TY  - JOUR
AU  - Leskovac, Andreja
AU  - Vujić, Dragana
AU  - Guć-Šćekić, Marija
AU  - Petrović, Sandra
AU  - Joksić, Ivana
AU  - Slijepcevic, Predrag
AU  - Joksić, Gordana
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4000
AB  - 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.
T2  - Tohoku Journal of Experimental Medicine
T1  - Fanconi Anemia Is Characterized by Delayed Repair Kinetics of DNA Double-Strand Breaks
VL  - 221
IS  - 1
SP  - 69
EP  - 76
DO  - 10.1620/tjem.221.69
ER  - 

@article{
author = "Leskovac, Andreja and Vujić, Dragana and Guć-Šćekić, Marija and Petrović, Sandra and Joksić, Ivana and Slijepcevic, Predrag and Joksić, Gordana",
year = "2010",
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.",
journal = "Tohoku Journal of Experimental Medicine",
title = "Fanconi Anemia Is Characterized by Delayed Repair Kinetics of DNA Double-Strand Breaks",
volume = "221",
number = "1",
pages = "69-76",
doi = "10.1620/tjem.221.69"
}

Leskovac, A., Vujić, D., Guć-Šćekić, M., Petrović, S., Joksić, I., Slijepcevic, P.,& Joksić, G.. (2010). Fanconi Anemia Is Characterized by Delayed Repair Kinetics of DNA Double-Strand Breaks. in Tohoku Journal of Experimental Medicine, 221(1), 69-76.
https://doi.org/10.1620/tjem.221.69

Leskovac A, Vujić D, Guć-Šćekić M, Petrović S, Joksić I, Slijepcevic P, Joksić G. Fanconi Anemia Is Characterized by Delayed Repair Kinetics of DNA Double-Strand Breaks. in Tohoku Journal of Experimental Medicine. 2010;221(1):69-76.
doi:10.1620/tjem.221.69 .

Leskovac, Andreja, Vujić, Dragana, Guć-Šćekić, Marija, Petrović, Sandra, Joksić, Ivana, Slijepcevic, Predrag, Joksić, Gordana, "Fanconi Anemia Is Characterized by Delayed Repair Kinetics of DNA Double-Strand Breaks" in Tohoku Journal of Experimental Medicine, 221, no. 1 (2010):69-76,
https://doi.org/10.1620/tjem.221.69 . .