TY  - JOUR
AU  - Filipović Tričković, Jelena G.
AU  - Mandušić, Vesna
AU  - Joksić, Ivana
AU  - Vujić, Dragana
AU  - Valenta-Šobot, Ana
AU  - Joksić, Gordana
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1882
AB  - Fanconi anemia is rare inherited disease characterized by wide spectrum of congenital anomalies, progressive pancytopenia, and predisposition to hematological malignancies and solid tumors. Molecular genetic analysis of mutations in FANC genes is of a great importance for diagnosis confirmation, prenatal and carrier testing, as well as for prediction of chemotherapy outcome and disease complications. In this study we performed screening of frequently affected regions of FANCD2 gene for sequence variants in six unrelated FA-D2 patients in Serbia. This is the first molecular analysis of FANCD2 gene in Serbian FA-D2 patients. A total of 10 sequence variants were detected, one in homozygous, and nine in heterozygous state. Two variants were found within exons, and eight within introns, in deep intronic regions. In-silico analysis showed that among all detected variants one exon variant and three intron variants might have impact on splicing mechanism. Heterozygous variants found in intron 3, c. 206-246delG; exon 26, c. 2396 C GT A and intron 28, c. 2715+573 C GT T were not previously reported. In-silico analysis revealed that among them, two (intron 3, c. 206-246 delG and exon 26, c. 2396 C GT A) could be novel disease-causing mutations. Many variants were found in more than one patient, including those unreported, indicating their possible ethnic association. Great number of variants in some patients suggests their non-random emergence in Fanconi anemia pathway.
T2  - Genetika
T1  - Genotyping Fanconi Anemia Patients from Serbia Reveals Three Novel Fancd2 Variants
VL  - 49
IS  - 2
SP  - 559
EP  - 572
DO  - 10.2298/GENSR1702559T
ER  - 

@article{
author = "Filipović Tričković, Jelena G. and Mandušić, Vesna and Joksić, Ivana and Vujić, Dragana and Valenta-Šobot, Ana and Joksić, Gordana",
year = "2017",
abstract = "Fanconi anemia is rare inherited disease characterized by wide spectrum of congenital anomalies, progressive pancytopenia, and predisposition to hematological malignancies and solid tumors. Molecular genetic analysis of mutations in FANC genes is of a great importance for diagnosis confirmation, prenatal and carrier testing, as well as for prediction of chemotherapy outcome and disease complications. In this study we performed screening of frequently affected regions of FANCD2 gene for sequence variants in six unrelated FA-D2 patients in Serbia. This is the first molecular analysis of FANCD2 gene in Serbian FA-D2 patients. A total of 10 sequence variants were detected, one in homozygous, and nine in heterozygous state. Two variants were found within exons, and eight within introns, in deep intronic regions. In-silico analysis showed that among all detected variants one exon variant and three intron variants might have impact on splicing mechanism. Heterozygous variants found in intron 3, c. 206-246delG; exon 26, c. 2396 C GT A and intron 28, c. 2715+573 C GT T were not previously reported. In-silico analysis revealed that among them, two (intron 3, c. 206-246 delG and exon 26, c. 2396 C GT A) could be novel disease-causing mutations. Many variants were found in more than one patient, including those unreported, indicating their possible ethnic association. Great number of variants in some patients suggests their non-random emergence in Fanconi anemia pathway.",
journal = "Genetika",
title = "Genotyping Fanconi Anemia Patients from Serbia Reveals Three Novel Fancd2 Variants",
volume = "49",
number = "2",
pages = "559-572",
doi = "10.2298/GENSR1702559T"
}

Filipović Tričković, J. G., Mandušić, V., Joksić, I., Vujić, D., Valenta-Šobot, A.,& Joksić, G.. (2017). Genotyping Fanconi Anemia Patients from Serbia Reveals Three Novel Fancd2 Variants. in Genetika, 49(2), 559-572.
https://doi.org/10.2298/GENSR1702559T

Filipović Tričković JG, Mandušić V, Joksić I, Vujić D, Valenta-Šobot A, Joksić G. Genotyping Fanconi Anemia Patients from Serbia Reveals Three Novel Fancd2 Variants. in Genetika. 2017;49(2):559-572.
doi:10.2298/GENSR1702559T .

Filipović Tričković, Jelena G., Mandušić, Vesna, Joksić, Ivana, Vujić, Dragana, Valenta-Šobot, Ana, Joksić, Gordana, "Genotyping Fanconi Anemia Patients from Serbia Reveals Three Novel Fancd2 Variants" in Genetika, 49, no. 2 (2017):559-572,
https://doi.org/10.2298/GENSR1702559T . .

TY  - JOUR
AU  - Filipović, Jelena G.
AU  - Joksić, Gordana
AU  - Vujić, Dragana
AU  - Joksić, Ivana
AU  - Mrasek, Kristin
AU  - Weise, Anja
AU  - Liehr, Thomas
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1239
AB  - Background: Fanconi anemia (FA) is a chromosomal instability syndrome characterized by increased frequency of chromosomal breakages, chromosomal radial figures and accelerated telomere shortening. In this work we performed detailed molecular-cytogenetic characterization of breakpoints in primary lymphocytes of FA-D2 patients in different stages of the disease using fluorescent in situ hybridization. Results: We found that chromosomal breakpoints co-localize on the molecular level with common fragile sites, whereas their distribution pattern depends on the severity of the disease. Telomere quantitative fluorescent in situ hybridization revealed that telomere fusions and radial figures, especially radials which involve telomere sequences are the consequence of critically shortened telomeres that increase with the disease progression and could be considered as a predictive parameter during the course of the disease. Sex chromosomes in FA cells are also involved in radial formation indicating that specific X chromosome regions share homology with autosomes and also could serve as repair templates in resolving DNA damage. Conclusions: FA-D2 chromosomal breakpoints co-localize with common fragile sites, but their distribution pattern depends on the disease stage. Telomere fusions and radials figures which involve telomere sequences are the consequence of shortened telomeres, increase with disease progression and could be of predictive value.
T2  - Molecular Cytogenetics
T1  - First molecular-cytogenetic characterization of Fanconi anemia fragile sites in primary lymphocytes of FA-D2 patients in different stages of the disease
VL  - 9
DO  - 10.1186/s13039-016-0280-6
ER  - 

@article{
author = "Filipović, Jelena G. and Joksić, Gordana and Vujić, Dragana and Joksić, Ivana and Mrasek, Kristin and Weise, Anja and Liehr, Thomas",
year = "2016",
abstract = "Background: Fanconi anemia (FA) is a chromosomal instability syndrome characterized by increased frequency of chromosomal breakages, chromosomal radial figures and accelerated telomere shortening. In this work we performed detailed molecular-cytogenetic characterization of breakpoints in primary lymphocytes of FA-D2 patients in different stages of the disease using fluorescent in situ hybridization. Results: We found that chromosomal breakpoints co-localize on the molecular level with common fragile sites, whereas their distribution pattern depends on the severity of the disease. Telomere quantitative fluorescent in situ hybridization revealed that telomere fusions and radial figures, especially radials which involve telomere sequences are the consequence of critically shortened telomeres that increase with the disease progression and could be considered as a predictive parameter during the course of the disease. Sex chromosomes in FA cells are also involved in radial formation indicating that specific X chromosome regions share homology with autosomes and also could serve as repair templates in resolving DNA damage. Conclusions: FA-D2 chromosomal breakpoints co-localize with common fragile sites, but their distribution pattern depends on the disease stage. Telomere fusions and radials figures which involve telomere sequences are the consequence of shortened telomeres, increase with disease progression and could be of predictive value.",
journal = "Molecular Cytogenetics",
title = "First molecular-cytogenetic characterization of Fanconi anemia fragile sites in primary lymphocytes of FA-D2 patients in different stages of the disease",
volume = "9",
doi = "10.1186/s13039-016-0280-6"
}

Filipović, J. G., Joksić, G., Vujić, D., Joksić, I., Mrasek, K., Weise, A.,& Liehr, T.. (2016). First molecular-cytogenetic characterization of Fanconi anemia fragile sites in primary lymphocytes of FA-D2 patients in different stages of the disease. in Molecular Cytogenetics, 9.
https://doi.org/10.1186/s13039-016-0280-6

Filipović JG, Joksić G, Vujić D, Joksić I, Mrasek K, Weise A, Liehr T. First molecular-cytogenetic characterization of Fanconi anemia fragile sites in primary lymphocytes of FA-D2 patients in different stages of the disease. in Molecular Cytogenetics. 2016;9.
doi:10.1186/s13039-016-0280-6 .

Filipović, Jelena G., Joksić, Gordana, Vujić, Dragana, Joksić, Ivana, Mrasek, Kristin, Weise, Anja, Liehr, Thomas, "First molecular-cytogenetic characterization of Fanconi anemia fragile sites in primary lymphocytes of FA-D2 patients in different stages of the disease" in Molecular Cytogenetics, 9 (2016),
https://doi.org/10.1186/s13039-016-0280-6 . .

