ArticleGene therapy2006
Oncolysis of pancreatic tumour cells by a gamma34.5-deleted HSV-1 does not rely upon Ras-activation, but on the PI 3-kinase pathway.
Article in Gene therapy, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 17 papers.
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
17 citing papers in PubMed, 28 citations in OpenAlex.
- Oncolytic viral therapy as a novel potential solution for treatment of pancreatic cancer.Gastroenterology and hepatology from bed to bench · 2025Review
- The Evolution and Future of Targeted Cancer Therapy: From Nanoparticles, Oncolytic Viruses, and Oncolytic Bacteria to the Treatment of Solid Tumors.Nanomaterials (Basel, Switzerland) · 2021Review
- Perspectives on immunotherapy via oncolytic viruses.Infectious agents and cancer · 2019Review
- Trial Watch-Oncolytic viruses and cancer therapy.Oncoimmunology · 2016Review
- Oncogenes: The Passport for Viral Oncolysis Through PKR Inhibition.Biomarkers in cancer · 2016Review
- Oncolytic viral therapy for pancreatic cancer: current research and future directions.Oncolytic virotherapy · 2014Review
- Critical analysis of an oncolytic herpesvirus encoding granulocyte-macrophage colony stimulating factor for the treatment of malignant melanoma.Oncolytic virotherapy · 2014Review
- Trial watch: Oncolytic viruses for cancer therapy.Oncoimmunology · 2013Article
- Oncolytic viruses & their specific targeting to tumour cells.The Indian journal of medical research · 2012Review
- Oncolytic virotherapy for ovarian cancer.Oncolytic virotherapy · 2012Article
- Vesicular stomatitis virus as an oncolytic agent against pancreatic ductal adenocarcinoma.Journal of virology · 2012Article
- A novel fusogenic herpes simplex virus for oncolytic virotherapy of squamous cell carcinoma.Virology journal · 2011Article
- Oncolytic virotherapy for pancreatic cancer.Expert reviews in molecular medicine · 2011Review
- Oncolytic herpes simplex virus vectors and chemotherapy: are combinatorial strategies more effective for cancer?Future oncology (London, England) · 2010Review
- Oncolytic virotherapy: molecular targets in tumor-selective replication and carrier cell-mediated delivery of oncolytic viruses.Biochimica et biophysica acta · 2008Review
- Oncolytic viruses in cancer therapy.Cancer letters · 2007Review
- Trial Watch:: Oncolytic viruses for cancer therapy.OncoimmunologyReview
Corrections and comments
- Retraction · 2024-08-16Concerns/Issues about Data · Concerns/Issues about Image · Duplication of/in Image · Investigation by Journal/Publisher · Investigation by Third Party · Manipulation of Images · Objections by Author(s) · Unreliable Data ·
- Retracted
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ability of viruses to selectively target, replicate within, and destroy tumour cells without deleterious effects in normal cells (oncolysis), makes the use of viruses as an attractive tool for cancer treatment. Pancreatic adenocarcinoma, being insensitive to traditional therapy and having a rather poor prognosis, represents a suitable target to evaluate viral oncolysis as a novel therapeutic approach. Herpes simplex virus (HSV) has been reported to produce an oncolytic effect in cells overexpressing Ras. As Ras signalling is frequently aberrant in pancreatic cancer, we compared four pancreatic cell lines (which differ in the presence of mutated or wild-type ras) for their ability to support growth of gamma34.5-replication attenuated HSV-1 (R3616). Our data show that permissiveness to viral replication is neither associated with enhanced Ras signalling nor with defective PKR activity. By contrast, we provide evidence that disregulation of the PI 3-kinase signalling pathway allows conditionally replication-defective R3616 virus to overcome the cellular antiviral activity.
Indexed as
Identifiers
What 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.