ArticleLeukemia2017
NUP98 is rearranged in 3.8% of pediatric AML forming a clinical and molecular homogenous group with a poor prognosis.
Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.
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Who cites it
83 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.
- Molecular Landscape of Acute Myeloid Leukemia in Pediatric Patient-Age-Related Correlations: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- [Clinical analysis of nine pediatric cases of acute myeloid leukemia with NUP98 rearrangement].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Article
- Article
- Comprehensive mutational profiling and clinical outcome of adult acute myeloid leukemia patients with NUP98 rearrangement.Leukemia · 2026Article
- Durable remission despite transplantation with active disease in therapy-related NUP98::TOP1-rearranged acute myeloid leukemia.Annals of hematology · 2026Article
- Review
- [Prognostic analysis of NUP98 rearrangement in patients with pediatric acute myeloid leukemia undergoing allogeneic hematopoietic stem cell transplantation].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Article
- NUP98 rearrangements in adult AML patients: evaluation of clinical implications and identification of novel fusion partners.Leukemia · 2026Article
- Evolutionary Restructuring and Systematic Review of theJournal of developmental biology · 2026Review
- Genetic landscape of pediatric acute myeloid leukemia in Taiwan.Scientific reports · 2026Article
- Clinical Integration of Menin Inhibitors in AML: Evolving Data and Therapeutic Perspectives.Oncology research · 2026Review
- RareAmerican journal of cancer research · 2026Article
- NSD Family-Mediated H3K36 Methylation in Human Cancer: Mechanisms and Therapeutic Opportunities.Biomedicines · 2025Review
- Allogeneic transplantation in adverse-risk acute myeloid leukemia: Challenges, strategies, and future directions.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025Article
- Challenges in accuracy in molecular genetic diagnosis of childhood AML: case series.Annals of hematology · 2025Article
- Review
- Application of Optical Genome Mapping for the Diagnosis and Risk Stratification of Myeloid and Lymphoid Malignancies.International journal of molecular sciences · 2025Article
- Novel NUP98:TNRC18 fusion transcript in acute myeloid leukemia: a case report and literature review.Blood science (Baltimore, Md.) · 2025Article
- Review
- Promising activity of Selinexor in the treatment of a patient with refractory NUP98-NSD1+/FLT3-ITD + acute myeloid leukemia.Annals of hematology · 2025Article
23 more citing papers are in PubMed but not listed here.
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Authors and funding
26 authors at 11 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pediatric acute myeloid leukemia (AML) is a rare disease whose prognosis is highly variable according to factors such as chromosomal abnormalities. Recurrent genomic rearrangements are detected in half of pediatric AML by karyotype. NUcleoPorin 98 (NUP98) gene is rearranged with 31 different fusion partner genes. These rearrangements are frequently undetected by conventional cytogenetics, as the NUP98 gene is located at the end of the chromosome 11 short arm (11p15). By screening a series of 574 pediatric AML, we detected a NUP98 rearrangement in 22 cases (3.8%), a frequency similar to CBFB-MYH11 fusion gene (4.0%). The most frequent NUP98 fusion gene partner is NSD1. These cases are homogeneous regarding their biological and clinical characteristics, and associated with bad prognosis only improved by bone marrow transplantation. We detailed the biological characteristics of these AML by exome sequencing which demonstrated few recurrent mutations (FLT3 ITD, WT1, CEBPA, NBPF14, BCR and ODF1). The analysis of the clonal structure in these cases suggests that the mutation order in the NUP98-rearranged pediatric AML begins with the NUP98 rearrangement leading to epigenetic dysregulations then followed by mutations of critical hematopoietic transcription factors and finally, activation of the FLT3 signaling pathway.
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