TY  - JOUR
AU  - Alhourani, Eyad
AU  - Othman, Moneeb A. K.
AU  - Melo, Joana B.
AU  - Carreira, Isabel M.
AU  - Grygalewicz, Beata
AU  - Vujić, Dragana
AU  - Zecevic, Zeljko
AU  - Joksić, Gordana
AU  - Glaser, Anita
AU  - Pohle, Beate
AU  - Schlie, Cordula
AU  - Hauke, Sven
AU  - Liehr, Thomas
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1011
AB  - Deletions within chromosome 11q22-23, are considered among the most common chromosomal aberrations in chronic lymphocytic leukemia (CLL), and are associated with a poor outcome. In addition to the ataxia telangiectasia mutated (ATM) gene, the baculoviral IAP repeat-containing 3 (BIRC3) gene is also located in the region. BIRC3 encodes a negative regulator of the non-canonical nuclear factor.-light-chain-enhancer of activated B cells (NF-kappa B) protein. Disruption of BIRC3 is known to be restricted to CLL fludarabine-refractory patients. The aim of the present study was to determine the frequency of copy number changes of BIRC3 and to assess its association with two known predictors of negative CLL outcome, ATM and tumor protein 53 (TP53) gene deletions. To evaluate the specificity of BIRC3 alterations to CLL, BIRC3 copy numbers were assessed in 117 CLL patients in addition to 45 B-cell acute lymphocytic leukemia (B-ALL) patients. A commercially available multiplex ligation dependent probe amplification kit, which includes four probes for the detection of TP53 and four probes for ATM gene region, was applied. Interphase-directed fluorescence in situ hybridization was used to apply commercially available probes for BIRC3, ATM and TP53. High resolution array-comparative genomic hybridization was conducted in selected cases. Genetic abnormalities of BIRC3 were detected in 23/117 (similar to 20%) of CLL and 2/45 (similar to 4%) of B-ALL cases. Overall, 20 patients with CLL and 1 with B-ALL possessed a BIRC3 deletion, whilst 3 patients with CLL and 1 with B-ALL harbored a BIRC3 duplication. All patients with an ATM deletion also carried a BIRC3 deletion. Only 2 CLL cases possessed deletions in BIRC3, ATM and TP53 simultaneously. Evidently, the deletion or duplication of BIRC3 may be observed rarely in B-ALL patients. BIRC3 duplication may occur in CLL patients, for which the prognosis requires additional studies in the future. The likelihood that TP53 deletions occur simultaneously with BIRC3 and/or ATM aberrations is low. However, as ATM deletions may, but not always, associate with BIRC3 deletions, each region should be considered in the future diagnostics of CLL in order to aid treatment decisions, notably whether to treat with or without fludarabine.
T2  - Oncology Letters
T1  - BIRC3 alterations in chronic and B-cell acute lymphocytic leukemia patients
VL  - 11
IS  - 5
SP  - 3240
EP  - 3246
DO  - 10.3892/ol.2016.4388
ER  - 

@article{
author = "Alhourani, Eyad and Othman, Moneeb A. K. and Melo, Joana B. and Carreira, Isabel M. and Grygalewicz, Beata and Vujić, Dragana and Zecevic, Zeljko and Joksić, Gordana and Glaser, Anita and Pohle, Beate and Schlie, Cordula and Hauke, Sven and Liehr, Thomas",
year = "2016",
abstract = "Deletions within chromosome 11q22-23, are considered among the most common chromosomal aberrations in chronic lymphocytic leukemia (CLL), and are associated with a poor outcome. In addition to the ataxia telangiectasia mutated (ATM) gene, the baculoviral IAP repeat-containing 3 (BIRC3) gene is also located in the region. BIRC3 encodes a negative regulator of the non-canonical nuclear factor.-light-chain-enhancer of activated B cells (NF-kappa B) protein. Disruption of BIRC3 is known to be restricted to CLL fludarabine-refractory patients. The aim of the present study was to determine the frequency of copy number changes of BIRC3 and to assess its association with two known predictors of negative CLL outcome, ATM and tumor protein 53 (TP53) gene deletions. To evaluate the specificity of BIRC3 alterations to CLL, BIRC3 copy numbers were assessed in 117 CLL patients in addition to 45 B-cell acute lymphocytic leukemia (B-ALL) patients. A commercially available multiplex ligation dependent probe amplification kit, which includes four probes for the detection of TP53 and four probes for ATM gene region, was applied. Interphase-directed fluorescence in situ hybridization was used to apply commercially available probes for BIRC3, ATM and TP53. High resolution array-comparative genomic hybridization was conducted in selected cases. Genetic abnormalities of BIRC3 were detected in 23/117 (similar to 20%) of CLL and 2/45 (similar to 4%) of B-ALL cases. Overall, 20 patients with CLL and 1 with B-ALL possessed a BIRC3 deletion, whilst 3 patients with CLL and 1 with B-ALL harbored a BIRC3 duplication. All patients with an ATM deletion also carried a BIRC3 deletion. Only 2 CLL cases possessed deletions in BIRC3, ATM and TP53 simultaneously. Evidently, the deletion or duplication of BIRC3 may be observed rarely in B-ALL patients. BIRC3 duplication may occur in CLL patients, for which the prognosis requires additional studies in the future. The likelihood that TP53 deletions occur simultaneously with BIRC3 and/or ATM aberrations is low. However, as ATM deletions may, but not always, associate with BIRC3 deletions, each region should be considered in the future diagnostics of CLL in order to aid treatment decisions, notably whether to treat with or without fludarabine.",
journal = "Oncology Letters",
title = "BIRC3 alterations in chronic and B-cell acute lymphocytic leukemia patients",
volume = "11",
number = "5",
pages = "3240-3246",
doi = "10.3892/ol.2016.4388"
}

Alhourani, E., Othman, M. A. K., Melo, J. B., Carreira, I. M., Grygalewicz, B., Vujić, D., Zecevic, Z., Joksić, G., Glaser, A., Pohle, B., Schlie, C., Hauke, S.,& Liehr, T.. (2016). BIRC3 alterations in chronic and B-cell acute lymphocytic leukemia patients. in Oncology Letters, 11(5), 3240-3246.
https://doi.org/10.3892/ol.2016.4388

Alhourani E, Othman MAK, Melo JB, Carreira IM, Grygalewicz B, Vujić D, Zecevic Z, Joksić G, Glaser A, Pohle B, Schlie C, Hauke S, Liehr T. BIRC3 alterations in chronic and B-cell acute lymphocytic leukemia patients. in Oncology Letters. 2016;11(5):3240-3246.
doi:10.3892/ol.2016.4388 .

Alhourani, Eyad, Othman, Moneeb A. K., Melo, Joana B., Carreira, Isabel M., Grygalewicz, Beata, Vujić, Dragana, Zecevic, Zeljko, Joksić, Gordana, Glaser, Anita, Pohle, Beate, Schlie, Cordula, Hauke, Sven, Liehr, Thomas, "BIRC3 alterations in chronic and B-cell acute lymphocytic leukemia patients" in Oncology Letters, 11, no. 5 (2016):3240-3246,
https://doi.org/10.3892/ol.2016.4388 . .

TY  - JOUR
AU  - Petrović, Sandra
AU  - Leskovac, Andreja
AU  - Joksić, Ivana
AU  - Vujić, Dragana
AU  - Valenta-Šobot, Ana
AU  - Filipović, Jelena G.
AU  - Joksić, Gordana
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/777
AB  - Fanconi anemia (FA) is a rare genetically heterogeneous disorder associated with bone marrow failure, birth defects and cancer susceptibility. Apart from the disease-causing mutations in FANC genes, the identification of specific DNA variations, such as single nucleotide polymorphisms (SNPs), in other candidate genes may lead to a better clinical description of this condition enabling individualized treatment with improvement of the prognosis. In this study, we have assessed 95 SNPs located in 52 key genes involved in base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), double strand break (DSB) repair and cell cycle control using a DNA repair chip (Asper Biotech, Estonia) which includes most of the common variants for the candidate genes. The SNP genotyping was performed in five FA-D2 patients and in one FA-A patient. The polymorphisms studied were synonymous (n=10), nonsynonymous (missense) (n=52) and in non-coding regions of the genome (introns and 5 and 3 untranslated regions (UTR)) (n=33). Polymorphisms found at the homozygous state are selected for further analysis. Our results have shown a significant inter-individual variability among patients in the type and the frequency of SNPs and also elucidate the need for further studies of polymorphisms located in ATM, APEX APE 1, XRCC1, ERCC2, MSH3, PARP4, NBS1, BARD1, CDKN1B, TP53 and TP53BP1 which may be of great importance for better clinical description of FA. In addition, the present report recommends the use of SNPs as predictive and prognostic genetic markers to individualize therapy of FA patients.
T2  - Genetika
T1  - Assessment of Single Nucleotide Polymorphisms in Screening 52 DNA Repair and Cell Cycle Control Genes in Fanconi Anemia Patients
VL  - 47
IS  - 2
SP  - 695
EP  - 710
DO  - 10.2298/GENSR1502695P
ER  - 

