ArticleNature cancer2026
Leptomeningeal metastatic cancer cells induce a permissive choroid plexus vasculature through extracellular-vesicle-derived 5-HIAA signaling.
Article in Nature cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- α-KG conformationally stabilizes nuclear GLUD1-SNAIL complex to fuel trans-endothelial migration in metastasis.Nature communications · 2026Article
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The choroid plexus acts as a crucial barrier in leptomeningeal metastasis (LM), yet the mechanisms through which cancer cells modulate supportive premetastasis niches remain unclear. Here, we show that remodeling of the metabolic microenvironment modifies the structure and function of choroid plexus vessels, which destroy vascular integrity to facilitate metastatic colonization. An abnormal increase in the metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid and choroid plexus indicates a predisposition. Before initially invading the choroid plexus through cancer cells, 5-HIAA-containing extracellular vesicles specifically target vessels, resulting in vascular distortion, abnormal hemodynamics, compromised permeability and facilitation of cancer cell traversal. Mechanistically, aryl hydrocarbon receptor pathway activation by 5-HIAA is linked to choroid plexus vascular remodeling, characterized by aberrant expression of mechanoreceptors and tight junction proteins. Hence, our findings underscore the key role of 5-HIAA in supportive niche formation and highlight metabolic determinants that govern choroidal plasticity to effectively prevent metastatic colonization in LM initiation.
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Registered trials
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