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dc.contributor.author
Palmitelli, Micaela
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dc.contributor.author
de Campos Nebel, Ildefonso Marcelo
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dc.contributor.author
Gonzalez Cid, Marcela Beatriz
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dc.date.available
2018-04-19T20:11:45Z
dc.date.issued
2015-12
dc.identifier.citation
Palmitelli, Micaela; de Campos Nebel, Ildefonso Marcelo; Gonzalez Cid, Marcela Beatriz; Progression of chromosomal damage induced by etoposide in G2 phase in a DNA-PKcs deficient context; Springer; Chromosome Research; 23; 4; 12-2015; 719-732
dc.identifier.issn
0967-3849
dc.identifier.uri
http://hdl.handle.net/11336/42753
dc.description.abstract
Etoposide (ETO), a drug used for the treatment of human tumors, is associated with the development of secondary malignancies. Recently, therapeutic strategies have incorporated chemosensitizing agents to improve the tumoral response to this drug. ETO creates DNA double strand breaks (DSB) via inhibition of DNA Topoisomerase II (Top2). To repair DSB, homologous recombination (HR) and non-homologous end-joining (NHEJ), involving D-NHEJ (dependent of DNA-PKcs) and B-NHEJ (backup repair pathway) are activated. We evaluated the progression of the DNA damage induced by the Top2 poison ETO in G2 HeLa human cells after chemical inhibition of DNA-PKcs. The inhibition by NU7026 together with ETO treatment resulted in a 2-fold higher rate of chromatid breaks and exchanges compared to ETO alone. Moreover, it was shown an increment in the percentage of micronuclei with H2AX positive signals in binucleated cells and a slight increase of dicentric chromosomes on second metaphases. It was also observed that in post-mitotic G1 phase, there is a closely association between unresolved DSB and MRE11 (Meiotic Recombination 11 homolog A) signals, demonstrating the contribution of MRE11 in the DSB repair by B-NHEJ. DNA-PKcs chemical inhibition impaired both D-NHEJ and HR repair pathways, altering the maintenance of chromosomal integrity and the cellular proliferative capacity. Thus, our results suggest that the chemosensitizing effectiveness of the DNA-PKcs inhibitor and the survival rate of aberrant cells may be determinants in the development of therapy-related tumors.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Springer
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Topoisomerase Ii Poison
dc.subject
Dna Damage
dc.subject
Dsb Repair Pathway
dc.subject
G2 Phase
dc.subject.classification
Bioquímica y Biología Molecular
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dc.subject.classification
Medicina Básica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Progression of chromosomal damage induced by etoposide in G2 phase in a DNA-PKcs deficient context
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-04-09T19:05:57Z
dc.identifier.eissn
1573-6849
dc.journal.volume
23
dc.journal.number
4
dc.journal.pagination
719-732
dc.journal.pais
Alemania
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dc.journal.ciudad
Berlin
dc.description.fil
Fil: Palmitelli, Micaela. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
dc.description.fil
Fil: de Campos Nebel, Ildefonso Marcelo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
dc.description.fil
Fil: Gonzalez Cid, Marcela Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
dc.journal.title
Chromosome Research
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs10577-015-9478-4
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1007/s10577-015-9478-4
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