ReviewCancer research2025
Mismatch Repair as a Dynamic and Clinically Actionable Vulnerability in Cancer.
Review in Cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Targeting the DNA Damage Response in Cancer.MedComm · 2026Review
- Pharmacologic Inhibition of PMS2 Induces MMR Deficiency and Response to Immune Checkpoint Blockade.Cancer discovery · 2026Article
- Review
- MYC at the tumor-immune interface: mechanisms of immune escape and immunotherapy resistance.Frontiers in immunology · 2026Review
- Chemoresistance in the era of immunotherapy: challenges and novel combinatorial strategies for digestive system tumors.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
DNA mismatch repair (MMR) preserves genomic integrity by correcting replication errors. Deficiency in MMR results in microsatellite instability, increased tumor mutational burden, neoantigen generation, and activation of the immune response. In this review, we first outline how MMR loss promotes immune activation and responsiveness to immune checkpoint blockade (ICB), establishing MMR-deficient (MMRd) status as the first tumor-agnostic biomarker for ICB therapy. Subsequently, we summarize the compelling evidence that defines MMR status as a dynamic, context-dependent process influenced by environmental and therapeutic pressures, rather than a fixed, binary trait. Accordingly, we discuss the implications of the spatial and temporal heterogeneity of MMR status for both the diagnosis and treatment of cancer, the differential response of MMRd tumors to ICB, as well as the occasional benefits observed in MMR-proficient immune-cold cancers. We then explore strategies to exploit MMR dynamics and mimic MMRd-like phenotypes through alkylating agents, pharmacologic MMR inhibition, and stress-mediated modulation, with the aim of sensitizing refractory tumors to immunotherapy. Finally, we report emerging therapeutic opportunities in MMRd tumors, including Werner helicase inhibition, nonsense-mediated decay blockade, and neoantigen-targeted vaccines. Altogether, reframing MMR as a dynamic and targetable axis may broaden immunotherapy applicability and advance precision immune oncology across different tumor types.
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Registered trials
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.