ArticleJournal of translational medicine2025
Innovative evaluation of selinexor and JQ1 synergy in leukemia therapy via C-MYC inhibition.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Preclinical characterization of a reversible XPO1 inhibitor for cancer therapy.Nature communications · 2026Article
- c-Medical sciences (Basel, Switzerland) · 2026Review
- Targeting the nuclear export receptor exportin-1 in acute myeloid leukaemia: From biology to clinical translation.Clinical and translational medicine · 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
8 authors.
Funding
Abstract
backgroundAcute myeloid leukemia (AML) remains a therapeutic challenge due to drug resistance and relapse. Selinexor, an XPO1 inhibitor, shows limited efficacy as monotherapy, necessitating combination strategies. JQ1, a BET inhibitor targeting MYC, may synergize with Selinexor to enhance antileukemic effects.
methodsAML cell lines, primary patient samples, and xenograft models (MLL-AF9, CDX, PDX) were treated with Selinexor and JQ1 alone or combined. Synergy was assessed via viability assays (Compusyn/SynergyFinder), apoptosis (flow cytometry/Western blot), and C-MYC suppression (qPCR/CRISPR). In vivo efficacy was evaluated by tumor burden (flow cytometry) and survival.
resultsThe combination demonstrated strong synergy (CI < 1, HSA > 10) across AML models, with > 80% inhibition in cell lines and primary samples. Mechanistically, it suppressed C-MYC (protein/mRNA), induced apoptosis (cleaved PARP), and arrested cell cycle. In vivo, the combination reduced leukemic burden in bone marrow, spleen, and liver, extending survival in xenografts. PDX models confirmed efficacy in primary AML cells.
conclusionsSelinexor and JQ1 synergistically target AML by dual C-MYC inhibition, offering a promising strategy to overcome resistance. Further clinical evaluation is warranted.
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Registered trials
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