@article{
author = "Petrović, Sandra and Leskovac, Andreja and Joksić, Ivana and Vujić, Dragana and Valenta-Šobot, Ana and Filipović, Jelena G. and Joksić, Gordana",
year = "2015",
abstract = "Fanconi anemia (FA) is a rare genetically heterogeneous disorder associated with bone marrow failure, birth defects and cancer susceptibility. Apart from the disease-causing mutations in FANC genes, the identification of specific DNA variations, such as single nucleotide polymorphisms (SNPs), in other candidate genes may lead to a better clinical description of this condition enabling individualized treatment with improvement of the prognosis. In this study, we have assessed 95 SNPs located in 52 key genes involved in base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), double strand break (DSB) repair and cell cycle control using a DNA repair chip (Asper Biotech, Estonia) which includes most of the common variants for the candidate genes. The SNP genotyping was performed in five FA-D2 patients and in one FA-A patient. The polymorphisms studied were synonymous (n=10), nonsynonymous (missense) (n=52) and in non-coding regions of the genome (introns and 5 and 3 untranslated regions (UTR)) (n=33). Polymorphisms found at the homozygous state are selected for further analysis. Our results have shown a significant inter-individual variability among patients in the type and the frequency of SNPs and also elucidate the need for further studies of polymorphisms located in ATM, APEX APE 1, XRCC1, ERCC2, MSH3, PARP4, NBS1, BARD1, CDKN1B, TP53 and TP53BP1 which may be of great importance for better clinical description of FA. In addition, the present report recommends the use of SNPs as predictive and prognostic genetic markers to individualize therapy of FA patients.",
journal = "Genetika",
title = "Assessment of Single Nucleotide Polymorphisms in Screening 52 DNA Repair and Cell Cycle Control Genes in Fanconi Anemia Patients",
volume = "47",
number = "2",
pages = "695-710",
doi = "10.2298/GENSR1502695P"
}

Petrović, S., Leskovac, A., Joksić, I., Vujić, D., Valenta-Šobot, A., Filipović, J. G.,& Joksić, G.. (2015). Assessment of Single Nucleotide Polymorphisms in Screening 52 DNA Repair and Cell Cycle Control Genes in Fanconi Anemia Patients. in Genetika, 47(2), 695-710.
https://doi.org/10.2298/GENSR1502695P

Petrović S, Leskovac A, Joksić I, Vujić D, Valenta-Šobot A, Filipović JG, Joksić G. Assessment of Single Nucleotide Polymorphisms in Screening 52 DNA Repair and Cell Cycle Control Genes in Fanconi Anemia Patients. in Genetika. 2015;47(2):695-710.
doi:10.2298/GENSR1502695P .

Petrović, Sandra, Leskovac, Andreja, Joksić, Ivana, Vujić, Dragana, Valenta-Šobot, Ana, Filipović, Jelena G., Joksić, Gordana, "Assessment of Single Nucleotide Polymorphisms in Screening 52 DNA Repair and Cell Cycle Control Genes in Fanconi Anemia Patients" in Genetika, 47, no. 2 (2015):695-710,
https://doi.org/10.2298/GENSR1502695P . .

TY  - JOUR
AU  - Leskovac, Andreja
AU  - Petrović, Sandra
AU  - Guć-Šćekić, Marija
AU  - Vujić, Dragana
AU  - Joksić, Gordana
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5986
AB  - Purpose: As the Fanconi anemia (FA) pathway is required for appropriate cell cycle progression through mitosis and the completion of cell division, the aim of the present study was to determine the destiny of FA cells after irradiation in vitro and to elucidate any difference in radiosensitivity between FA and control cells. Materials and methods: Analyses of phosphorylated histone H2AX (gamma-H2AX) foci, micronuclei formation and cell cycle analysis were performed in unirradiated (0 min) and irradiated primary FA fibroblasts and in a control group at different post-irradiation times (30 min, 2 h, 5 h and 24 h). Results: The accumulation of gamma-H2AX foci in irradiated FA fibroblasts was observed. At 24 h post-irradiation, 57% of FA cells were gamma-H2AX foci-positive, significantly higher than in the control (p LT 0.01). The cell cycle analysis has shown the transient G2/M arrest in irradiated FA fibroblasts. The portion of cells in the G2/M phase showed initial increase at 30 min post-irradiation and afterwards decreased over time reaching the pretreatment level 24 h after irradiation. Irradiated FA fibroblasts progressed to abnormal mitosis, as is shown by the production of cells with different nuclear morphologies from binucleated to multinucleated surrounded with micronuclei, and also by a high percentage of foci-positive micronuclei. The majority of radiation-induced micronuclei were gamma-H2AX foci-positive, indicating that radiation-induced micronuclei contain fragments of damaged chromosomes. In contrast, in the control group, most of the micronuclei were classified as gamma-H2AX foci-negative, which indicates that cells with unrepaired damage were blocked before entering mitosis. Conclusion: The results clearly indicate that mitotic catastrophe might be an important cell-death mechanism involved in the response of FA fibroblasts to ionizing radiation.
T2  - International Journal of Radiation Biology
T1  - Radiation-induced mitotic catastrophe in FANCD2 primary fibroblasts
VL  - 90
IS  - 5
SP  - 373
EP  - 381
DO  - 10.3109/09553002.2014.892224
ER  - 

@article{
author = "Leskovac, Andreja and Petrović, Sandra and Guć-Šćekić, Marija and Vujić, Dragana and Joksić, Gordana",
year = "2014",
abstract = "Purpose: As the Fanconi anemia (FA) pathway is required for appropriate cell cycle progression through mitosis and the completion of cell division, the aim of the present study was to determine the destiny of FA cells after irradiation in vitro and to elucidate any difference in radiosensitivity between FA and control cells. Materials and methods: Analyses of phosphorylated histone H2AX (gamma-H2AX) foci, micronuclei formation and cell cycle analysis were performed in unirradiated (0 min) and irradiated primary FA fibroblasts and in a control group at different post-irradiation times (30 min, 2 h, 5 h and 24 h). Results: The accumulation of gamma-H2AX foci in irradiated FA fibroblasts was observed. At 24 h post-irradiation, 57% of FA cells were gamma-H2AX foci-positive, significantly higher than in the control (p LT 0.01). The cell cycle analysis has shown the transient G2/M arrest in irradiated FA fibroblasts. The portion of cells in the G2/M phase showed initial increase at 30 min post-irradiation and afterwards decreased over time reaching the pretreatment level 24 h after irradiation. Irradiated FA fibroblasts progressed to abnormal mitosis, as is shown by the production of cells with different nuclear morphologies from binucleated to multinucleated surrounded with micronuclei, and also by a high percentage of foci-positive micronuclei. The majority of radiation-induced micronuclei were gamma-H2AX foci-positive, indicating that radiation-induced micronuclei contain fragments of damaged chromosomes. In contrast, in the control group, most of the micronuclei were classified as gamma-H2AX foci-negative, which indicates that cells with unrepaired damage were blocked before entering mitosis. Conclusion: The results clearly indicate that mitotic catastrophe might be an important cell-death mechanism involved in the response of FA fibroblasts to ionizing radiation.",
journal = "International Journal of Radiation Biology",
title = "Radiation-induced mitotic catastrophe in FANCD2 primary fibroblasts",
volume = "90",
number = "5",
pages = "373-381",
doi = "10.3109/09553002.2014.892224"
}

Leskovac, A., Petrović, S., Guć-Šćekić, M., Vujić, D.,& Joksić, G.. (2014). Radiation-induced mitotic catastrophe in FANCD2 primary fibroblasts. in International Journal of Radiation Biology, 90(5), 373-381.
https://doi.org/10.3109/09553002.2014.892224

Leskovac A, Petrović S, Guć-Šćekić M, Vujić D, Joksić G. Radiation-induced mitotic catastrophe in FANCD2 primary fibroblasts. in International Journal of Radiation Biology. 2014;90(5):373-381.
doi:10.3109/09553002.2014.892224 .

Leskovac, Andreja, Petrović, Sandra, Guć-Šćekić, Marija, Vujić, Dragana, Joksić, Gordana, "Radiation-induced mitotic catastrophe in FANCD2 primary fibroblasts" in International Journal of Radiation Biology, 90, no. 5 (2014):373-381,
https://doi.org/10.3109/09553002.2014.892224 . .

TY  - JOUR
AU  - Petrović, Sandra
AU  - Leskovac, Andreja
AU  - Joksić, Ivana
AU  - Filipović, Jelena G.
AU  - Vujić, Dragana
AU  - Guć-Šćekić, Marija
AU  - Joksić, Gordana
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5606
AB  - Fanconi anemia (FA) is a rare cancer-prone genetic disease characterized by impaired oxygen metabolism and defects in DNA damage repair. Response of FA cells to ionizing radiation has been an issue intensively debated in the literature. To study in vitro radiosensitivity in patients suffering from FA and their parents (heterozygous carriers), we determined radiation-induced leukocyte apoptosis using flow cytometry. As TP53 gene is involved in the control of apoptosis, we studied its status in FA lymphocytes using dual colour fluorescence in situ hybridization (FISH). FA patients and female heterozygous carriers display radiosensitive response to ionizing radiation seen as abnormal elimination of cells via apoptosis. By employment of FISH, the TP53 allele loss in FA lymphocytes was not observed. In diseases related to oxidative stress, determination of radiation-induced apoptosis is the method of choice for testing the radiosensitivity.
T2  - Current Science
T1  - Leukocyte apoptosis as a predictor of radiosensitivity in Fanconi anemia
VL  - 105
IS  - 1
SP  - 56
EP  - 60
UR  - https://hdl.handle.net/21.15107/rcub_vinar_5606
ER  - 

