Evidence map›Paper›PMID 41107859›Full record

ArticleJournal of translational medicine2025

IL33-ST2 axis is a predictive biomarker for anti-PD1 therapeutic efficacy in advanced gastric cancer.

Chie Kudo-Saito, Hiroshi Imazeki, Kengo Nagashima, Hirokazu Shoji, Kai Tsugaru, Naoki Takahashi, Takeshi Kawakami, Yusuke Amanuma, Takeru Wakatsuki, Naohiro Okano and 6 more

Abstract read
In one paragraph

Article in Journal of translational medicine, 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. 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

16 authors.

Chie Kudo-SaitoDepartment of Immune Medicine, National Cancer Center Research Institute, Tokyo, Japan. ckudo@ncc.go.jp.ORCID 0000-0003-4644-9404
Hiroshi ImazekiDepartment of Immune Medicine, National Cancer Center Research Institute, Tokyo, Japan.
Kengo NagashimaBiostatistics Unit, Clinical and Translational Research Center, Keio University Hospital, Tokyo, Japan.
Hirokazu ShojiDepartment of Gastrointestinal Medical Oncology, National Cancer Center Hospital, Tokyo, Japan.
Kai TsugaruDivision of Gastroenterology and Hepatology, Keio University Hospital, Tokyo, Japan.
Naoki TakahashiDepartment of Gastroenterology, Saitama Cancer Center, Saitama, Japan.
Takeshi KawakamiDivision of Gastrointestinal Oncology, Shizuoka Cancer Center, Shizuoka, Japan.
Yusuke AmanumaClinical Trial Promotion Department, Chiba Cancer Center, Chiba, Japan.
Takeru WakatsukiDepartment of Gastrointestinal Medical Oncology, Cancer Institute Hospital of JFCR, Tokyo, Japan.
Naohiro OkanoDepartment of Medical Oncology, Faculty of Medicine, Kyorin University, Tokyo, Japan.
Yukiya NaritaDepartment of Clinical Oncology, Aichi Cancer Center Hospital, Nagoya, Japan.
Yoshiyuki YamamotoDepartment of Gastroenterology, University of Tsukuba Hospital, Tsukuba, Japan.
Rika KizawaDepartment of Medical Oncology, Toranomon Hospital, Tokyo, Japan.
Kei MuroDepartment of Clinical Oncology, Aichi Cancer Center Hospital, Nagoya, Japan.
Hitoshi IchikawaDepartment of Clinical Genomics, National Cancer Center Research Institute, Tokyo, Japan.
Narikazu BokuDepartment of Gastrointestinal Medical Oncology, National Cancer Center Hospital, Tokyo, Japan.

Funding

Bristol-Myers Squibb A2018-032Ono Pharmaceutical A2018-032
6 · The paper itself

Abstract

backgroundWe previously demonstrated that interleukin-33 (IL33) plays a key role in treatment resistance through tumor polyploidization and the consequent immune dysfunction by recruiting and expanding various immunosuppressive cells that express its receptor ST2, and that anti-IL33 blockade therapy induces potent anti-tumor effect in mouse tumor models resistant to anti-PD1 therapy. These suggest that IL33 and ST2 are potentially promising targets that could contribute to anti-PD1/PDL1 therapy. Recently, an increasing number of clinical studies have shown a significant correlation between IL33 expression in tumor tissues and poor prognosis in patients with gastric cancer (GC). However, the clinical significance of targeting the IL33-ST2 axis in anti-PD1/PDL1 therapy for GC remains unclear.

methodsTumor tissues and peripheral blood were collected from patients with advanced GC before and after nivolumab monotherapy in the WJOG10417GTR study. Gene expression of il33 in tumor tissues, IL33 in plasma, and ST2

resultsThe levels of tumor il33 gene expression and peripheral IL33 and ST2

conclusionsThese data suggest high IL33/ST2 levels are significant poor prognostic factors for nivolumab therapy for advanced GC. The IL33/ST2 axis may be useful as a biomarker for predicting and pre-selecting possible responders/nonresponders to anti-PD1/PDL1 therapy for GC, and hopefully as a druggable target for developing new drugs for treating GC. The IL33/ST2-targeting strategy will contribute to improving clinical outcomes in the treatment of GC.

Indexed as

Biomarkers, TumorInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Programmed Cell Death 1 ReceptorStomach NeoplasmsAgedFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedPrognosisTreatment OutcomeBiomarkers, TumorIL1RL1 protein, humanIL33 protein, humanInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Programmed Cell Death 1 ReceptorBiomarkerGastric cancerIL33Immune checkpoint inhibitorNivolumabPD1Peripheral bloodPrognosisST2Tumor tissue

Identifiers

PMID41107859
PMCPMC12534944

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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.