ArticleCancer cell2018
Mutant NPM1 Maintains the Leukemic State through HOX Expression.
Article in Cancer cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 212 papers, 1 of them a synthesis that pooled it.
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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
212 citing papers in PubMed, 1 synthesis or guideline pooled it, 309 citations in OpenAlex.
- Acute Myeloid Leukemia: From Biology to Clinical Practices Through Development and Pre-Clinical Therapeutics.Frontiers in oncology · 2020Pooled it
- Ziftomenib in Relapsed or RefractoryJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025Trial
- Reduced dose azacitidine plus venetoclax as maintenance therapy in acute myeloid leukaemia following intensive or low-intensity induction: a single-centre, single-arm, phase 2 trial.The Lancet. Haematology · 2024Trial
- The landscape of gene co-expression modules correlating with prognostic genetic abnormalities in AML.Journal of translational medicine · 2021Trial
- How do low-complexity domain interactions control transcription?Biochemical Society transactions · 2026Review
- Thrombotic and hemorrhagic complications in NPM1-mutated AML: Association with APL-like immunophenotype and impact on early mortality.Journal of thrombosis and thrombolysis · 2026Article
- Ziftomenib with venetoclax and azacitidine for relapsed/refractory NPM1-mutated acute myeloid leukemia.Blood · 2026Article
- The cellular landscape of druggable RNA-binding proteins.Nature reviews. Drug discovery · 2026Review
- Two Decades ofCancers · 2026Review
- The interaction between NPMc+ and Orai1 induces abnormal calcium influx to facilitate leukemogenesis.The FEBS journal · 2026Article
- NPM1-rearranged AML: clinical features, molecular pathogenesis, and therapeutic perspectives.International journal of hematology · 2026Review
- Beyond nuclear export: chromatin-bound XPO1/CRM1 as a transcriptional scaffold.International journal of hematology · 2026Review
- Identification of GSE1 as a PAX5 fusion partner and characterization of PAX5 fusion signature in B-cell acute lymphoblastic leukaemia.British journal of haematology · 2026Article
- Menin inhibitors as a treatment for acute leukemia: from bench to the clinic.Blood neoplasia · 2026Review
- Article
- Systematic Targeting of Protein Complexes with Molecular COUPLrs.Cancer discovery · 2026Article
- Newly diagnosed acute myeloid leukemia in Fit patients: 2026 treatment algorithms.Blood cancer journal · 2026Review
- Targeting SMC3 deacetylation synergizes with XPO1 inhibition to reprogram the epigenetic landscape and suppress NPM1-mutated acute myeloid leukemia.Nature communications · 2026Article
- Menin Inhibition in Acute Myeloid Leukemia: Rewiring Leukemic Transcriptional Networks.International journal of molecular sciences · 2026Review
- Outstanding Questions to Understand and Target Splicing Factor-Mutant Blood Cancers.Blood cancer discovery · 2026Article
152 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 6 institutions in 2 countries.
Funding
Abstract
NPM1 is the most frequently mutated gene in cytogenetically normal acute myeloid leukemia (AML). In AML cells, NPM1 mutations result in abnormal cytoplasmic localization of the mutant protein (NPM1c); however, it is unknown whether NPM1c is required to maintain the leukemic state. Here, we show that loss of NPM1c from the cytoplasm, either through nuclear relocalization or targeted degradation, results in immediate downregulation of homeobox (HOX) genes followed by differentiation. Finally, we show that XPO1 inhibition relocalizes NPM1c to the nucleus, promotes differentiation of AML cells, and prolongs survival of Npm1-mutated leukemic mice. We describe an exquisite dependency of NPM1-mutant AML cells on NPM1c, providing the rationale for the use of nuclear export inhibitors in AML with mutated NPM1.
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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.