ReviewBritish journal of cancer2024
DNA repair-dependent immunogenic liabilities in colorectal cancer: opportunities from errors.
Review in British journal of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- Modulating the gut microbiota to enhance immune checkpoint inhibitor efficacy in colorectal cancer: mechanisms, therapeutic strategies, and clinical perspectives.Gut microbes · 2026Review
- A prospective clinical study on the effectiveness ofJournal of traditional and complementary medicine · 2026Article
- Piroctone olamine promotes BECN1 transcription and activates autophagy by targeting HDAC6 in colorectal cancer.Acta pharmacologica Sinica · 2026Article
- The Mechanistic Crosstalk between Probiotics, ncRNAs, and Autophagy: Implications for Colorectal Cancer Precision Medicine.Expert reviews in molecular medicine · 2026Review
- Overexpression of ENDOD1 inhibits proliferation, migration, and invasion of colorectal cancer.Cell division · 2026Article
- Review
- Degrees of H2AX phosphorylation correlate with unique features of the intratumoral immune microenvironment in colorectal carcinomas.The oncologist · 2026Article
- Review
- Review
- Predicting homologous recombination deficiency and treatment responses using a computed tomography-based foundation model: a preclinical study.NPJ precision oncology · 2026Article
- Immune checkpoint inhibitors in dMMR-MSI-H colorectal cancer: rationale, progress and prospects.Frontiers in immunology · 2026Review
- Digital immune twins and ai-integrated multi-omic biomarkers: Redefining personalized immunotherapy in non-small cell lung cancer.Iranian journal of basic medical sciences · 2026Review
- HMGB1 reduce DNA damage by binding KU70 to activate NHEJ pathway in colorectal cancer cells after radiation.PloS one · 2026Article
- Mismatch Repair as a Dynamic and Clinically Actionable Vulnerability in Cancer.Cancer research · 2025Review
- Confounder-Adjusted Differentiation of Colorectal Cancer via Dynamic Propagation of Pathway Influence.International journal of molecular sciences · 2025Article
- EPS8L2 drives colorectal cancer cell proliferation and migration via YBX1-dependent activation of G3BP2 transcription.Cell death & disease · 2025Article
- Reassessing the Prognostic Value of Lymph Node Metastasis in Deficient Mismatch Repair Colorectal Cancer.Current oncology (Toronto, Ont.) · 2025Article
- Metabolic crossroads: unravelling immune cell dynamics in gastrointestinal cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Colorectal cancer (CRC) remains one of the major causes of cancer death worldwide. Chemotherapy continues to serve as the primary treatment modality, while immunotherapy is largely ineffective for the majority of CRC patients. Seminal discoveries have emphasized that modifying DNA damage response (DDR) mechanisms confers both cell-autonomous and immune-related vulnerabilities across various cancers. In CRC, approximately 15% of tumours exhibit alterations in the mismatch repair (MMR) machinery, resulting in a high number of neoantigens and the activation of the type I interferon response. These factors, in conjunction with immune checkpoint blockades, collectively stimulate anticancer immunity. Furthermore, although less frequently, somatic alterations in the homologous recombination (HR) pathway are observed in CRC; these defects lead to genome instability and telomere alterations, supporting the use of poly (ADP-ribose) polymerase (PARP) inhibitors in HR-deficient CRC patients. Additionally, other DDR inhibitors, such as Ataxia Telangiectasia and Rad3-related protein (ATR) inhibitors, have shown some efficacy both in preclinical models and in the clinical setting, irrespective of MMR proficiency. The aim of this review is to elucidate how preexisting or induced vulnerabilities in DNA repair pathways represent an opportunity to increase tumour sensitivity to immune-based therapies in CRC.
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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.