Evidence map›Paper›PMID 40011711›Full record

ArticleCancer gene therapy2025

A conditionally replicative adenovirus vector containing the synNotch receptor gene for the treatment of muscle-invasive bladder cancer.

Ruhan A, Hideto Ueki, Shunya Nishioka, Rion Yamazaki, Marina Maekawa, Koichi Kitagawa, Hideaki Miyake, Toshiro Shirakawa

Abstract read
In one paragraph

Article in Cancer gene therapy, 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

8 authors.

Ruhan ADepartment of Advanced Medical Science, Kobe University Graduate School of Science, Technology and Innovation, Kobe, Japan.
Hideto UekiDepartment of Advanced Medical Science, Kobe University Graduate School of Science, Technology and Innovation, Kobe, Japan.ORCID http://orcid.org/0000-0002-7742-4528
Shunya NishiokaDepartment of Advanced Medical Science, Kobe University Graduate School of Science, Technology and Innovation, Kobe, Japan.
Rion YamazakiDepartment of Advanced Medical Science, Kobe University Graduate School of Science, Technology and Innovation, Kobe, Japan.
Marina MaekawaDepartment of Advanced Medical Science, Kobe University Graduate School of Science, Technology and Innovation, Kobe, Japan.
Koichi KitagawaDepartment of Advanced Medical Science, Kobe University Graduate School of Science, Technology and Innovation, Kobe, Japan.ORCID http://orcid.org/0000-0003-4508-2671
Hideaki MiyakeDivision of Urology, Kobe University Graduate School of Medicine, Kobe, Japan.
Toshiro ShirakawaDepartment of Advanced Medical Science, Kobe University Graduate School of Science, Technology and Innovation, Kobe, Japan. toshiro@med.kobe-u.ac.jp.ORCID http://orcid.org/0000-0003-3925-8730

Funding

Japan Society for the Promotion of Science London (JSPS London) 22K07252
6 · The paper itself

Abstract

Muscle-invasive bladder cancer (MIBC), a highly heterogeneous disease, shows genomic instability and a high mutation rate, making it difficult to treat. Recent studies revealed that cancer stem cells (CSCs) play a critical role in MIBC frequent recurrence and high morbidity. Previous research has shown that Cyclooxygenases-2 (COX-2) is particularly highly expressed in bladder cancer cells. In recent years, the development of oncolytic adenoviruses and their use in clinical trials have gained increased attention. In this study, we composed a conditionally replicative adenovirus vector (CRAd-synNotch) that carries the COX-2 promotor driving adenoviral E1 gene, the synNotch receptor therapeutic gene, and the Ad5/35 fiber gene. Activation of the COX-2 promoter gene causes replication only within COX-2 expressing cancer cells, thereby leading to tumor oncolysis. Also, CD44 and HIF signals contribute to cancer stemness and maintaining CSCs in bladder cancer, and the transduced synNotch receptor inhibits both CD44 and HIF signals simultaneously. We performed an in vivo study using a mouse xenograft model of T24 human MIBC cells and confirmed the significant antitumor activity of CRAd-synNotch. Our findings in this study warrant the further development of CRAd-synNotch for treating patients with MIBC.

Indexed as

AdenoviridaeGenetic TherapyGenetic VectorsUrinary Bladder NeoplasmsAnimalsCell Line, TumorHumansMiceOncolytic VirotherapyXenograft Model Antitumor Assays

Identifiers

PMID40011711
PMCPMC11946899

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.