ArticleCancer gene therapy2003
Quantification and characterization of the bystander effect in prostate cancer cells following adenovirus-mediated FasL expression.
Article in Cancer gene therapy, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
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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.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- Identification of blood protein biomarkers associated with prostate cancer risk using genetic prediction models: analysis of over 140,000 subjects.Human molecular genetics · 2023Article
- Prostate Microbiota and Prostate Cancer: A New Trend in Treatment.Frontiers in oncology · 2021Review
- Impact of Induced Syncytia Formation on the Oncolytic Potential of Myxoma Virus.Oncolytic virotherapy · 2019Article
- Targeted nonviral gene therapy in prostate cancer.International journal of nanomedicine · 2018Review
- Enhancing the bystander killing effect of an oncolytic HSV by arming it with a secretable apoptosis activator.Gene therapy · 2015Article
- Glucocorticoid receptor over-expression promotes human small cell lung cancer apoptosis in vivo and thereby slows tumor growth.Endocrine-related cancer · 2010Article
- The effects of FasL on inflammation and tumor survival are dependent on its expression levels.Cancer gene therapy · 2007Article
- International Society for Cell and Gene Therapy of Cancer: 2005 meeting in Shenzhen, China.Cancer gene therapy · 2007Article
- Combined therapeutic use of AdGFPFasL and small molecule inhibitors of ceramide metabolism in prostate and head and neck cancers: a status report.Cancer gene therapy · 2006Review
- FasL gene therapy: a new therapeutic modality for head and neck cancer.Cancer gene therapy · 2006Article
- An improved Tet-On regulatable FasL-adenovirus vector system for lung cancer therapy.Journal of molecular medicine (Berlin, Germany) · 2006Article
- Cancer gene therapy: combination with radiation therapy and the role of bystander cell killing in the anti-tumor effect.Pathology oncology research : POR · 2006Article
- In vitro efficacy of Fas ligand gene therapy for the treatment of bladder cancer.Cancer gene therapy · 2005Article
- Exceptionally potent anti-tumor bystander activity of an scFv:sTRAIL fusion protein with specificity for EGP2 toward target antigen-negative tumor cells.Neoplasia (New York, N.Y.)Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Inducing Fas-mediated apoptosis in prostate cancer (PCa) is a promising new therapeutic approach with the potential to overcome delivery issues currently problematic in cancer gene therapy. We have previously demonstrated that a Fas Ligand (FasL) expressing adenovirus (AdGFPFasL(TET)) was able to induce Fas-mediated apoptosis in a panel of PCa cell lines regardless of their Fas-sensitivity as determined by the agonistic Fas antibody CH-11. We now report that AdGFPFasL(TET)-infected cells produce apoptotic bodies and cellular debris that continues to elicit FasL-mediated bystander killing in uninfected neighboring cells. Using light microscopy, we demonstrate that AdGFPFasL(TET)-infected cells release apoptotic bodies and cellular debris into the local environment and that this material will induce bystander killing in Jurkat, PPC-1, and PC-3 target cells, but not in DU145 and K-562 cells. The bystander killing mechanism is mediated through Fas/FasL interaction because it is significantly inhibited if target cells are pretreated with the pan spectrum caspase inhibitor Z-VAD-FMK or the Fas neutralizing antibody ZB-4. Coincubation of PPC-1 target cells with apoptotic bodies and cellular debris (effector material) induce nearly complete target cell killing at a ratio of 1:1 target to effector. Collectively, these data indicate that AdGFPFasL(TET)-infected PCa cells release apoptotic and cellular debris capable of inducing bystander killing in PCa and supports the development of FasL as a gene therapy agent.
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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.