Evidence map›Paper›PMID 40047938›Full record

ArticleCancer immunology, immunotherapy : CII2025

Prostaglandin F2 receptor negative regulator as a potential target for chimeric antigen receptor-T cell therapy for glioblastoma.

Hideki Kuroda, Noriyuki Kijima, Tetsuro Tachi, Shunya Ikeda, Koki Murakami, Tomoyoshi Nakagawa, Moto Yaga, Kanji Nakagawa, Reina Utsugi, Ryuichi Hirayama and 4 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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

14 authors.

Hideki KurodaDepartment of Neurosurgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, 5650871, Japan.
Noriyuki KijimaDepartment of Neurosurgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, 5650871, Japan. n-kijima@nsurg.med.osaka-u.ac.jp.
Tetsuro TachiDepartment of Neurosurgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, 5650871, Japan.
Shunya IkedaWorld Premier International Immunology Frontier Research Center, Osaka University, Suita, Osaka, Japan.
Koki MurakamiDepartment of Neurosurgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, 5650871, Japan.
Tomoyoshi NakagawaDepartment of Neurosurgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, 5650871, Japan.
Moto YagaDepartment of Respiratory Medicine, Osaka General Hospital, Osaka, Osaka, Japan.
Kanji NakagawaDepartment of Neurosurgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, 5650871, Japan.
Reina UtsugiDepartment of Neurosurgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, 5650871, Japan.
Ryuichi HirayamaDepartment of Neurosurgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, 5650871, Japan.
Yoshiko OkitaDepartment of Neurosurgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, 5650871, Japan.
Naoki KagawaDepartment of Neurosurgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, 5650871, Japan.
Naoki HosenWorld Premier International Immunology Frontier Research Center, Osaka University, Suita, Osaka, Japan. hnaoki@bldon.med.osaka-u.ac.jp.
Haruhiko KishimaDepartment of Neurosurgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, 5650871, Japan.

Funding

Japan Society for the Promotion of Science 22J14291Japan Society for the Promotion of Science 22K09231
6 · The paper itself

Abstract

backgroundChimeric antigen receptor (CAR)-T cell therapy targeting novel glioblastoma (GBM)-specific cell surface antigens is a promising approach. However, transcriptome analyses have revealed few GBM-specific target antigens.

methodsA library of monoclonal antibodies (mAbs) against tumor cell lines derived from patients with GBM was generated. mAbs reacting with tumor cells in resected tissues from patients with GBM but not with nonmalignant human brain cells were detected. The antigens that were recognized were identified through expression cloning. CAR-T cells derived from a candidate mAb were generated, and their functionality was tested in vitro and in vivo.

resultsApproximately 3,200 clones were established. Among them, 5E17 reacted with tumor cells in six of seven patients with GBM, but not with nonmalignant human brain cells. Prostaglandin F2 receptor negative regulator (PTGFRN) was identified as an antigen recognized by 5E17. CAR-T cells derived from 5E17 produced cytokines and exerted cytotoxicity upon co-culture with tumor cells from patients with GBM. Furthermore, intracranial injection of 5E17-CAR-T cells demonstrated antitumor effects in an orthotopic xenograft murine model with patient-derived GBM cells.

conclusionsCell surface PTGFRN is a candidate target for intracranial CAR-T cell therapy for GBM. On-target off-tumor toxicity in alternative normal tissues needs to be carefully tested.

Indexed as

Brain NeoplasmsGlioblastomaImmunotherapy, AdoptiveReceptors, Chimeric AntigenT-LymphocytesAnimalsAntibodies, MonoclonalCell Line, TumorFemaleHumansMaleMiceXenograft Model Antitumor AssaysAntibodies, MonoclonalReceptors, Chimeric AntigenCAR-T cell therapyExpression cloningGlioblastoma (GBM)Monoclonal antibodiesPTGFRN

Identifiers

PMID40047938
PMCPMC11885767

What OpenQuestion holds

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Registered trials

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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.