ArticleCancer research2025
Immune Checkpoint Blockade Delays Cancer Development and Extends Survival in DNA Polymerase Mutator Syndromes.
Article in Cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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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Who cites it
4 citing papers in PubMed.
- An antibody-PROTAC conjugate targets BRD4/c-Myc/PD-L1 to enhance immunotherapy efficacy in triple-negative breast cancer.Cell reports. Medicine · 2026Article
- Identification of DNA Replication Stress-Related Genes as Prognostic Biomarkers for Bladder Cancer.Combinatorial chemistry & high throughput screening · 2026Article
- Respiration defects limit serine synthesis required for lung cancer growth and survival.Nature communications · 2025Article
- Beyond proofreading: POLD1 mutations as dynamic orchestrators of genomic instability and immune evasion in cancer.Frontiers in immunology · 2025Review
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13 authors.
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Abstract
Mutations in the exonuclease domains of the replicative nuclear DNA polymerases POLD1 and POLE are associated with increased cancer incidence, elevated tumor mutation burden (TMB), and enhanced response to immune checkpoint blockade (ICB). Although ICB is approved for treatment of several cancers, not all tumors with elevated TMB respond, highlighting the need for a better understanding of how TMB affects tumor biology and subsequently immunotherapy response. To address this, we generated mice with germline and conditional mutations in the exonuclease domains of Pold1 and Pole. Engineered mice with Pold1 and Pole mutator alleles presented with spontaneous cancers, primarily lymphomas, lung cancer, and intestinal tumors, whereas Pold1 mutant mice also developed tail skin carcinomas. These cancers had highly variable tissue type-dependent increased TMB with mutational signatures associated with POLD1 and POLE mutations found in human cancers. The Pold1 mutant tail tumors displayed increased TMB; however, only a subset of established tumors responded to ICB. Similarly, introducing the mutator alleles into mice with lung cancer driven by mutant Kras and Trp53 deletion did not improve survival, whereas passaging these tumor cells in vitro without immune editing and subsequently implanting them into immunocompetent mice caused tumor rejection in vivo. These results demonstrated the efficiency by which cells with antigenic mutations are eliminated in vivo. Finally, ICB treatment of mutator mice earlier, before observable tumors had developed delayed cancer onset, improved survival and selected for tumors without aneuploidy, suggesting the potential of ICB in high-risk individuals for cancer prevention. Significance: Treating high-mutation burden mice with immunotherapy prior to cancer onset significantly improves survival, raising the possibility of utilizing immune checkpoint blockade for cancer prevention, especially in individuals with increased risk.
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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.