SynthesisMedical oncology (Northwood, London, England)2025
Targeting DNA damage response to enhance cancer immunotherapy efficacy: molecular mechanisms and clinical advances.
Synthesis in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed.
- DNA-PKcs and PARP1 at the interface between DNA damage responses and cGAS-STING signaling: context-dependent roles and therapeutic implications.Cancer biology & therapy · 2026Review
- Targeting the DNA Damage Response in Cancer.MedComm · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
The DNA damage response (DDR) is a critical cellular mechanism for maintaining genomic stability and integrity. Over the past decade, targeting DDR pathways in tumors has led to significant therapeutic advances but faces limitations such as drug resistance and combinatorial toxicity. Meanwhile, cancer immunotherapy has shown remarkable efficacy in some solid tumors, yet response rates to single-agent therapies remain modest and are often hindered by immunosuppression in the tumor microenvironment (TME). DDR inhibitors (DDRi) can potentiate antitumor immunity via mechanisms such as increased neoantigen release and activation of the cGAS-STING pathway, providing a rationale for combining DDRi with immunotherapy. Indeed, the combination of DDRi with immune checkpoint inhibitors (ICIs) has shown synergistic promise in clinical studies, while combinations of DDRi with novel immunotherapeutic approaches are now in early development. Here, we systematically review DDR-targeted cancer therapies and their molecular mechanisms for enhancing tumor immunogenicity, along with recent clinical advances in combining DDRi with immunotherapy. Our goal is to provide a theoretical foundation and translational insight for optimizing these combination strategies.
Indexed as
Identifiers
41331183What OpenQuestion holds
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.