@article{
author = "Petrović, Sandra and Leskovac, Andreja and Joksić, Ivana and Filipović, Jelena G. and Vujić, Dragana and Guć-Šćekić, Marija and Joksić, Gordana",
year = "2013",
abstract = "Fanconi anemia (FA) is a rare cancer-prone genetic disease characterized by impaired oxygen metabolism and defects in DNA damage repair. Response of FA cells to ionizing radiation has been an issue intensively debated in the literature. To study in vitro radiosensitivity in patients suffering from FA and their parents (heterozygous carriers), we determined radiation-induced leukocyte apoptosis using flow cytometry. As TP53 gene is involved in the control of apoptosis, we studied its status in FA lymphocytes using dual colour fluorescence in situ hybridization (FISH). FA patients and female heterozygous carriers display radiosensitive response to ionizing radiation seen as abnormal elimination of cells via apoptosis. By employment of FISH, the TP53 allele loss in FA lymphocytes was not observed. In diseases related to oxidative stress, determination of radiation-induced apoptosis is the method of choice for testing the radiosensitivity.",
journal = "Current Science",
title = "Leukocyte apoptosis as a predictor of radiosensitivity in Fanconi anemia",
volume = "105",
number = "1",
pages = "56-60",
url = "https://hdl.handle.net/21.15107/rcub_vinar_5606"
}

Petrović, S., Leskovac, A., Joksić, I., Filipović, J. G., Vujić, D., Guć-Šćekić, M.,& Joksić, G.. (2013). Leukocyte apoptosis as a predictor of radiosensitivity in Fanconi anemia. in Current Science, 105(1), 56-60.
https://hdl.handle.net/21.15107/rcub_vinar_5606

Petrović S, Leskovac A, Joksić I, Filipović JG, Vujić D, Guć-Šćekić M, Joksić G. Leukocyte apoptosis as a predictor of radiosensitivity in Fanconi anemia. in Current Science. 2013;105(1):56-60.
https://hdl.handle.net/21.15107/rcub_vinar_5606 .

Petrović, Sandra, Leskovac, Andreja, Joksić, Ivana, Filipović, Jelena G., Vujić, Dragana, Guć-Šćekić, Marija, Joksić, Gordana, "Leukocyte apoptosis as a predictor of radiosensitivity in Fanconi anemia" in Current Science, 105, no. 1 (2013):56-60,
https://hdl.handle.net/21.15107/rcub_vinar_5606 .

TY  - JOUR
AU  - Joksić, Ivana
AU  - Petrović, Sandra
AU  - Leskovac, Andreja
AU  - Filipović, Jelena G.
AU  - Guć-Šćekić, Marija
AU  - Vujić, Dragana
AU  - Joksić, Gordana
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5798
AB  - Fanconi anemia (FA) is a rare genetically heterogeneous disease characterized by developmental abnormalities, progressive bone marrow failure, and cancer susceptibility. We examined spontaneous, diepoxybutane (DEB)-induced and radiation-induced sister chromatid exchanges (SCEs) in wholeblood lymphocyte cultures of bone marrow failure (BMF) patients including Fanconi anemia, mothers of affected individuals, and healthy controls. The baseline frequency of SCE in FA cells was similar to that observed in controls. However, in response to DEB SCE frequencies in FA patients and their mothers were significantly increased compared to both non-FA BMF families and healthy controls. In response to ionizing radiation, cells displayed increased frequency of SCE, but no differences between FA patients and non-FA BMF patients were seen. Our data confirm and expand previous findings by showing that SCE induced by DEB can be used as an adjunct diagnostic test not only for FA patients, but also for female heterozygous carriers, at least for complementation groups FANCA and FANCD2.
T2  - Genetika
T1  - Enhanced Frequency of Sister Chromatid Exchanges Induced By Diepoxybutane Is Specific Characteristic of Fanconi Anemia Cellular Phenotype
VL  - 45
IS  - 2
SP  - 393
EP  - 403
DO  - 10.2298/GENSR1302393J
ER  - 

@article{
author = "Joksić, Ivana and Petrović, Sandra and Leskovac, Andreja and Filipović, Jelena G. and Guć-Šćekić, Marija and Vujić, Dragana and Joksić, Gordana",
year = "2013",
abstract = "Fanconi anemia (FA) is a rare genetically heterogeneous disease characterized by developmental abnormalities, progressive bone marrow failure, and cancer susceptibility. We examined spontaneous, diepoxybutane (DEB)-induced and radiation-induced sister chromatid exchanges (SCEs) in wholeblood lymphocyte cultures of bone marrow failure (BMF) patients including Fanconi anemia, mothers of affected individuals, and healthy controls. The baseline frequency of SCE in FA cells was similar to that observed in controls. However, in response to DEB SCE frequencies in FA patients and their mothers were significantly increased compared to both non-FA BMF families and healthy controls. In response to ionizing radiation, cells displayed increased frequency of SCE, but no differences between FA patients and non-FA BMF patients were seen. Our data confirm and expand previous findings by showing that SCE induced by DEB can be used as an adjunct diagnostic test not only for FA patients, but also for female heterozygous carriers, at least for complementation groups FANCA and FANCD2.",
journal = "Genetika",
title = "Enhanced Frequency of Sister Chromatid Exchanges Induced By Diepoxybutane Is Specific Characteristic of Fanconi Anemia Cellular Phenotype",
volume = "45",
number = "2",
pages = "393-403",
doi = "10.2298/GENSR1302393J"
}

Joksić, I., Petrović, S., Leskovac, A., Filipović, J. G., Guć-Šćekić, M., Vujić, D.,& Joksić, G.. (2013). Enhanced Frequency of Sister Chromatid Exchanges Induced By Diepoxybutane Is Specific Characteristic of Fanconi Anemia Cellular Phenotype. in Genetika, 45(2), 393-403.
https://doi.org/10.2298/GENSR1302393J

Joksić I, Petrović S, Leskovac A, Filipović JG, Guć-Šćekić M, Vujić D, Joksić G. Enhanced Frequency of Sister Chromatid Exchanges Induced By Diepoxybutane Is Specific Characteristic of Fanconi Anemia Cellular Phenotype. in Genetika. 2013;45(2):393-403.
doi:10.2298/GENSR1302393J .

Joksić, Ivana, Petrović, Sandra, Leskovac, Andreja, Filipović, Jelena G., Guć-Šćekić, Marija, Vujić, Dragana, Joksić, Gordana, "Enhanced Frequency of Sister Chromatid Exchanges Induced By Diepoxybutane Is Specific Characteristic of Fanconi Anemia Cellular Phenotype" in Genetika, 45, no. 2 (2013):393-403,
https://doi.org/10.2298/GENSR1302393J . .

TY  - JOUR
AU  - Vujić, Dragana
AU  - Petrović, Sandra
AU  - Leskovac, Andreja
AU  - Joksić, Ivana
AU  - Filipović, Jelena G.
AU  - Valenta-Šobot, Ana
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5595
AB  - In this paper we present the data of lymphocyte radiosensitivity testing used for characterization of radiosensitive cellular phenotype and diagnostics of ataxia-telangiectasia disease. We point out the advantage of lymphocyte micronucleus test (CBMN) over other cellular tests for assessment of radiosensitivity: the first advantage of CBMN is that primary patient cells are used (less than 1 ml), the second one is that the results of testing are obtained within 3 days and there is no need for establishing a patient-derived cell line, which requires additional time and application of more expensive methods. The third advantage of CBMN method is that it gives information about proliferative ability of cells, which can recognize dysfunctional ataxia-telangiectasia mutated protein. The results are fast and accurate in diagnostics of ataxia-telagiectasia diseases.
T2  - Nuclear technology and radiation protection
T1  - Accurate Diagnostics of Ataxia-Telangiectasia Cellular Phenotype By Employing in Vitro Lymphocyte Radiosensitivity Testing
VL  - 28
IS  - 2
SP  - 221
EP  - 224
DO  - 10.2298/NTRP1302221V
ER  - 

@article{
author = "Vujić, Dragana and Petrović, Sandra and Leskovac, Andreja and Joksić, Ivana and Filipović, Jelena G. and Valenta-Šobot, Ana",
year = "2013",
abstract = "In this paper we present the data of lymphocyte radiosensitivity testing used for characterization of radiosensitive cellular phenotype and diagnostics of ataxia-telangiectasia disease. We point out the advantage of lymphocyte micronucleus test (CBMN) over other cellular tests for assessment of radiosensitivity: the first advantage of CBMN is that primary patient cells are used (less than 1 ml), the second one is that the results of testing are obtained within 3 days and there is no need for establishing a patient-derived cell line, which requires additional time and application of more expensive methods. The third advantage of CBMN method is that it gives information about proliferative ability of cells, which can recognize dysfunctional ataxia-telangiectasia mutated protein. The results are fast and accurate in diagnostics of ataxia-telagiectasia diseases.",
journal = "Nuclear technology and radiation protection",
title = "Accurate Diagnostics of Ataxia-Telangiectasia Cellular Phenotype By Employing in Vitro Lymphocyte Radiosensitivity Testing",
volume = "28",
number = "2",
pages = "221-224",
doi = "10.2298/NTRP1302221V"
}

Vujić, D., Petrović, S., Leskovac, A., Joksić, I., Filipović, J. G.,& Valenta-Šobot, A.. (2013). Accurate Diagnostics of Ataxia-Telangiectasia Cellular Phenotype By Employing in Vitro Lymphocyte Radiosensitivity Testing. in Nuclear technology and radiation protection, 28(2), 221-224.
https://doi.org/10.2298/NTRP1302221V

Vujić D, Petrović S, Leskovac A, Joksić I, Filipović JG, Valenta-Šobot A. Accurate Diagnostics of Ataxia-Telangiectasia Cellular Phenotype By Employing in Vitro Lymphocyte Radiosensitivity Testing. in Nuclear technology and radiation protection. 2013;28(2):221-224.
doi:10.2298/NTRP1302221V .

