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• W2168412437 abstract "Background: Conditionally replicating adenoviruses (CRAds) can be engineered to replicate selectively in cancer cells and cause cancer-specific cell lysis; thus they are considered a promising cancer therapy. Methods: To elucidate the mechanisms by which CRAds induce cancer-specific cell death, we infected normal human fibroblasts (MRC5, telomerase negative), human malignant glioma (U373-MG and U87-MG), human cervical cancer (HeLa), and human prostate cancer (PC3) cells (all telomerase positive) with CRAds regulated by the human telomerase reverse transcriptase promoter (hTERT-Ad) or control nonreplicating adenoviruses (Ad-GFP). Nonapoptotic autophagy was assessed in Ad-GFP- and hTERT-Ad–infected cells by examining cell morphology, the development of acidic vesicular organelles, and the conversion of microtubule-associated protein 1 light chain 3 from the cytoplasmic form to the autophagosome membrane form; signaling via mammalian target of rapamycin (mTOR), an autophagy-associated molecule, was monitored by western blot analysis. We also compared the growth of subcutaneous gliomas in nude mice that were treated by intratumoral injection with Ad-GFP or hTERT-Ad. Survival of athymic mice carrying intracranial gliomas treated by intratumoral injection with Ad-GFP or hTERT-Ad was compared by using the Kaplan–Meier method and the Cox–Mantel log-rank analysis. All statistical tests were two-sided. Results: hTERT-Ad induced tumor-specific autophagic cell death in tumor cells and in subcutaneous gliomas. hTERT-Ad–induced autophagy was associated with hTERT-Ad infection kinetics. The mTOR signaling pathway was suppressed in tumor cells and in subcutaneous gliomas treated with hTERT-Ad compared with GFP-Ad or no treatment as shown by reduced phosphorylation of mTOR's downstream target p70S6 kinase (p70S6K). hTERT-Ad treatment of mice (n = 7) slowed growth of subcutaneous gliomas (mean tumor volume = 39 mm 3 , 95% confidence interval [CI] = 23 to 54 mm 3 ) compared with GFP-Ad treatment (n = 7) (mean tumor volume = 200 mm 3 , 95% CI = 149 to 251 mm 3 ) at day 7 (volume difference = 161 mm 3 , 95% CI = 126 to 197 mm 3 ; P <.001). Mice carrying intracranial tumors that were treated with three intratumoral injections of hTERT-Ad survived longer (53 days) than after treatment with GFP-Ad (29 days) (seven mice per group, difference = 24 days, 95% CI = 20 to 28 days; P <.001). Conclusions: hTERT-Ad may kill telomerase-positive cancer cells by inducing autophagic cell death." @default.
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• W2168412437 date "2006-05-03" @default.
• W2168412437 modified "2023-10-03" @default.
• W2168412437 title "Autophagic Cell Death of Malignant Glioma Cells Induced by a Conditionally Replicating Adenovirus" @default.
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• W2168412437 doi "https://doi.org/10.1093/jnci/djj161" @default.
• W2168412437 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16670388" @default.
• W2168412437 hasPublicationYear "2006" @default.
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