Evidence map›Paper›PMID 40595396›Full record

ArticleScientific reports2025

Stromal modifying CHST15 siRNA enhances antitumor effect synergistically with anti-PD-1 immune checkpoint antibody in murine pancreatic cancer.

Juanjuan Ye, Futoshi Suizu, Keiko Yamakawa, Hiroyuki Yoneyama, Jiro Kondo, Motohiko Kato, Akira Nishiyama, Naohisa Yahagi, Kyuichi Kadota

Abstract read
In one paragraph

Article in Scientific reports, 2025. 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

9 authors.

Juanjuan YeMolecular Oncologic Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, Kita-gun, Takamatsu, Kagawa, Japan.
Futoshi SuizuMolecular Oncologic Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, Kita-gun, Takamatsu, Kagawa, Japan. suizu-f@kagawa-puhs.ac.jp.
Keiko YamakawaMolecular Oncologic Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, Kita-gun, Takamatsu, Kagawa, Japan.
Hiroyuki YoneyamaTME Therapeutics Inc., Minato-ku, Tokyo, Japan.
Jiro KondoDepartment of Materials and Life Sciences, Sophia University, Chiyoda-ku, Tokyo, Japan.
Motohiko KatoCenter for Diagnostic and Therapeutic Endoscopy, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Akira NishiyamaDepartment of Pharmacology, Faculty of Medicine, Kagawa University, Kita-gun, Takamatsu, Kagawa, Japan.
Naohisa YahagiDivision of Research and Development for Minimally Invasive Treatment, Cancer Center, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Kyuichi KadotaMolecular Oncologic Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, Kita-gun, Takamatsu, Kagawa, Japan. kadota.kyuichi@kagawa-u.ac.jp.

Funding

Japan Society for the Promotion of Science 19H03447Japan Society for the Promotion of Science 23H02702
6 · The paper itself

Abstract

Tumor stromal remodeling is an obstacle for immune checkpoint inhibitors (ICI). A stroma modifying small interfering RNA (siRNA) to carbohydrate sulfotransferase 15 (CHST15) was recently shown to enhance tumor-infiltrating T cells, yet its impact on antitumor response of ICI remains unexplored. In mouse pancreatic cancer KPC and Pan02 subcutaneous syngeneic tumor models, mice were divided into 4 groups for treatment; (1) control, (2) CHST15 siRNA monotherapy, (3) anti-programmed death receptor 1 (PD-1) monotherapy, and (4) combination therapy with CHST15 siRNA and anti-PD-1 antibody. Mice were sacrificed after 2 week-treatments and anti-tumor effects were evaluated by immunohistochemistry for KPC and flow cytometry for Pan02 model, respectively. In the KPC model, combination treatment with intratumoral CHST15 siRNA (0.9-1.0 mg/kg) and systemic anti-PD-1 antibody (5 mg/kg) synergistically and robustly suppressed tumor growth with a significant increase of tumor-infiltrating CD4

Indexed as

Immune Checkpoint InhibitorsPancreatic NeoplasmsProgrammed Cell Death 1 ReceptorRNA, Small InterferingSulfotransferasesAnimalsCell Line, TumorDisease Models, AnimalDrug SynergismFemaleLymphocytes, Tumor-InfiltratingMiceTumor MicroenvironmentImmune Checkpoint InhibitorsPdcd1 protein, mouseProgrammed Cell Death 1 ReceptorRNA, Small InterferingSulfotransferasesCarbohydrate sulfotransferase 15 (CHST15)Chondroitin sulfate E (CS-E)Immune checkpoint inhibitors (ICI)Myeloid-derived suppressor cells (MDSCs)Pancreatic ductal adenocarcinoma (PDAC)T cell

Identifiers

PMID40595396
PMCPMC12216279

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.