ReviewFrontiers in immunology2025
Beyond proofreading: POLD1 mutations as dynamic orchestrators of genomic instability and immune evasion in cancer.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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
6 citing papers in PubMed.
- Genotype-phenotype heterogeneity among patients with lipodystrophy harboring rare POLD1 variants.The Journal of clinical endocrinology and metabolism · 2026Article
- Screening, Prognostic, and Predictive Molecular Tools for Colorectal Cancer: Recent Advances in the Classical Background.International journal of molecular sciences · 2026Review
- Case Report: Tumor regression and neurological recovery in paraplegia from POLD1-mutated hepatocellular carcinoma treated with targeted immunotherapy and electroacupuncture.Frontiers in immunology · 2026Article
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Defying the Prognostic Odds: A Case Report of Unexpected Complete Remission of Metastatic Ampullary Carcinoma With Palliative Chemotherapy.Case reports in oncological medicine · 2025Article
- Case Report: Expansion of theFrontiers in oncology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA polymerase delta (Pol δ) is a cornerstone of genomic stability, orchestrating DNA replication and repair through its catalytic subunit, POLD1. This subunit's 3'-5' exonuclease domain proofreads replication errors, ensuring fidelity. However, POLD1 mutations-particularly in this domain-disrupt this function, triggering genomic instability and a hypermutated state in cancers. This review delves into the multifaceted roles of POLD1 mutations, spotlighting their contributions to tumorigenesis and immunotherapy responses. Beyond their established link to syndromes like polymerase proofreading-associated polyposis (PPAP), these mutations unexpectedly enhance tumor immunogenicity in microsatellite-stable (MSS) tumors, previously considered largely resistant to immune checkpoint inhibitors (ICIs). By elevating tumor mutation burden and generating unique mutational signatures (e.g., SBS10d), POLD1 mutations sensitize MSS tumors to ICIs, challenging the dominance of microsatellite instability (MSI) as an immunotherapy predictor. Integrating structural insights, molecular mechanisms, and clinical data, this review positions POLD1 mutations as both a driver of cancer progression and a promising biomarker, redefining therapeutic possibilities in precision oncology.
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