Evidence map›Paper›PMID 41331183›Full record

SynthesisMedical oncology (Northwood, London, England)2025

Targeting DNA damage response to enhance cancer immunotherapy efficacy: molecular mechanisms and clinical advances.

Ziyi Tang, Pan Chen, Bo Xiang, Wei Xiong, Pan Wu, Zhaoyang Zeng

Abstract readSystematic Review
PubMed Publisher
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Ziyi TangNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410078, China.
Pan ChenNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410078, China.
Bo XiangKey Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Xiangya School of Basic Medical Sciences, Central South University, Changsha, Hunan, China.
Wei XiongKey Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Xiangya School of Basic Medical Sciences, Central South University, Changsha, Hunan, China.
Pan WuNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410078, China. 1554520342@qq.com.
Zhaoyang ZengNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410078, China. zengzhaoyang@csu.edu.cn.ORCID http://orcid.org/0000-0002-0648-0565

Funding

National Natural Science Foundation of China 82403859Natural Science Foundation of Changsha kq2402235Natural Science Foundation of Hunan Province 2024JJ6544
6 · The paper itself

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

DNA DamageImmunotherapyNeoplasmsAnimalsDNA RepairHumansImmune Checkpoint InhibitorsMolecular Targeted TherapyTumor MicroenvironmentImmune Checkpoint InhibitorsCancer immunotherapyDNA damage responseDNA damage response inhibitors

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.