Vujić, Dragana, Petrović, Sandra, Leskovac, Andreja, Joksić, Ivana, Filipović, Jelena G., Valenta-Šobot, Ana, "Accurate Diagnostics of Ataxia-Telangiectasia Cellular Phenotype By Employing in Vitro Lymphocyte Radiosensitivity Testing" in Nuclear technology and radiation protection, 28, no. 2 (2013):221-224,
https://doi.org/10.2298/NTRP1302221V . .

TY  - JOUR
AU  - Petrović, Sandra
AU  - Leskovac, Andreja
AU  - Kotur-Stevuljevic, Jelena
AU  - Joksić, Jelena
AU  - Guć-Šćekić, Marija
AU  - Vujić, Dragana
AU  - Joksić, Gordana
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4379
AB  - Fanconi anemia (FA) is a rare cancer-prone genetic disorder characterized by progressive bone marrow failure, chromosomal instability and redox abnormalities. There is much biochemical and genetic data, which strongly suggest that FA cells experience increased oxidative stress. The present study was designed to elucidate if differences in oxidant state exist between control, idiopathic bone marrow failure (idBMF) and FA cells, and to analyze oxidant state of cells in FA heterozygous carriers as well. The results of the present study confirm an in vivo prooxidant state of FA cells and clearly indicate that FA patients can be distinguished from idBMF patients based on the oxidant state of cells. Female carriers of FA mutation also exhibited hallmarks of an in vivo prooxidant state behaving in a similar manner as FA patients. On the other hand, the oxidant state of cells in FA male carriers and idBMF families failed to show any significant difference vs. controls. We demonstrate that the altered oxidant state influences susceptibility of cells to apoptosis in both FA patients and female carriers. The results highlight the need for further research of the possible role of mitochondrial inheritance in the pathogenesis of FA.
T2  - Biological Chemistry
T1  - Gender-related differences in the oxidant state of cells in Fanconi anemia heterozygotes
VL  - 392
IS  - 7
SP  - 625
EP  - 632
DO  - 10.1515/BC.2011.064
ER  - 

@article{
author = "Petrović, Sandra and Leskovac, Andreja and Kotur-Stevuljevic, Jelena and Joksić, Jelena and Guć-Šćekić, Marija and Vujić, Dragana and Joksić, Gordana",
year = "2011",
abstract = "Fanconi anemia (FA) is a rare cancer-prone genetic disorder characterized by progressive bone marrow failure, chromosomal instability and redox abnormalities. There is much biochemical and genetic data, which strongly suggest that FA cells experience increased oxidative stress. The present study was designed to elucidate if differences in oxidant state exist between control, idiopathic bone marrow failure (idBMF) and FA cells, and to analyze oxidant state of cells in FA heterozygous carriers as well. The results of the present study confirm an in vivo prooxidant state of FA cells and clearly indicate that FA patients can be distinguished from idBMF patients based on the oxidant state of cells. Female carriers of FA mutation also exhibited hallmarks of an in vivo prooxidant state behaving in a similar manner as FA patients. On the other hand, the oxidant state of cells in FA male carriers and idBMF families failed to show any significant difference vs. controls. We demonstrate that the altered oxidant state influences susceptibility of cells to apoptosis in both FA patients and female carriers. The results highlight the need for further research of the possible role of mitochondrial inheritance in the pathogenesis of FA.",
journal = "Biological Chemistry",
title = "Gender-related differences in the oxidant state of cells in Fanconi anemia heterozygotes",
volume = "392",
number = "7",
pages = "625-632",
doi = "10.1515/BC.2011.064"
}

Petrović, S., Leskovac, A., Kotur-Stevuljevic, J., Joksić, J., Guć-Šćekić, M., Vujić, D.,& Joksić, G.. (2011). Gender-related differences in the oxidant state of cells in Fanconi anemia heterozygotes. in Biological Chemistry, 392(7), 625-632.
https://doi.org/10.1515/BC.2011.064

Petrović S, Leskovac A, Kotur-Stevuljevic J, Joksić J, Guć-Šćekić M, Vujić D, Joksić G. Gender-related differences in the oxidant state of cells in Fanconi anemia heterozygotes. in Biological Chemistry. 2011;392(7):625-632.
doi:10.1515/BC.2011.064 .

Petrović, Sandra, Leskovac, Andreja, Kotur-Stevuljevic, Jelena, Joksić, Jelena, Guć-Šćekić, Marija, Vujić, Dragana, Joksić, Gordana, "Gender-related differences in the oxidant state of cells in Fanconi anemia heterozygotes" in Biological Chemistry, 392, no. 7 (2011):625-632,
https://doi.org/10.1515/BC.2011.064 . .

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 . .

TY  - CONF
AU  - Petrović, Sandra
AU  - Vujić, Dragana
AU  - Guć-Šćekić, Marija
AU  - Joksić, Ivana
AU  - Leskovac, Andreja
AU  - Joksić, Gordana
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/11708
AB  - Fankonijeva anemija (FA) je genetičko oboljenje karakterisano progresivnom pancitopenijom i predispozicijom ka malignitetima. Asocirano je sa poremećajima u redoks procesima u ćeliji što ga čini i bolešću oksidativnog stresa. FA ćelije ispoljavaju veliku osetljivost na DNK klastogene agense, dok su podaci o njihovoj osetljivosti na jonizujuće zračenje kontradiktorni. Cilj ove studije je ispitivanje in vitro radioosetljivosti FA homozigota i heterozigota i utvrđivanje uticaja antioksidativnih enzima na ukupan radiobiološki odgovor ćelija. FA pacijenti ispoljavaju značajno sniženje aktivnosti katalaza, sniženu vrednost superoksid dismutaza i povećani bazalni nivo mikronukleusa u odnosu na kontrolu. Radiorezistentni odgovor na jonizujuće zračenje utvrđen je kod većine pacijenata i praćen je značajno većim procentom zračenjem indukovane apoptoze. Utvrđena je negativna korelacija između aktivnosti katalaza i procenta apoptotskih ćelija. Heterozigoti-roditelji imaju visok procenat zračenjem indukovane apoptoze koja je kod nosioca-majki praćena značajnim sniženjem aktivnosti katalaza. Rezultati pokazuju da snižena vrednost katalaza značajno doprinosi ukupnom radiobiološkom odgovoru ćelija.
PB  - Beograd : Društvo genetičara Srbije
C3  - IV Kongres genetičara Srbije : zbornik abstrakata; Jun 1-5, Tara
T1  - Uticaj antioksidativniih enzima na ukupni radiobiološki odgovor limfocita pacienata obolelih od Fankonijeve anemije
SP  - 52
EP  - 52
UR  - https://hdl.handle.net/21.15107/rcub_vinar_11708
ER  - 

@conference{
author = "Petrović, Sandra and Vujić, Dragana and Guć-Šćekić, Marija and Joksić, Ivana and Leskovac, Andreja and Joksić, Gordana",
year = "2009",
abstract = "Fankonijeva anemija (FA) je genetičko oboljenje karakterisano progresivnom pancitopenijom i predispozicijom ka malignitetima. Asocirano je sa poremećajima u redoks procesima u ćeliji što ga čini i bolešću oksidativnog stresa. FA ćelije ispoljavaju veliku osetljivost na DNK klastogene agense, dok su podaci o njihovoj osetljivosti na jonizujuće zračenje kontradiktorni. Cilj ove studije je ispitivanje in vitro radioosetljivosti FA homozigota i heterozigota i utvrđivanje uticaja antioksidativnih enzima na ukupan radiobiološki odgovor ćelija. FA pacijenti ispoljavaju značajno sniženje aktivnosti katalaza, sniženu vrednost superoksid dismutaza i povećani bazalni nivo mikronukleusa u odnosu na kontrolu. Radiorezistentni odgovor na jonizujuće zračenje utvrđen je kod većine pacijenata i praćen je značajno većim procentom zračenjem indukovane apoptoze. Utvrđena je negativna korelacija između aktivnosti katalaza i procenta apoptotskih ćelija. Heterozigoti-roditelji imaju visok procenat zračenjem indukovane apoptoze koja je kod nosioca-majki praćena značajnim sniženjem aktivnosti katalaza. Rezultati pokazuju da snižena vrednost katalaza značajno doprinosi ukupnom radiobiološkom odgovoru ćelija.",
publisher = "Beograd : Društvo genetičara Srbije",
journal = "IV Kongres genetičara Srbije : zbornik abstrakata; Jun 1-5, Tara",
title = "Uticaj antioksidativniih enzima na ukupni radiobiološki odgovor limfocita pacienata obolelih od Fankonijeve anemije",
pages = "52-52",
url = "https://hdl.handle.net/21.15107/rcub_vinar_11708"
}

Petrović, S., Vujić, D., Guć-Šćekić, M., Joksić, I., Leskovac, A.,& Joksić, G.. (2009). Uticaj antioksidativniih enzima na ukupni radiobiološki odgovor limfocita pacienata obolelih od Fankonijeve anemije. in IV Kongres genetičara Srbije : zbornik abstrakata; Jun 1-5, Tara
Beograd : Društvo genetičara Srbije., 52-52.
https://hdl.handle.net/21.15107/rcub_vinar_11708

Petrović S, Vujić D, Guć-Šćekić M, Joksić I, Leskovac A, Joksić G. Uticaj antioksidativniih enzima na ukupni radiobiološki odgovor limfocita pacienata obolelih od Fankonijeve anemije. in IV Kongres genetičara Srbije : zbornik abstrakata; Jun 1-5, Tara. 2009;:52-52.
https://hdl.handle.net/21.15107/rcub_vinar_11708 .

