Evidence map›Paper›PMID 40767963›Full record

ArticleCancer immunology, immunotherapy : CII2025

IL-1R2 promotes tumorigenesis and modulates the tumor immune microenvironment in colorectal cancer.

Yanyan Lang, Hao Huang, Hongwei Jiang, Shaoxian Wu, Zhang Fang, Dachuan Zhang, Heya Qian, Yingting Liu, Maoling Yuan, Bin Xu and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. STAT3 Inhibition to Treat Ulcerative Colitis-Associated Colorectal Cancer.International journal of molecular sciences · 2025
    Article
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

13 authors.

Yanyan LangDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Jiangsu, 213003, Changzhou, China.
Hao HuangDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Jiangsu, 213003, Changzhou, China.
Hongwei JiangDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Jiangsu, 213003, Changzhou, China.
Shaoxian WuDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Jiangsu, 213003, Changzhou, China.
Zhang FangDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Jiangsu, 213003, Changzhou, China.
Dachuan ZhangDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Jiangsu, 213003, Changzhou, China.
Heya QianDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Jiangsu, 213003, Changzhou, China.
Yingting LiuDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Jiangsu, 213003, Changzhou, China.
Maoling YuanDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Jiangsu, 213003, Changzhou, China.
Bin XuDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Jiangsu, 213003, Changzhou, China.
Lujun ChenDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Jiangsu, 213003, Changzhou, China.
Xiao ZhengDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Jiangsu, 213003, Changzhou, China.
Jingting JiangDepartment of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Jiangsu, 213003, Changzhou, China. jiangjingting@suda.edu.cn.

Funding

Changzhou Clinical Medical Center CZZX202201Jiangsu Provincial Medical Key Discipline YXZDXK202236National Natural Science Foundation of China 32270955Provincial-level Talent Program for National Center of Technology Innovation for Biopharmaceuticals NCTIB2024JS0101the Key R&D Project of Jiangsu Province BE2022719
6 · The paper itself

Abstract

Colorectal cancer (CRC) continues to be a major global health challenge due to its high incidence and mortality rates, emphasizing the critical need for innovative therapeutic strategies. IL-1R2, a member of the IL-1 receptor family, plays a pivotal role in both tumorigenesis and antitumor immunity. However, its precise role in tumor development and its impact on immune checkpoint inhibitors (ICIs) therapy in CRC remain poorly understood. We examined tumor progression in wild-type and IL-1R2-deficient mice using an AOM/DSS-induced colitis-associated colorectal cancer model treated with combined ICIs therapy. Our findings revealed that IL-1R2 deficient mice exhibited a significant reduction in tumor burden, accompanied by alterations in the carcinogenic program and enhanced immunogenicity of tumor cells. Furthermore, the deletion of IL-1R2 resulted in an increased proportion of exhausted CD8

Indexed as

CarcinogenesisColorectal NeoplasmsReceptors, Interleukin-1 Type IITumor MicroenvironmentAnimalsCD8-Positive T-LymphocytesHumansImmune Checkpoint InhibitorsMiceMice, Inbred C57BLMice, KnockoutImmune Checkpoint InhibitorsReceptors, Interleukin-1 Type IIColorectal cancerCTLA-4Immune checkpointInterleukin-1 receptor 2PD-1

Identifiers

PMID40767963
PMCPMC12328880

What OpenQuestion holds

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LicenceCC BY
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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.