ArticleCancer cell2026
IFNγ-dependent metabolic reprogramming restrains an immature, pro-metastatic lymphatic state in melanoma.
Article in Cancer cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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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
7 citing papers in PubMed.
- The effects of IFNγ on tissue physiology through structural cells.Nature reviews. Immunology · 2026Review
- Lymphatic Endothelial Cells in Health and Disease.MedComm · 2026Review
- Glioma-Associated Microglia Augment Neuronal Hyper-Excitability in Glioma.Brain tumor research and treatment · 2026Review
- Kynurenic acid mediates epicardial fat-induced lymphatic metabolic dysfunction in atrial fibrillation.Nature communications · 2026Article
- Lymphatic egress recycles tumor-experienced effector CD8 T cells to sustain immune surveillance.bioRxiv : the preprint server for biology · 2026Article
- Pancreatic Lymphatics in Health and Disease: Evolution, Embryology, and Neural Control.Lymphatics · 2026Article
- Editorial: Challenges and opportunities in tumor metabolomics.Frontiers in molecular biosciences · 2026Article
Corrections and comments
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Authors and funding
26 authors.
Funding
Abstract
Lymphatic vessels activate anti-tumor immune surveillance and support metastasis. Whether there are distinct lymphatic phenotypes that govern immunity and metastasis remains unclear. Here we reveal that cytotoxic immunity normalizes lymphatic function and uncouples immune and metastatic potential. We demonstrate that intratumoral lymphatic vessel density negatively correlates with cytotoxic immunity and that IFNγ reprograms the intratumoral lymphatic state. Lymphatic deletion of Ifngr1 expanded the intratumoral lymphatic network and drove the emergence of a tip-like state that promotes lymph node metastasis but not dendritic cell migration or response to immune checkpoint blockade (ICB). Mechanistically, IFNγ restrains proliferation and cell state programs through inhibition of mitochondrial respiration. Lymphatic-specific inhibition of mitochondrial complex III restrained the intratumoral tip-like state, blocked metastasis, and enhanced the response to ICB. Our data reveal that IFNγ induces a metabolic and phenotypic switch in tumor-associated lymphatic vessels that blocks regional metastasis and reinforces immune surveillance.
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Registered trials
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