Petrović, Sandra, Vujić, Dragana, Guć-Šćekić, Marija, Joksić, Ivana, Leskovac, Andreja, Joksić, Gordana, "Uticaj antioksidativniih enzima na ukupni radiobiološki odgovor limfocita pacienata obolelih od Fankonijeve anemije" in IV Kongres genetičara Srbije : zbornik abstrakata; Jun 1-5, Tara (2009):52-52,
https://hdl.handle.net/21.15107/rcub_vinar_11708 .

TY  - CONF
AU  - Joksić, Ivana
AU  - Guć-Šćekić, Marija
AU  - Vujić, Dragana
AU  - Petrović, Sandra
AU  - Leskovac, Andreja
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/11709
AB  - Telomere su nukleoproteinski kompleksi smešteni na krajevima hromozoma koji imaju ključnu funkciju u očuvanju integriteta hromozomskih sekvenci, sprečavajući degradaciju DNK egzonukleazama i neadekvatnu aktivaciju kontrolnih tačaka ćelijskog ciklusa i puteva popravke DNK. TIF metoda (fokusi indukovani telomernom disfunkcijom), predstvalja ko-lokalizaciju faktora DNK repera (53BP1 i γH2AX) i telomera i omogućava kvantifikaciju nefunkcionalnih telomera u različitim tkivima. U primarnim ćelijskim linijama fibroblasta kože devet pacijenata sa sindromom aplazije kostne srži i fenotipom Fankonijeve anemije određivana je bazalna incidenca SCE, T-SCE, γH2AX i TIF. Prosečna učestalost SCE iznoslia je 4.42±0.96 (3.38 do 6.5) po ćeliji, dok je incidenca T-SCE iznoslia 1.91±0.81 (1 do 3.33) po ćeliji. Bazalne vrednosti γH2AX iznosile su 2.27±1.55 (0.8 do 4.2), dok je prosečna učestalosta TIF iznoslia 2.97±1.47 (od 1.44 do 5) po ćeliji. Statistički značajna pozitivna korelacija uočena je između incidence SCE i TIF (0.77 p<0.05), ukazujući da je disfunkcija telomera verovatno nastala mehanizmom homologe rekombinacije.
PB  - Beograd : Društvo genetičara Srbije
C3  - IV Kongres genetičara Srbije : zbornik abstrakata; Jun 1-5, Tara
T1  - Disfunkcija telomera pozitivno koreliše sa incidencom izmena sestrinskih hromatida kod pacijenata obolelih of Fankonijeve anemije
SP  - 103
EP  - 103
UR  - https://hdl.handle.net/21.15107/rcub_vinar_11709
ER  - 

@conference{
author = "Joksić, Ivana and Guć-Šćekić, Marija and Vujić, Dragana and Petrović, Sandra and Leskovac, Andreja",
year = "2009",
abstract = "Telomere su nukleoproteinski kompleksi smešteni na krajevima hromozoma koji imaju ključnu funkciju u očuvanju integriteta hromozomskih sekvenci, sprečavajući degradaciju DNK egzonukleazama i neadekvatnu aktivaciju kontrolnih tačaka ćelijskog ciklusa i puteva popravke DNK. TIF metoda (fokusi indukovani telomernom disfunkcijom), predstvalja ko-lokalizaciju faktora DNK repera (53BP1 i γH2AX) i telomera i omogućava kvantifikaciju nefunkcionalnih telomera u različitim tkivima. U primarnim ćelijskim linijama fibroblasta kože devet pacijenata sa sindromom aplazije kostne srži i fenotipom Fankonijeve anemije određivana je bazalna incidenca SCE, T-SCE, γH2AX i TIF. Prosečna učestalost SCE iznoslia je 4.42±0.96 (3.38 do 6.5) po ćeliji, dok je incidenca T-SCE iznoslia 1.91±0.81 (1 do 3.33) po ćeliji. Bazalne vrednosti γH2AX iznosile su 2.27±1.55 (0.8 do 4.2), dok je prosečna učestalosta TIF iznoslia 2.97±1.47 (od 1.44 do 5) po ćeliji. Statistički značajna pozitivna korelacija uočena je između incidence SCE i TIF (0.77 p<0.05), ukazujući da je disfunkcija telomera verovatno nastala mehanizmom homologe rekombinacije.",
publisher = "Beograd : Društvo genetičara Srbije",
journal = "IV Kongres genetičara Srbije : zbornik abstrakata; Jun 1-5, Tara",
title = "Disfunkcija telomera pozitivno koreliše sa incidencom izmena sestrinskih hromatida kod pacijenata obolelih of Fankonijeve anemije",
pages = "103-103",
url = "https://hdl.handle.net/21.15107/rcub_vinar_11709"
}

Joksić, I., Guć-Šćekić, M., Vujić, D., Petrović, S.,& Leskovac, A.. (2009). Disfunkcija telomera pozitivno koreliše sa incidencom izmena sestrinskih hromatida kod pacijenata obolelih of Fankonijeve anemije. in IV Kongres genetičara Srbije : zbornik abstrakata; Jun 1-5, Tara
Beograd : Društvo genetičara Srbije., 103-103.
https://hdl.handle.net/21.15107/rcub_vinar_11709

Joksić I, Guć-Šćekić M, Vujić D, Petrović S, Leskovac A. Disfunkcija telomera pozitivno koreliše sa incidencom izmena sestrinskih hromatida kod pacijenata obolelih of Fankonijeve anemije. in IV Kongres genetičara Srbije : zbornik abstrakata; Jun 1-5, Tara. 2009;:103-103.
https://hdl.handle.net/21.15107/rcub_vinar_11709 .

Joksić, Ivana, Guć-Šćekić, Marija, Vujić, Dragana, Petrović, Sandra, Leskovac, Andreja, "Disfunkcija telomera pozitivno koreliše sa incidencom izmena sestrinskih hromatida kod pacijenata obolelih of Fankonijeve anemije" in IV Kongres genetičara Srbije : zbornik abstrakata; Jun 1-5, Tara (2009):103-103,
https://hdl.handle.net/21.15107/rcub_vinar_11709 .

TY  - CONF
AU  - Leskovac, Andreja
AU  - Petrović, Sandra
AU  - Joksić, Ivana
AU  - Vujić, Dragana
AU  - Guć-Šćekić, Marija
AU  - Slijepčević, Predrag
AU  - Joksić, Gordana
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/11710
AB  - Ćelije obolelih od Fankonijeve anemije pokazuju preosetljivost na DNK-unakrsno vezujuće agense, ali je njihov odgovor na jonizujuće zračenje još uvek nedovoljno proučen. Cilj ove studije bio je ispitati radioosetljivost fibroblasta obolelih od aplastične (AA) i fankonijeve (FA) anemije in vitro, praćenjem fosforilisanog histona γH2AX i procenta ćelija u apoptozi. Imunofluorescentnom metodom određeni γH2AX fokusi korišćeni su za kvantifikaciju dvolančanih prekida. Najveći broj γH2AX fokusa u FA ćelijama utvrđen je 30 min, a u AA ćelijama 24 h nakon ozračivanja. U kontrolnim ćelijama najveći broj apoptotičnih ćelija utvrđen je 30 min i 24 h, a kod obolelih od FA i AA, 2 i 24 h nakon ozračivanja. Odogođena apoptoza i zastoj u ćelijskom ciklusu u FA i AA ćelijama nakon ozračivanja ukazuje na poremećaj u radiobiološkom odgovoru, dok merenje dvolančanih prekida preko γH2AX 30 min nakon ozračivanja može biti značajan parametar za diferencijalnu dijagnostiku FA i AA ćelijskog fenotipa. Ovo istraživanje je pokazalo da praćenje γH2AX fokusa predstavlja veoma osetljivu metodu značajnu za procenu genomske radioosetljivosti, kao i da postoji jasna razlika u ponašanju FA, AA i normalnih fibroblasta u odgovoru na jonizujuće zračenje.
PB  - Beograd : Društvo genetičara Srbije
C3  - IV Kongres genetičara Srbije : zbornik abstrakata; Jun 1-5, Tara
T1  - Radioosetljivost fibroblasta pacijenata obolelih of Fankonijeve anemije
SP  - 53
EP  - 53
UR  - https://hdl.handle.net/21.15107/rcub_vinar_11710
ER  - 

