ArticleProceedings of the National Academy of Sciences of the United States of America2025
DDX54 downregulation enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- DARS2 serves as an independent prognostic factor and participates in multiple biological processes in bladder urothelial carcinoma.Translational andrology and urology · 2026Article
- Correlation between tumor mutational burden and CT radiographic features in EGFR exon 19 deletion-mutated lung adenocarcinoma: a diagnostic accuracy study.Frontiers in medicine · 2026Article
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4 authors.
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Abstract
High tumor mutational burden (TMB-H) is a predictive biomarker for the responsiveness of cancer to immune checkpoint inhibitor (ICI) therapy that indicates whether immune cells can sufficiently recognize cancer cells as nonself. However, about 30% of all cancers from The Cancer Genome Atlas (TCGA) are classified as immune-desert tumors lacking T cell infiltration despite TMB-H. Since the underlying mechanism of these immune-desert tumors has yet to be unraveled, there is a pressing need to transform such immune-desert tumors into immune-inflamed tumors and thereby enhance their responsiveness to anti-PD1 therapy. Here, we present a systems framework for identifying immuno-oncotargets, based on analysis of gene regulatory networks, and validating the effect of these targets in transforming immune-desert into immune-inflamed tumors. In particular, we identify DEAD-box helicases 54 (DDX54) as a master regulator of immune escape in immune-desert lung cancer with TMB-H and show that knockdown of DDX54 can increase immune cell infiltration and lead to improved sensitivity to anti-PD1 therapy.
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