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• W4313145832 endingPage "25" @default.
• W4313145832 startingPage "15" @default.
• W4313145832 abstract "When selected tumor cells in a large <i>in vitro</i> population are exposed to ionizing radiation, they can send pro-survival signals to non-exposed counterparts (bystander cells). If there is no physical contact between irradiated and bystander cells, the latter respond to mediators from targeted cells that diffuse through the medium. One such mediator is known to be nitric oxide (NO). It was recently discovered that non-ionizing anti-tumor photodynamic therapy (PDT) can also elicit pro-survival/expansion bystander effects in a variety of human cancer cells. A novel silicone ring-based approach was used for distinguishing photodynamically-targeted cells from non-targeted bystanders. A key finding was that NO from upregulated iNOS in surviving targeted cells diffused to the bystanders and caused iNOS/NO upregulation there, which in turn stimulated cell proliferation and migration. The intensity of these responses depended on the extent of iNOS/NO induction in targeted cells of different cancer lines. Moreover, the responses could be replicated using NO from the chemical donor DETA/NO. This review will focus on these and related findings, their negative implications for clinical PDT, and how these might be averted by using pharmacologic inhibitors of iNOS activity or transcription." @default.
• W4313145832 created "2023-01-06" @default.
• W4313145832 creator A5045290396 @default.
• W4313145832 creator A5079595535 @default.
• W4313145832 date "2023-01-01" @default.
• W4313145832 modified "2023-10-14" @default.
• W4313145832 title "Hyper-aggressiveness of Bystander Cells in an Anti-tumor Photodynamic Therapy Model: Role of Nitric Oxide Produced by Targeted Cells" @default.
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• W4313145832 doi "https://doi.org/10.1615/critrevoncog.2022040016" @default.
• W4313145832 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37824384" @default.
• W4313145832 hasPublicationYear "2023" @default.
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