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Antisenescence effect of REAC biomodulation to counteract the evolution of myelodysplastic syndrome
M. Maioli, S. Rinaldi, S. Cruciani, A. Necas, V. Fontani, G. Corda, S. Santaniello, A. Rinaldi, A. Pinheiro Barcessat, A. Necasova, A. Castagna, Z. Filipejova, C. Ventura, C. Fozza
Jazyk angličtina Země Česko
Typ dokumentu časopisecké články
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
PubMed Central
od 2020
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- akutní myeloidní leukemie * MeSH
- buněčná diferenciace MeSH
- lidé MeSH
- myelodysplastické syndromy * genetika metabolismus terapie MeSH
- nádorový supresorový protein p53 metabolismus MeSH
- telomerasa * metabolismus MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
About 30 percent of patients diagnosed with myelodysplastic syndromes (MDS) progress to acute myeloid leukemia (AML). The senescence of bone marrow?derived mesenchymal stem cells (BMSCs) seems to be one of the determining factors in inducing this drift. Research is continuously looking for new methodologies and technologies that can use bioelectric signals to act on senescence and cell differentiation towards the phenotype of interest. The Radio Electric Asymmetric Conveyer (REAC) technology, aimed at reorganizing the endogenous bioelectric activity, has already shown to be able to determine direct cell reprogramming effects and counteract the senescence mechanisms in stem cells. Aim of the present study was to prove if the anti-senescence results previously obtained in different kind of stem cells with the REAC Tissue optimization - regenerative (TO-RGN) treatment, could also be observed in BMSCs, evaluating cell viability, telomerase activity, p19ARF, P21, P53, and hTERT gene expression. The results show that the REAC TO-RGN treatment may be a useful tool to counteract the BMSCs senescence which can be the basis of AML drift. Nevertheless, further clinical studies on humans are needed to confirm this hypothesis.
Blood Diseases Department of Clinical and Experimental Medicine University of Sassari Sassari Italy
Department of Biomedical Sciences University of Sassari Sassari Italy
Department of Regenerative Medicine Rinaldi Fontani Institute Florence Italy
Faculty of Veterinary Medicine University of Veterinary and Sciences Brno Czech Republic
Health and Biological Sciences Department Federal University of Amapá Macapá Brazil
Research Department Rinaldi Fontani Foundation Florence Italy
Citace poskytuje Crossref.org
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