@conference{
author = "Leskovac, Andreja and Petrović, Sandra and Joksić, Ivana and Vujić, Dragana and Guć-Šćekić, Marija and Slijepčević, Predrag and Joksić, Gordana",
year = "2009",
abstract = "Ćelije obolelih od Fankonijeve anemije pokazuju preosetljivost na DNK-unakrsno vezujuće agense, ali je njihov odgovor na jonizujuće zračenje još uvek nedovoljno proučen. Cilj ove studije bio je ispitati radioosetljivost fibroblasta obolelih od aplastične (AA) i fankonijeve (FA) anemije in vitro, praćenjem fosforilisanog histona γH2AX i procenta ćelija u apoptozi. Imunofluorescentnom metodom određeni γH2AX fokusi korišćeni su za kvantifikaciju dvolančanih prekida. Najveći broj γH2AX fokusa u FA ćelijama utvrđen je 30 min, a u AA ćelijama 24 h nakon ozračivanja. U kontrolnim ćelijama najveći broj apoptotičnih ćelija utvrđen je 30 min i 24 h, a kod obolelih od FA i AA, 2 i 24 h nakon ozračivanja. Odogođena apoptoza i zastoj u ćelijskom ciklusu u FA i AA ćelijama nakon ozračivanja ukazuje na poremećaj u radiobiološkom odgovoru, dok merenje dvolančanih prekida preko γH2AX 30 min nakon ozračivanja može biti značajan parametar za diferencijalnu dijagnostiku FA i AA ćelijskog fenotipa. Ovo istraživanje je pokazalo da praćenje γH2AX fokusa predstavlja veoma osetljivu metodu značajnu za procenu genomske radioosetljivosti, kao i da postoji jasna razlika u ponašanju FA, AA i normalnih fibroblasta u odgovoru na jonizujuće zračenje.",
publisher = "Beograd : Društvo genetičara Srbije",
journal = "IV Kongres genetičara Srbije : zbornik abstrakata; Jun 1-5, Tara",
title = "Radioosetljivost fibroblasta pacijenata obolelih of Fankonijeve anemije",
pages = "53-53",
url = "https://hdl.handle.net/21.15107/rcub_vinar_11710"
}

Leskovac, A., Petrović, S., Joksić, I., Vujić, D., Guć-Šćekić, M., Slijepčević, P.,& Joksić, G.. (2009). Radioosetljivost fibroblasta pacijenata obolelih of Fankonijeve anemije. in IV Kongres genetičara Srbije : zbornik abstrakata; Jun 1-5, Tara
Beograd : Društvo genetičara Srbije., 53-53.
https://hdl.handle.net/21.15107/rcub_vinar_11710

Leskovac A, Petrović S, Joksić I, Vujić D, Guć-Šćekić M, Slijepčević P, Joksić G. Radioosetljivost fibroblasta pacijenata obolelih of Fankonijeve anemije. in IV Kongres genetičara Srbije : zbornik abstrakata; Jun 1-5, Tara. 2009;:53-53.
https://hdl.handle.net/21.15107/rcub_vinar_11710 .

Leskovac, Andreja, Petrović, Sandra, Joksić, Ivana, Vujić, Dragana, Guć-Šćekić, Marija, Slijepčević, Predrag, Joksić, Gordana, "Radioosetljivost fibroblasta pacijenata obolelih of Fankonijeve anemije" in IV Kongres genetičara Srbije : zbornik abstrakata; Jun 1-5, Tara (2009):53-53,
https://hdl.handle.net/21.15107/rcub_vinar_11710 .

TY  - CONF
AU  - Joksić, I.
AU  - Vujić, Dragana
AU  - Guć-Šćekić, Marija
AU  - Leskovac, Andreja
AU  - Petrović, Sandra
AU  - Miković, Z.
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/11711
AB  - Telomeres consist of repeated DNA sequences and associated proteins that lie at the termini of linear chromosomes and are critical to the protection and stability of internal chromosome sequences, a function known as telomere “capping”. In capping chromosomes ends, telomeres restrict chromosome end resection by exonucleases and prevent the improper activation of checkpoint response factors and DNA damage response pathways such as homologous recombination (HR) and non-homologous end joining (NHEJ). Telomeres shorten as cell divide, but also due to action of restriction exonucleases, oxidative damage and inappropriate recombination. When telomere shorten to a critical length, they become uncapped, which can lead to permanent cell cycle arrest. The development of the “TIF” (telomere dysfunction induced foci) assay that is based on colocalization of the DNA repair factors 53BP1 and γH2AX with uncapped telomeres enables measurement of telomere uncapping in different tissues. Our aim was to investigate correlation between homologous DNA recombination processes and function of telomeres. In nine primary fibroblast cell lines, obtained from patients presenting with bone marrow failure syndrome and Fanconi anemia clinical and cellular (diepoxybutane- DEB positive) phenotype, baseline incidence of SCE, T-SCE, γH2AX and TIF were examined. The average incidence of SCE was 4.42+-0.96, ranging from 3.38 to 6.5 per cell, whereas incidence of T-SCE was 1.91+-0.81 ranging from 1 to 3.33. Baseline level of γH2AX foci was 2.27+-1.55 ranging from 0.8 to 4.2, whereas average incidence of TIF was 2.97+-1.47, ranging from 1.44 to 5 per cell. Statistically significant positive correlation between incidence of SCE and TIF was observed (0.77 p<0.05) indicating a connection between uncapped telomeres in these cells and homologous recombination, a link which should be further investigated.
C3  - ICEM 2009 : 10th 10th International Conference on Enviromental Mutagens : programme and the book of abstracts; Aug 20-25, 2009; Firenze, Italy
T1  - Telomere dysfunction induced foci correlates positively with incidence of sister chromatid exchanges in cells of Fanconi anemia patients
SP  - 135
SP  - 135
UR  - https://hdl.handle.net/21.15107/rcub_vinar_11711
ER  - 

@conference{
author = "Joksić, I. and Vujić, Dragana and Guć-Šćekić, Marija and Leskovac, Andreja and Petrović, Sandra and Miković, Z.",
year = "2009",
abstract = "Telomeres consist of repeated DNA sequences and associated proteins that lie at the termini of linear chromosomes and are critical to the protection and stability of internal chromosome sequences, a function known as telomere “capping”. In capping chromosomes ends, telomeres restrict chromosome end resection by exonucleases and prevent the improper activation of checkpoint response factors and DNA damage response pathways such as homologous recombination (HR) and non-homologous end joining (NHEJ). Telomeres shorten as cell divide, but also due to action of restriction exonucleases, oxidative damage and inappropriate recombination. When telomere shorten to a critical length, they become uncapped, which can lead to permanent cell cycle arrest. The development of the “TIF” (telomere dysfunction induced foci) assay that is based on colocalization of the DNA repair factors 53BP1 and γH2AX with uncapped telomeres enables measurement of telomere uncapping in different tissues. Our aim was to investigate correlation between homologous DNA recombination processes and function of telomeres. In nine primary fibroblast cell lines, obtained from patients presenting with bone marrow failure syndrome and Fanconi anemia clinical and cellular (diepoxybutane- DEB positive) phenotype, baseline incidence of SCE, T-SCE, γH2AX and TIF were examined. The average incidence of SCE was 4.42+-0.96, ranging from 3.38 to 6.5 per cell, whereas incidence of T-SCE was 1.91+-0.81 ranging from 1 to 3.33. Baseline level of γH2AX foci was 2.27+-1.55 ranging from 0.8 to 4.2, whereas average incidence of TIF was 2.97+-1.47, ranging from 1.44 to 5 per cell. Statistically significant positive correlation between incidence of SCE and TIF was observed (0.77 p<0.05) indicating a connection between uncapped telomeres in these cells and homologous recombination, a link which should be further investigated.",
journal = "ICEM 2009 : 10th 10th International Conference on Enviromental Mutagens : programme and the book of abstracts; Aug 20-25, 2009; Firenze, Italy",
title = "Telomere dysfunction induced foci correlates positively with incidence of sister chromatid exchanges in cells of Fanconi anemia patients",
pages = "135-135",
url = "https://hdl.handle.net/21.15107/rcub_vinar_11711"
}

Joksić, I., Vujić, D., Guć-Šćekić, M., Leskovac, A., Petrović, S.,& Miković, Z.. (2009). Telomere dysfunction induced foci correlates positively with incidence of sister chromatid exchanges in cells of Fanconi anemia patients. in ICEM 2009 : 10th 10th International Conference on Enviromental Mutagens : programme and the book of abstracts; Aug 20-25, 2009; Firenze, Italy, 135.
https://hdl.handle.net/21.15107/rcub_vinar_11711

Joksić I, Vujić D, Guć-Šćekić M, Leskovac A, Petrović S, Miković Z. Telomere dysfunction induced foci correlates positively with incidence of sister chromatid exchanges in cells of Fanconi anemia patients. in ICEM 2009 : 10th 10th International Conference on Enviromental Mutagens : programme and the book of abstracts; Aug 20-25, 2009; Firenze, Italy. 2009;:135.
https://hdl.handle.net/21.15107/rcub_vinar_11711 .

Joksić, I., Vujić, Dragana, Guć-Šćekić, Marija, Leskovac, Andreja, Petrović, Sandra, Miković, Z., "Telomere dysfunction induced foci correlates positively with incidence of sister chromatid exchanges in cells of Fanconi anemia patients" in ICEM 2009 : 10th 10th International Conference on Enviromental Mutagens : programme and the book of abstracts; Aug 20-25, 2009; Firenze, Italy (2009):135,
https://hdl.handle.net/21.15107/rcub_vinar_11711 .

