine Methyltransferase 2A) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • MECOM (MDS1 And EVI1 Complex Locus)
2ms
Genetic landscape of pediatric acute myeloid leukemia in Taiwan. (PubMed, Sci Rep)
Patients with RUNX1 mutations had inferior 5 year OS in multivariable analysis (p-value = 0.009). These findings suggest specific genomic alterations that may refine risk stratification and guide future therapeutic protocols in Taiwanese pediatric patients with AML.
Journal
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FLT3 (Fms-related tyrosine kinase 3) • RUNX1 (RUNX Family Transcription Factor 1) • KMT2A (Lysine Methyltransferase 2A) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)
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RUNX1 mutation