Evidence map›Paper›PMID 42800308›Full record

ReviewEBioMedicine2026

Tumour-associated dsRNA accumulation and innate immune activation: mechanistic basis and therapeutic strategies.

Shaoping Li, Yanfei Huo, Hangwei Fa, Linyu Han, Huiwen Luan, Pengxiao Han, Yi Liu, Lixin Zheng, Chang Liu, Kaiyue Fan and 2 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in EBioMedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Shaoping LiSchool of Clinical Medicine, Shandong Second Medical University, Weifang, China; Shandong Provincial Key Laboratory of Precision Oncology, Cancer Research Center, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong Province, 250117, China.
Yanfei HuoShandong Provincial Key Laboratory of Precision Oncology, Cancer Research Center, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong Province, 250117, China.
Hangwei FaIntegrative Center for Frontier Biotech and Pharmaceutical Sciences, School of Life Sciences, Shandong First Medical University and Shandong Academy of Medical Sciences, Taian, Shandong Province, 271021, China.
Linyu HanShandong Provincial Key Laboratory of Precision Oncology, Cancer Research Center, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong Province, 250117, China.
Huiwen LuanShandong Provincial Key Laboratory of Precision Oncology, Cancer Research Center, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong Province, 250117, China.
Pengxiao HanShandong Provincial Key Laboratory of Precision Oncology, Cancer Research Center, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong Province, 250117, China; Department of Radiation Oncology, Shandong Cancer Hospital and Institute, Jinan, Shandong Province, 250117, China.
Yi LiuShandong Provincial Key Laboratory of Precision Oncology, Cancer Research Center, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong Province, 250117, China; Integrative Center for Frontier Biotech and Pharmaceutical Sciences, School of Life Sciences, Shandong First Medical University and Shandong Academy of Medical Sciences, Taian, Shandong Province, 271021, China.
Lixin ZhengShandong Provincial Key Laboratory of Precision Oncology, Cancer Research Center, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong Province, 250117, China; Integrative Center for Frontier Biotech and Pharmaceutical Sciences, School of Life Sciences, Shandong First Medical University and Shandong Academy of Medical Sciences, Taian, Shandong Province, 271021, China.
Chang LiuShandong Provincial Key Laboratory of Precision Oncology, Cancer Research Center, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong Province, 250117, China.
Kaiyue FanSchool of Clinical Medicine, Shandong Second Medical University, Weifang, China; Shandong Provincial Key Laboratory of Precision Oncology, Cancer Research Center, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong Province, 250117, China.
Nasha ZhangDepartment of Radiation Oncology, Shandong Cancer Hospital and Institute, Jinan, Shandong Province, 250117, China.
Ming YangSchool of Clinical Medicine, Shandong Second Medical University, Weifang, China; Shandong Provincial Key Laboratory of Precision Oncology, Cancer Research Center, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong Province, 250117, China; Integrative Center for Frontier Biotech and Pharmaceutical Sciences, School of Life Sciences, Shandong First Medical University and Shandong Academy of Medical Sciences, Taian, Shandong Province, 271021, China; Medical Science and Technology Innovation Center, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong Province, 250117, China. Electronic address: yangm@sdu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endogenous double-stranded RNA (dsRNA) links disrupted RNA homoeostasis in cancer to innate immunity. Tumour-associated dsRNA arises from complementary repeat transcripts, mitochondrial transcriptional imbalance, defective RNA processing and cellular stress. Its immunogenicity depends on ligand structure, editing, persistence, localisation, sensor access and pathway competence. ADAR1 and RNA-binding or decay factors buffer self-dsRNA, allowing tumour cells to tolerate potentially immunogenic RNA. Disruption of this control engages RIG-I-MAVS, MDA5-MAVS, TLR3-TRIF, PKR-eIF2α, and OAS-RNase L pathways; Z-conformation RNA can activate ZBP1. Outputs include interferon responses, translational arrest, RNA degradation, and regulated cell death, which can promote antigen presentation and immune-cell recruitment or drive chronic interferon adaptation, suppressive inflammation and treatment resistance. This Review examines critical-target and cumulative-burden models, methods for ligand identification, biomarker-guided patient selection and therapeutic strategies based on viral mimicry, ADAR1 targeting, engineered dsRNA agonists, and delivery platforms.

Indexed as

ADAR1Cancer therapyDouble-stranded RNAInnate immune sensingTumour microenvironmentViral mimicry

Identifiers

PMID42800308
PMCPMC13638791

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.