TY  - JOUR
AU  - Petrović, Sandra
AU  - Vujić, Dragana
AU  - Guć-Šćekić, Marija
AU  - Leskovac, Andreja
AU  - Jevtic, Dragana
AU  - Joksić, Gordana
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3751
AB  - Fanconi anemia (FA) is a genetic disease characterized by progressive pancytopenia and cancer susceptibility. The clinical and cellular phenotypes of Fanconi anemia are associated with a set of redox abnormalities, indicating that FA is an oxidative stress-related disorder. Fanconi anemia cells are highly sensitive to DNA clastogen agents, but their response to ionizing radiation is still unclear. The aim of this study was to evaluate the in vitro radiosensitivity of Fanconi anemia homozygotes and heterozygotes, and to assess the contribution of catalase and superoxide dismutase (SOD) to the overall radiobiological response of the cells. The incidence of radiation-induced lymphocyte micronuclei was used as the indicator of radiation sensitivity in vitro, whereas the activity of antioxidant enzymes was determined in erythrocytes. Patients with FA exhibited a two-fold decrease in catalase activity, accompanied by lowered activity of SOD, and increased incidence of baseline micronuclei. In the entire group of patients (with one exception), a reduced yield of radiation-induced micronuclei in lymphocytes was observed, and this was categorized as a radioresistant response. A mild radioresistant in vitro response was also observed in carrier-mothers, accompanied by reduced activity of catalase. The radiosensitivity of carrier-fathers was normal. The results of this study suggest that reduced activity of catalase is an important contributor to the radiobiological response of cells.
T2  - Archives of Biological Sciences
T1  - Influence of Catalase on the Radiosensitivity of Fanconi Anemia Lymphocytes in Vitro
VL  - 61
IS  - 2
SP  - 195
EP  - 204
DO  - 10.2298/ABS0901195P
ER  - 

@article{
author = "Petrović, Sandra and Vujić, Dragana and Guć-Šćekić, Marija and Leskovac, Andreja and Jevtic, Dragana and Joksić, Gordana",
year = "2009",
abstract = "Fanconi anemia (FA) is a genetic disease characterized by progressive pancytopenia and cancer susceptibility. The clinical and cellular phenotypes of Fanconi anemia are associated with a set of redox abnormalities, indicating that FA is an oxidative stress-related disorder. Fanconi anemia cells are highly sensitive to DNA clastogen agents, but their response to ionizing radiation is still unclear. The aim of this study was to evaluate the in vitro radiosensitivity of Fanconi anemia homozygotes and heterozygotes, and to assess the contribution of catalase and superoxide dismutase (SOD) to the overall radiobiological response of the cells. The incidence of radiation-induced lymphocyte micronuclei was used as the indicator of radiation sensitivity in vitro, whereas the activity of antioxidant enzymes was determined in erythrocytes. Patients with FA exhibited a two-fold decrease in catalase activity, accompanied by lowered activity of SOD, and increased incidence of baseline micronuclei. In the entire group of patients (with one exception), a reduced yield of radiation-induced micronuclei in lymphocytes was observed, and this was categorized as a radioresistant response. A mild radioresistant in vitro response was also observed in carrier-mothers, accompanied by reduced activity of catalase. The radiosensitivity of carrier-fathers was normal. The results of this study suggest that reduced activity of catalase is an important contributor to the radiobiological response of cells.",
journal = "Archives of Biological Sciences",
title = "Influence of Catalase on the Radiosensitivity of Fanconi Anemia Lymphocytes in Vitro",
volume = "61",
number = "2",
pages = "195-204",
doi = "10.2298/ABS0901195P"
}

Petrović, S., Vujić, D., Guć-Šćekić, M., Leskovac, A., Jevtic, D.,& Joksić, G.. (2009). Influence of Catalase on the Radiosensitivity of Fanconi Anemia Lymphocytes in Vitro. in Archives of Biological Sciences, 61(2), 195-204.
https://doi.org/10.2298/ABS0901195P

Petrović S, Vujić D, Guć-Šćekić M, Leskovac A, Jevtic D, Joksić G. Influence of Catalase on the Radiosensitivity of Fanconi Anemia Lymphocytes in Vitro. in Archives of Biological Sciences. 2009;61(2):195-204.
doi:10.2298/ABS0901195P .

Petrović, Sandra, Vujić, Dragana, Guć-Šćekić, Marija, Leskovac, Andreja, Jevtic, Dragana, Joksić, Gordana, "Influence of Catalase on the Radiosensitivity of Fanconi Anemia Lymphocytes in Vitro" in Archives of Biological Sciences, 61, no. 2 (2009):195-204,
https://doi.org/10.2298/ABS0901195P . .

TY  - CONF
AU  - Joksić, Gordana
AU  - Guč-Šćekić, Marija
AU  - Vujić, Dragana
AU  - Petrović, Sandra
AU  - Leskovac, Andreja
AU  - Jevtić, D.
AU  - Mićić, D.
PY  - 2007
PY  - 1
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/11735
AB  - Fanconi anemia (FA) is an autosomal recessive disorder characterized by bone-marrow failure and cancer susceptibility. Early studies pointed to the specific sensitivity of FA cells to MMC and DEB which became the tools for the current diagnostic tests for FA. Although there is the long-standing clinical impression of radiosensitivity, in vitro studies have yielded conflicting results. We exposed peripheral blood mononuclear cells of FA patients (10 subjects) and carriers (20 subjects) to γ-rays (60Co), dose of 2 Gy in vitro with aim to determine their radiosensitivity using CB micronucleus (MN) test. Incidence of spontaneous occurring chromosomal aberrations and MN in unirradiatedcontrol samples also was examined. Mean incidence of chromosomal aberrations in FA patients was 0.088±0.08; which is 3.5 fold higher than in carriers, baseline level of MN was 11.66±6.7 whereas average incidence of radiation-induced micronuclei was 122.63±95.6. Baseline level of micronuclei find in parents lymphocytes was 16.29±8.4 (fathers); 14.04±11.17 (mothers), which is 2.3 fold higher compared to common population. Radioresponse of FA lymphocyte in vitro in most cases corresponds to resistant in vitro response, (with exception of one case where radiosensitive in vitro response was observed). Incidence of spontaneously occurring chromosomal aberration highly correlates with baseline incidence of MN, number of cell carrying aberrations and radiosensitivity (r=0.81, p<0.05) Mild radioresistant in vitro response was observed in mothers lymphocytes, whereas fathers response could be described normal-as in the common population. The authors will discuss the possible explanations for resistant response of FA lymphocytes in vitro
PB  - Nature Publishing Group
C3  - Proceedings of the European Journal of Human Genetics
T1  - Radiosensitivity of Fanconi anemia lymphocytes in vitro measured by CBMN assay
VL  - 15
SP  - 108
EP  - 109
UR  - https://hdl.handle.net/21.15107/rcub_vinar_11735
ER  - 

@conference{
author = "Joksić, Gordana and Guč-Šćekić, Marija and Vujić, Dragana and Petrović, Sandra and Leskovac, Andreja and Jevtić, D. and Mićić, D.",
year = "2007, 1",
abstract = "Fanconi anemia (FA) is an autosomal recessive disorder characterized by bone-marrow failure and cancer susceptibility. Early studies pointed to the specific sensitivity of FA cells to MMC and DEB which became the tools for the current diagnostic tests for FA. Although there is the long-standing clinical impression of radiosensitivity, in vitro studies have yielded conflicting results. We exposed peripheral blood mononuclear cells of FA patients (10 subjects) and carriers (20 subjects) to γ-rays (60Co), dose of 2 Gy in vitro with aim to determine their radiosensitivity using CB micronucleus (MN) test. Incidence of spontaneous occurring chromosomal aberrations and MN in unirradiatedcontrol samples also was examined. Mean incidence of chromosomal aberrations in FA patients was 0.088±0.08; which is 3.5 fold higher than in carriers, baseline level of MN was 11.66±6.7 whereas average incidence of radiation-induced micronuclei was 122.63±95.6. Baseline level of micronuclei find in parents lymphocytes was 16.29±8.4 (fathers); 14.04±11.17 (mothers), which is 2.3 fold higher compared to common population. Radioresponse of FA lymphocyte in vitro in most cases corresponds to resistant in vitro response, (with exception of one case where radiosensitive in vitro response was observed). Incidence of spontaneously occurring chromosomal aberration highly correlates with baseline incidence of MN, number of cell carrying aberrations and radiosensitivity (r=0.81, p<0.05) Mild radioresistant in vitro response was observed in mothers lymphocytes, whereas fathers response could be described normal-as in the common population. The authors will discuss the possible explanations for resistant response of FA lymphocytes in vitro",
publisher = "Nature Publishing Group",
journal = "Proceedings of the European Journal of Human Genetics",
title = "Radiosensitivity of Fanconi anemia lymphocytes in vitro measured by CBMN assay",
volume = "15",
pages = "108-109",
url = "https://hdl.handle.net/21.15107/rcub_vinar_11735"
}

Joksić, G., Guč-Šćekić, M., Vujić, D., Petrović, S., Leskovac, A., Jevtić, D.,& Mićić, D.. (2007). Radiosensitivity of Fanconi anemia lymphocytes in vitro measured by CBMN assay. in Proceedings of the European Journal of Human Genetics
Nature Publishing Group., 15, 108-109.
https://hdl.handle.net/21.15107/rcub_vinar_11735

Joksić G, Guč-Šćekić M, Vujić D, Petrović S, Leskovac A, Jevtić D, Mićić D. Radiosensitivity of Fanconi anemia lymphocytes in vitro measured by CBMN assay. in Proceedings of the European Journal of Human Genetics. 2007;15:108-109.
https://hdl.handle.net/21.15107/rcub_vinar_11735 .

Joksić, Gordana, Guč-Šćekić, Marija, Vujić, Dragana, Petrović, Sandra, Leskovac, Andreja, Jevtić, D., Mićić, D., "Radiosensitivity of Fanconi anemia lymphocytes in vitro measured by CBMN assay" in Proceedings of the European Journal of Human Genetics, 15 (2007):108-109,
https://hdl.handle.net/21.15107/rcub_vinar_11735 .