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Fanconi Anemia Is Characterized by Delayed Repair Kinetics of DNA Double-Strand Breaks
dc.creator | Leskovac, Andreja | |
dc.creator | Vujić, Dragana | |
dc.creator | Guć-Šćekić, Marija | |
dc.creator | Petrović, Sandra | |
dc.creator | Joksić, Ivana | |
dc.creator | Slijepcevic, Predrag | |
dc.creator | Joksić, Gordana | |
dc.date.accessioned | 2018-03-01T21:13:30Z | |
dc.date.available | 2018-03-01T21:13:30Z | |
dc.date.issued | 2010 | |
dc.identifier.issn | 0040-8727 | |
dc.identifier.issn | 1349-3329 | |
dc.identifier.uri | https://vinar.vin.bg.ac.rs/handle/123456789/4000 | |
dc.description.abstract | Among patients with bone marrow failure (BMF) syndrome, some are happened to have underlying Fanconi anemia (FA), a genetically heterogeneous disease, which is characterized by progressive pancytopenia and cancer susceptibility. Due to heterogeneous nature of the disease, a single genetic test, as in vitro response to DNA cross-linking agents, usually is not enough to make correct diagnosis. The aim of this study was to evaluate whether measuring repair kinetics of radiation-induced DNA double-strand breaks (DSBs) can distinguish Fanconi anemia from other BMF patients. An early step in repair of DSBs is phosphorylation of the histone H2AX, generating gamma-H2AX histone, which extends over mega base-pair regions of DNA from the break site and is visualised as foci (gamma-H2AX foci) with specific antibodies. The primary fibroblasts, established from FA patients, were exposed to gamma-rays, a dose of 2 Gy (Co-60), incubated for up to 24 hours under repair-permissive conditions, and assayed for the level of gamma-H2AX foci and apoptosis at different recovery times after the treatment. Cell lines originating from FA patients displayed a significant delay in the repair of radiation-induced DNA DSBs relative to non-FA bone marrow failure (non-FA BMF) and control cell lines. The delay is especially evident at recovery time of 24 hours, and is seen as about 8-fold increase of residual gamma-H2AX foci compared to self-state before irradiation. The delay in repair kinetics of FA cells represents the unique feature of FA cellular phenotype, which should be exploited to distinguish FA cellular phenotype. | en |
dc.relation | Serbian Ministry of Science and Technological Development [143046] | |
dc.rights | openAccess | en |
dc.source | Tohoku Journal of Experimental Medicine | en |
dc.subject | double-strand breaks | en |
dc.subject | repair kinetics | en |
dc.subject | gamma-H2AX foci | en |
dc.subject | apoptosis | en |
dc.subject | irradiation | en |
dc.title | Fanconi Anemia Is Characterized by Delayed Repair Kinetics of DNA Double-Strand Breaks | en |
dc.type | article | en |
dcterms.abstract | Лесковац Aндреја; Петровић, Сандра; Јоксић Ивана; Јоксић Гордана; Вујиц, Драгана; Гуц-Сцекиц, Марија; Слијепцевиц, Предраг; | |
dc.citation.volume | 221 | |
dc.citation.issue | 1 | |
dc.citation.spage | 69 | |
dc.citation.epage | 76 | |
dc.identifier.wos | 000277671800010 | |
dc.identifier.doi | 10.1620/tjem.221.69 | |
dc.citation.rank | M22 | |
dc.identifier.pmid | 20453460 | |
dc.identifier.scopus | 2-s2.0-77951710441 | |
dc.identifier.fulltext | https://vinar.vin.bg.ac.rs//bitstream/id/12630/3996.pdf |