ArticleBritish journal of cancer2026
Efficacy and safety of GC001: an oncolytic vaccinia virus expressing STRIP1 shRNA.
Article in British journal of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGC001, a thymidine kinase deleted oncolytic vaccinia virus expressing striatin-interacting protein 1 (STRIP1) shRNA, has been approved by National Medical Products Administration (NMPA) of China to enter phase I clinical trial in 2023.
methodsAnti-tumour efficacy of GC001 across multiple cancer types was evaluated in mouse xenograft models. Anti-tumour immune responses were investigated in immunocompetent or humanised cancer mouse model. The mechanism of GC001 activity was elucidated including ROS accumulation, NRF2 degradation, and mitochondrial metabolic reprogramming.
resultsGC001 showed potent and broad-spectrum anti-tumour activity across multiple mouse xenograft models, and stimulated anti-tumour immune responses in both immunocompetent and humanised mouse models. Importantly, GC001 did not elicit significant toxicity and was well tolerated in the nonhuman primate model. Mechanistically, GC001 induced ROS accumulation, which was driven by NRF2 degradation and mitochondrial metabolic reprogramming through the combinatorial activity of STRIP1 knockdown and oncolytic vaccinia virus backbone, whereas STRIP1 knockdown alone did not induce ROS accumulation.
conclusionsOur study reveals dual mechanisms of GC001: viral replication and cytotoxicity potentiation through ROS-Hippo pathway, and oxidative stress-mediated anti-tumour immune responses. Studies have demonstrated robust anti-tumour efficacy and favourable safety profile of GC001, thereby establishing it as a promising oncolytic VV candidate for clinical development.
Identifiers
42791319What OpenQuestion holds
Registered trials
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.