Ask about this productRelated genes to: XPO1 antibody
- Gene:
- XPO1 NIH gene
- Name:
- exportin 1
- Previous symbol:
- -
- Synonyms:
- CRM1, CRM-1, emb
- Chromosome:
- 2p15
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-12
- Date modifiied:
- 2019-03-12
Related products to: XPO1 antibody
Related articles to: XPO1 antibody
- Neuroblastoma, a pediatric cancer derived from sympathetic ganglia of the peripheral nervous system, frequently metastasizes, driving poor outcomes. Primary neuroblastomas are well-characterized, but the mechanisms underlying metastasis remain poorly understood. Here, by using single-cell and spatial multiomics, we identified that lymph node metastases in high-risk neuroblastomas display distinctive cellular heterogeneity and plasticity, marked by mesenchymal-like and stem-like states and heightened epithelial-to-mesenchymal transition activity compared to primary adrenal tumors. In addition, compared to primary adrenal masses, the metastatic niche display increased immunosuppressive myeloid programs, heightened immune checkpoint signaling, and lymphocyte exhaustion, which are indicative of immune evasion and dysfunction. Notably, metastatic neuroblastomas show elevated eIF4F translation machinery and XPO1 levels. Dual inhibition of eIF4A and XPO1 synergistically halted tumor growth and prolonged survival in xenograft models. Together, our multiomics studies reveal the molecular and cellular plasticity that contributes to therapy resistance and highlight exploitable therapeutic vulnerabilities in high-risk metastatic neuroblastomas. - Source: PubMed
Publication date: 2026/07/17
Wu Lai Man NatalieOblinger Janet LXin DazhuanRao RohitZhang FengAdam MikeLopez-Nunez OscarSzabo Saravon Allmen DanielChang Long-ShengWeiss Brian DLu Qing Richard - Glioblastoma (GBM) remains associated with poor outcomes, with most recurrences occurring within the high-dose radiation field suggesting persistent radioresistance. Exportin 1 (XPO1) inhibition with Selinexor has demonstrated radiosensitizing effects in preclinical models. We conducted a phase I trial to evaluate the safety, tolerability, and preliminary efficacy of Selinexor in combination with standard chemoradiation for newly diagnosed GBM. - Source: PubMed
Publication date: 2026/07/07
Mathen PeterChaudhry HumaMackey MeganCooley-Zgela TheresaMasciocchi MatthewLi BoHuang ErichWu JingSmart DeeDeeKrauze AndraCamphausen Kevin - Myelofibrosis (MF) is a chronic myeloproliferative neoplasm (MPN) characterized by splenomegaly, constitutional symptoms, marrow fibrosis, cytopenias and inflammation. Janus kinase 2 (JAK2) inhibitors, such as ruxolitinib, reduce splenomegaly and alleviate symptoms but have limited disease-modifying activity, and resistance frequently develops. Selinexor, an oral selective exportin (XPO1) inhibitor, restores nuclear retention of tumour suppressors and inhibitors of inflammatory signalling. Dual XPO1/JAK2 inhibition targets complementary downstream pathways, enhancing suppression of MF progenitor cell fitness. We evaluated selinexor plus ruxolitinib in MF models, including JAK2V617F or calreticulin (CALR) exon 9-mutant MPN cell lines and samples from patients with MF. The combination showed greater anti-proliferative activity than JAK2 inhibition alone and suppressed colony formation from MF Cluster of Differentiation 34 (CD34)+ cells. Selinexor remained active in a ruxolitinib-resistant MPN cell line, inducing G1 arrest and apoptosis. Multi-omic analyses demonstrated increased nuclear retention of p53 and disruption of Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) signalling, complementing and extending ruxolitinib-targeted pathways. The combination suppressed NF-κB transcriptional activity and reduced Tumor Necrosis Factor alpha (TNFα), Interleukin-6 (IL-6) and Monocyte Chemoattractant Protein-1 (MCP-1) secretion from MF patient peripheral blood mononuclear cells. These findings highlight that selinexor plus ruxolitinib affects both MF haematopoietic cell-intrinsic and microenvironment-related pathways, providing a novel disease-modifying strategy with the potential to improve clinical outcomes in patients with MF. - Source: PubMed
Publication date: 2026/07/14
Kashyap TrinayanEllero Andrea AWalker Christopher JMaloof Marie ELu MinXia LijuanHoffman RonaldTaverna Pietro - Relapsed or refractory extranodal natural killer/T-cell lymphoma (R/R NKTCL) remains a highly lethal disease, particularly after failure of PD-1 blockade-based therapy. Preclinical data suggest that inhibition of exportin-1 (XPO1) may enhance antitumor immunity and synergize with PD-1 blockade. - Source: PubMed
Publication date: 2026/07/11
Liu ChuanxuLi DahuiGao YanZhang WenhaoGuo ZhiZhao JunHuang HuiqiangTao Rong - Asparaginase-based regimens and anti-PD-1 therapies have significantly improved survival in patients with extranodal natural killer/T-cell lymphoma (ENKTL) and are now increasingly incorporated into earlier treatment lines. However, clinical outcomes for patients with dual resistance to asparaginase and PD-1 inhibitors remain poorly defined. We conducted a multicenter retrospective study of 61 patients with dual resistance from a cohort of 900 ENKTL patients across 12 academic centers in China. Among 61 patients, median overall survival from initial diagnosis (OS-1) was 21.9 months (95% CI: 14.7-43.1). After the onset of dual resistance, the median post-resistance survival (OS-2) was 4.9 months (95% CI: 2.8-9.9). Rechallenge with asparaginase-based regimens or anti-PD-1 agents resulted in only limited benefit, yielding median progression-free survival (PFS) of 3.2 months (95% CI: 1.4-5.0) and 2.7 months (95% CI: 2.1-3.3), respectively. Chidamide-containing regimens were associated with a significantly longer OS-2 compared to regimens without chidamide (HR, 0.46; 95% CI: 0.24-0.88; P = 0.019). Other novel agents, including inhibitors of XPO1, PI3K, and JAK1, along with brentuximab vedotin, did not demonstrate a significant survival benefit in patients with dual-resistant ENKTL. This is the first comprehensive analysis of dual-resistant ENKTL, revealing poor prognosis and suggesting a potential signal of benefit associated with chidamide-containing regimens. - Source: PubMed
Publication date: 2026/07/09
Li RanSheng LixiaMa JieLu XuzhangWang XiranLiu HailingChen LvwenShen HaoruiXia YiZhang JingHuang HongmingShi JinningWang WeiZhao XiaXu XiaohongWang ChunlingSun MeiDing KaiyangFan Lei