ReviewClinical and translational medicine2026
Targeting the nuclear export receptor exportin-1 in acute myeloid leukaemia: From biology to clinical translation.
Review in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Diagnosis-Driven Targeted Therapy in Acute Myeloid Leukemia: Clinical Integration of Tyrosine Kinase, BCL-2, and CD33-Directed Strategies with Midostaurin, Venetoclax, and Gemtuzumab Ozogamicin.Journal of clinical medicine · 2026Review
- Nuclear-Cytoplasmic Axis in Cancer: From Protein Mislocalization to Anticancer Drug Resistance.Oncology research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
backgroundExportin-1 (XPO1), a key regulator of nucleocytoplasmic transport, is frequently dysregulated in acute myeloid leukemia (AML) and contributes to leukemogenesis, disease progression and therapeutic resistance. Selective inhibitors of nuclear export (SINEs), especially selinexor and eltanexor, have shown promising antileukemic potential. However, their clinical value, optimal therapeutic positioning and rational use in AML remain to be fully clarified.
methodsWe collected and reviewed relevant literature to summarize the biological roles of XPO1 in AML and the therapeutic potential of XPO1 inhibitors in preclinical and clinical settings.
resultsIn this review, we focus on the nuclear export function of XPO1 and its pathogenic role in AML. We summarize the mechanisms of action, preclinical evidence, clinical trial results, adverse effects, resistance mechanisms and potential response biomarkers associated with XPO1 inhibitors in AML.
conclusionsXPO1 inhibition has emerged as a promising therapeutic strategy for AML, offering a novel approach to targeting aberrant nucleocytoplasmic transport and overcoming treatment resistance. Future studies should focus on optimizing dosing schedules, identifying predictive biomarkers and developing effective combination strategies in molecularly selected AML populations. KEY POINTS: XPO1 hyperactivation rewires nucleocytoplasmic transport and sustains leukaemogenic programs in genetically defined acute myeloid leukaemia (AML) subsets. Selective XPO1 inhibitors (selinexor, eltanexor) show preferential activity in NPM1-mutated, DEK::NUP214-positive and SF3B1-mutated myeloid neoplasms. Combination strategies with hypomethylating agents, BCL-2 inhibitors and other targeted therapies enhance depth and durability of responses but are limited by toxicity. Future clinical trials should focus on molecularly selected populations, biomarker-guided dosing and translational endpoints such as measurable residual disease (MRD) and clonal dynamics.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.