Evidence map›Paper›PMID 41806197›Full record

ReviewInternational journal of clinical oncology2026

Interleukin-1 receptor type 1 in pancreatic cancer progression and metastasis: a review.

Kenta Saito, Yoichi Matsuo, Yuki Denda, Keisuke Nonoyama, Hiromichi Murase, Tomokatsu Kato, Yushi Yamakawa, Takafumi Sato, Hiroyuki Sagawa, Ryo Ogawa and 1 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in International journal of clinical oncology, 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

11 authors.

Kenta SaitoDepartment of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi, 4678601, Japan.ORCID http://orcid.org/0000-0003-3590-2189
Yoichi MatsuoDepartment of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi, 4678601, Japan. nukemat0328@gmail.com.
Yuki DendaDepartment of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi, 4678601, Japan.
Keisuke NonoyamaDepartment of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi, 4678601, Japan.
Hiromichi MuraseDepartment of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi, 4678601, Japan.
Tomokatsu KatoDepartment of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi, 4678601, Japan.
Yushi YamakawaDepartment of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi, 4678601, Japan.
Takafumi SatoDepartment of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi, 4678601, Japan.
Hiroyuki SagawaDepartment of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi, 4678601, Japan.
Ryo OgawaDepartment of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi, 4678601, Japan.
Shuji TakiguchiDepartment of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi, 4678601, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a global lethal malignancy, with increasing incidence and dismal survival rates. Inflammation plays a central role in shaping PDAC biology, and interleukin-1 receptor type 1 (IL-1R1) is a key mediator linking oncogenic signaling, stromal activation, and immune suppression. This review summarizes current insights into IL-1R1 signaling in PDAC, focusing on its role in tumor microenvironment remodeling, tumor progression, and metastasis. IL-1R1 activation by IL-1α or IL-1β triggers MyD88-dependent pathways, including NF-κB, MAPK, and STAT3, which induce pro-inflammatory cytokines, angiogenic factors, and immune checkpoints. These events contribute to the desmoplastic and immunosuppressive tumor microenvironment characteristic of PDAC. IL-1R1 orchestrates crosstalk between cancer cells, cancer-associated fibroblasts, and tumor-associated macrophages, promoting epithelial-mesenchymal transition, extracellular matrix remodeling, and immune evasion. Moreover, IL-1R1 promotes metastatic dissemination by enhancing the survival of circulating tumor cells through platelet shielding and neutrophil extracellular traps, while fostering angiogenesis and lymphangiogenesis to establish niches in the liver and peritoneum. Clinically, high IL-1R1 expression correlates with advanced disease, metastasis, and poor prognosis. Therapeutic blockade of the IL-1 pathway with agents, such as anakinra, canakinumab, or rilonacept, reduces tumor growth, metastasis, and immune suppression in preclinical PDAC models. Combination strategies with chemotherapy, radiotherapy, or immune checkpoint inhibitors further enhance anti-tumor efficacy. However, major challenges remain, including limited clinical trial data, infection risk, and the absence of predictive biomarkers. Summarily, IL-1R1 is a central driver of PDAC aggressiveness and a therapeutic target. Targeting this pathway may enable biomarker-guided strategies to improve outcomes in this disease.

Indexed as

Epithelial–mesenchymal transitionIL-1 receptor type 1Immunotherapy resistancePancreatic ductal adenocarcinomaTumor-associated macrophagesTumor microenvironment

Identifiers

What OpenQuestion holds

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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.