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Tytuł pozycji:

Optimization of Thymidine Kinase-Based Safety Switch for Neural Cell Therapy.

Tytuł:
Optimization of Thymidine Kinase-Based Safety Switch for Neural Cell Therapy.
Autorzy:
Locatelli M; Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, CH-1211 Geneva, Switzerland.
Delhaes F; Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, CH-1211 Geneva, Switzerland.
Cherpin O; Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, CH-1211 Geneva, Switzerland.
Black ME; School of Molecular Biosciences, Washington State University, Pullman, WA 99163, USA.
Carnesecchi S; Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, CH-1211 Geneva, Switzerland.
Preynat-Seauve O; Laboratory of Therapy and Stem Cells, Geneva University Hospitals, CH-1211 Geneva, Switzerland.; Department of Medicine, Faculty of Medicine, University of Geneva, CH-1211 Geneva, Switzerland.
Hibaoui Y; Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, CH-1211 Geneva, Switzerland.
Krause KH; Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, CH-1211 Geneva, Switzerland.; Department of Genetic Medicine and Laboratory, Geneva Hospitals, CH-1211 Geneva, Switzerland.
Źródło:
Cells [Cells] 2022 Jan 31; Vol. 11 (3). Date of Electronic Publication: 2022 Jan 31.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Original Publication: Basel, Switzerland : MDPI
MeSH Terms:
Nucleosides*
Thymidine Kinase*/genetics
Thymidine Kinase*/metabolism
Cell- and Tissue-Based Therapy ; Ganciclovir/pharmacology ; Humans ; Neurons/metabolism
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Grant Information:
Grp Krause Clayton Foundation
Contributed Indexing:
Keywords: SR39; penciclovir; pluripotent stem cell therapy; post-transplantation tumor; teratoma
Substance Nomenclature:
0 (Nucleosides)
EC 2.7.1.21 (Thymidine Kinase)
P9G3CKZ4P5 (Ganciclovir)
Entry Date(s):
Date Created: 20220215 Date Completed: 20220408 Latest Revision: 20220408
Update Code:
20240105
PubMed Central ID:
PMC8834506
DOI:
10.3390/cells11030502
PMID:
35159311
Czasopismo naukowe
Cell therapies based on pluripotent stem cells (PSC), have opened new therapeutic strategies for neurodegenerative diseases. However, insufficiently differentiated PSC can lead to tumor formation. Ideally, safety switch therapies should selectively kill proliferative transplant cells while preserving post-mitotic neurons. In this study, we evaluated the potential of nucleoside analogs and thymidine kinase-based suicide genes. Among tested thymidine kinase variants, the humanized SR39 (SR39h) variant rendered cells most sensitive to suicide induction. Unexpectedly, post-mitotic neurons with ubiquitous SR39h expression were killed by ganciclovir, but were spared when SR39h was expressed under the control of the cell cycle-dependent Ki67 promoter. The efficacy of six different nucleoside analogs to induce cell death was then evaluated. Penciclovir (PCV) showed the most interesting properties with an efficiency comparable to ganciclovir (GCV), but low toxicity. We tested three nucleoside analogs in vivo: at concentrations of 40 mg/kg/day, PCV and GCV prevented tumor formation, while acyclovir (ACV) did not. In summary, SR39h under the control of a cell cycle-dependent promoter appears most efficient and selective as safety switch for neural transplants. In this setting, PCV and GCV are efficient inducers of cell death. Because of its low toxicity, PCV might become a preferred alternative to GCV.
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