ReviewNature reviews. Clinical oncology2025
Therapeutic targeting of mismatch repair-deficient cancers.
Review in Nature reviews. Clinical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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Who cites it
19 citing papers in PubMed.
- Colorectal Cancer: Epidemiology, Risk Factors, Signaling Pathways, Clinical Features, Screening, Diagnosis, and Management.MedComm · 2026Review
- An antibody-PROTAC conjugate targets BRD4/c-Myc/PD-L1 to enhance immunotherapy efficacy in triple-negative breast cancer.Cell reports. Medicine · 2026Article
- Pharmacologic Inhibition of PMS2 Induces MMR Deficiency and Response to Immune Checkpoint Blockade.Cancer discovery · 2026Article
- G-Quadruplexes: Structural Diversity and Emerging Roles in Biomolecular Condensation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- DNA repair pathways in Mycobacterium leprae: insights from reductive genome evolution and therapeutic opportunities.Archives of microbiology · 2026Review
- Genomic loss of MLH1/PMS2 loci defines a mismatch repair deficient subgroup in monomorphic epitheliotropic intestinal T-cell lymphoma.Blood cancer journal · 2026Article
- Reconsidering adjuvant and perioperative immune-checkpoint inhibition: de-escalation, expansion and personalization.Nature reviews. Clinical oncology · 2026Review
- Cytotoxic and apoptotic effects of kaempferol 3-O-rhamnoside from Schima wallichii in HepG2 cells.Scientific reports · 2026Article
- Impact of germline MMR gene variants on immune checkpoint inhibitors response in patients with MSI-H/dMMR digestive cancers: a retrospective cohort analysis.Hereditary cancer in clinical practice · 2026Article
- Molecular Testing for Intrahepatic Cholangiocarcinoma: What, When, How?Journal of gastrointestinal cancer · 2026Review
- Reference-Free Microsatellite Instability Detection from Tumor Sequencing Using Intrasample Variability Modeling.Computational and structural biotechnology journal · 2026Article
- COL10A1 beyond skeletal development: a hypertrophic chondrocyte-specific collagen emerging as a potential biomarker and tumor microenvironment regulator in solid cancers.American journal of cancer research · 2026Review
- Umbralisib antagonizes multidrug resistance in ABCB1-overexpressing cancer cells.Frontiers in oncology · 2026Article
- Relationship between MLH1, MSH2, MSH6, and PMS2 protein expression status and clinicopathological characteristics in colorectal cancer tissues.Frontiers in medicine · 2026Article
- A Double-Edged Role for SIRT7 in Cancer: Can Anti-Cancer Immunity Tip the Balance?Pharmaceuticals (Basel, Switzerland) · 2025Review
- A common food mutagen promotes intestinal carcinogenesis by multiple mechanisms in mouse models of Lynch syndrome.NAR cancer · 2025Article
- Immune checkpoint inhibitors for the treatment of solid tumors and lymphoma in the past 26 years (2000-2025).Journal of hematology & oncology · 2025Review
- Soluble immune checkpoints in endometrial cancer - a discovery study.Frontiers in immunology · 2025Article
- Is there a role for impaired DNA mismatch repair system in the pathogenesis of ameloblastomas? A scoping review.Journal of oral biology and craniofacial researchReview
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA mismatch repair (MMR) is one of many evolutionarily conserved processes that act as guardians of genomic integrity. MMR proteins recognize errors that occur during DNA replication and initiate countermeasures to rectify those mistakes. MMR deficiency (MMRd) therefore leads to a dramatic accumulation of mutations. The MMRd genomic signature is characterized by a high frequency of single-base substitutions as well as insertions and/or deletions that preferentially occur in short nucleotide repeat sequences known as microsatellites. This accumulation leads to a phenomenon termed microsatellite instability, which accordingly serves as a marker of underlying MMRd. MMRd is associated with hereditary cancer syndromes such as Lynch syndrome and constitutional MMRd as well as with sporadic tumour development across a variety of tissues. High baseline immune cell infiltration is a characteristic feature of MMRd/microsatellite instability-high tumours, as is the upregulation of immune checkpoints. Importantly, the molecular profile of MMRd tumours confers remarkable sensitivity to immune-checkpoint inhibitors (ICIs). Many patients with MMRd disease derive durable clinical benefit when treated with these agents regardless of the primary tumour site. Nevertheless, a substantial subset of these patients will fail to respond to ICI, and increasing research is focused on identifying the factors that confer resistance. In this Review, we begin by discussing the biological function of the MMR machinery as well as the genomic sequelae of MMRd before then examining the clinical implications of MMRd with a specific focus on cancer predisposition, diagnostic approaches, therapeutic strategies and potential mechanisms of resistance to ICIs.
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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.