Ask about this productRelated genes to: NUP98 Blocking Peptide
- Gene:
- NUP98 NIH gene
- Name:
- nucleoporin 98
- Previous symbol:
- -
- Synonyms:
- NUP96
- Chromosome:
- 11p15.4
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-04
- Date modifiied:
- 2016-10-05
Related products to: NUP98 Blocking Peptide
Related articles to: NUP98 Blocking Peptide
- NUP98 rearrangements define a high-risk, genetically heterogeneous subtype of paediatric acute myeloid leukaemia (AML), yet comprehensive clinicogenetic and survival data remain limited. This retrospective, single-centre study of 32 paediatric patients (2017-2025) found a median age of 8.7 years and predominance of the NUP98::NSD1 fusion (68.8%), frequently co-mutated with FLT3-ITD (50%) and WT1 (43.8%). Complete remission (CR) rates increased from 53.1% to 87.5% after first and second induction. With a median follow-up of 41.7 months, the estimated 3-year overall survival (OS), event-free survival (EFS) and cumulative incidence of relapse (CIR) were 81.2% (95% confidence interval [CI], 65.9%-96.5%), 62.8% (95% CI, 43.8%-81.8%) and 28.1% (95% CI, 12.9%-45.6%), respectively; corresponding rates among the 29 transplanted patients were 79.8% (95% CI, 63.5%-96.1%), 68.7% (95% CI, 50.3%-87.1%) and 26.0% (95% CI, 11.1%-43.9%) respectively. Exploratory multivariate analysis identified failure to achieve CR after induction 2 as a risk factor for OS, WT1 mutation for relapse in the entire cohort and pretransplant minimal residual disease (MRD) positivity for relapse in the transplant subgroup. This confirms that NUP98-rearranged AML necessitates intensive therapy including transplant and highlights WT1 and pretransplant MRD as key prognostic markers for risk-adapted strategies. - Source: PubMed
Publication date: 2026/04/28
Zhang Zhi-XiaoZhang LinLu Ai-DongZhang Le-PingJia Yue-PingZeng Hui-Min - T-lymphoblastic lymphoma (T-LBL) is an aggressive malignancy of T-lymphoid precursors, rarely co-occurring with consequent rearrangement of nucleoporin 98 () gene. The fusion gene was first reported in a de novo T-cell acute lymphoblastic leukemia (T-ALL) patient. However, it has not yet been reported in patients with T-LBL. We report a case of T-LBL with the fusion gene. The fusion gene was discovered by RNA sequencing (RNA-seq) in the patient's bone marrow cells and verified in various tissues through direct sequencing and reverse transcriptase polymerase chain reaction (RT-PCR). Unfortunately, despite the use of various treatment methods, including traditional chemotherapy, anti-CD7 CAR-T cell therapy, and CD38-targeted therapy, the patient showed no improvement and ultimately died from disease progression. To our knowledge, this is the first report of the translocation involving and genes in T-LBL. It is necessary to collect additional cases and conduct carefully designed experiments to establish the recurrence of this fusion in other T-LBL cohorts and confirm its role as a novel oncogenic rearrangement in T-LBL, providing a basis for managing such patients. - Source: PubMed
Publication date: 2026/03/25
Chen XiaoyongWang LinlinZou JunyanZhou JihaoZhou YayingZuo MinHu LinaDong XiaoyingKe PengHou Junjie - Myelodysplastic syndrome (MDS) is a heterogeneous group of myeloid neoplasms characterized by treatment difficulties and a propensity to progress to acute myeloid leukemia. Impaired natural killer (NK) cell surveillance is a hallmark of MDS, yet the underlying molecular mechanisms remain poorly understood. This study aims to elucidate the mechanism by which HIF-1α regulates NK cell differentiation disorders and its impact on NK cell cytotoxicity in MDS. Flow cytometry was employed to compare HIF-1α expression and NK cell differentiation between wild-type and NUP98/HOXD13 (NHD13) mice. Our results demonstrated a significant increase in HIF-1α expression in the bone marrow and peripheral blood of MDS mice, accompanied by a notable decrease in immature NK cell subsets and activating receptors (NKG2D, NKp44, and DNAM-1). Overexpression of HIF-1α in human NK cells or pharmacological stabilization with CoCl2 inhibits the differentiation into mature NK cells, suppresses the expression of degranulation molecules such as Granzyme B, and impairs NK cell cytotoxicity. Western blot analysis indicated that HIF-1α regulates NK cell differentiation and function via the JAK1/STAT5/SOCS2 signaling pathway. Collectively, these findings suggest that the hypoxic microenvironment in MDS enhances HIF-1α expression, which subsequently impairs NK cell maturation and inhibits their cytotoxicity. Targeting HIF-1α may delay MDS progression by enhancing NK cell function via the JAK1/STAT5/SOCS2 signaling pathway. - Source: PubMed
Xu ShujuanJiang YixiangWang ShengtaoChen BeiliLin WenyuanJiang FangWu XianyiTang RongfangNie YuweiChen TongtongWang Xiaotao - Osteoarthritis (OA) existed as a degenerative arthropathy that involved the cartilage and many of its surrounding tissues. SUMOylation was an important post-translational modification. Some studies had confirmed that SUMOylation was associated with the occurrence of OA. However, there were relatively few related studies, and the explicit action mechanism of SUMOylation-related genes (SRGs) in OA remained unclear. The objective of this research was to detect and verify key genes related to SRGs in OA. - Source: PubMed
Publication date: 2026/03/31
Liu AnsongYang YanlinXiang JieHu YihengYang JifaZhang YuDeng YueChen Yong - Chronic myeloid leukemia (CML) is a hematologic malignancy originating from hematopoietic stem cells with the fusion oncogene BCR-ABL1 on the Philadelphia chromosome, which drives the abnormal proliferation of leukemic blast cells within the bone marrow microenvironment. While previous research has primarily focused on the hematopoietic compartment, the functional contribution of the bone marrow microenvironment to the CML pathology remains understudied. We investigated the changes in the peripheral nervous system in the bone marrow with myeloid leukemia via immunofluorescence staining of tyrosine hydroxylase (TH) and calcitonin gene-related peptide (CGRP) antibodies in mouse with NUP98-HOXA9- and BCR-ABL1-expressing myeloid leukemia. We found that the TH-positive fibers were significantly reduced, while no overt changes were observed in CGRP-positive nerves in the bone marrow. The reduction in TH-positive nerve cells was also evident in the spleen. Human patient gene expression data suggested that the levels of sympathetic nerve receptor expression change during the blastic transformation of human CML. Our findings indicate that the sympathetic nervous system regulates the pathogenesis of myeloid leukemia and could play a crucial role in the disease progression of myeloid leukemia. - Source: PubMed
Publication date: 2026/04/13
Okigawa SayumiInafuku HibikiHattori AyunaIto Takahiro