17 results on '"Badie, C"'
Search Results
2. RENEB Inter-Laboratory Comparison 2021: The Gene Expression Assay
- Author
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Abend, M., primary, Amundson, S.A., additional, Badie, C., additional, Brzoska, K., additional, Kriehuber, R., additional, Lacombe, J., additional, Lopez-Riego, M., additional, Lumniczky, K., additional, Endesfelder, D., additional, O'Brien, G., additional, Doucha-Senf, S., additional, Ghandhi, S.A., additional, Hargitai, R., additional, Kis, E., additional, Lundholm, L., additional, Oskamp, D., additional, Ostheim, P., additional, Schüle, S., additional, Schwanke, D., additional, Shuryak, I., additional, Siebenwith, C., additional, Unverricht-Yeboah, M., additional, Wojcik, A., additional, Yang, J., additional, Zenhausern, F., additional, and Port, M., additional
- Published
- 2023
- Full Text
- View/download PDF
3. RENEB Inter-Laboratory Comparison 2021: Inter-Assay Comparison of Eight Dosimetry Assays
- Author
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Port, M., primary, Barquinero, J-F., additional, Endesfelder, D., additional, Moquet, J., additional, Oestreicher, U., additional, Terzoudi, G., additional, Trompier, F., additional, Vral, A., additional, Abe, Y., additional, Ainsbury, L., additional, Alkebsi, L, additional, Amundson, S.A., additional, Badie, C., additional, Baeyens, A., additional, Balajee, A.S., additional, Balázs, K., additional, Barnard, S., additional, Bassinet, C., additional, Beaton-Green, L.A., additional, Beinke, C., additional, Bobyk, L., additional, Brochard, P., additional, Brzoska, K., additional, Bucher, M., additional, Ciesielski, B., additional, Cuceu, C., additional, Discher, M., additional, D,Oca, M.C., additional, Domínguez, I., additional, Doucha-Senf, S., additional, Dumitrescu, A., additional, Duy, P.N., additional, Finot, F., additional, Garty, G., additional, Ghandhi, S.A., additional, Gregoire, E., additional, Goh, V.S.T., additional, Güçlü, I., additional, Hadjiiska, L., additional, Hargitai, R., additional, Hristova, R., additional, Ishii, K., additional, Kis, E., additional, Juniewicz, M., additional, Kriehuber, R., additional, Lacombe, J., additional, Lee, Y., additional, Lopez Riego, M., additional, Lumniczky, K., additional, Mai, T.T., additional, Maltar-Strmečki, N., additional, Marrale, M., additional, Martinez, J.S., additional, Marciniak, A., additional, Maznyk, N., additional, McKeever, S.W.S., additional, Meher, P.K., additional, Milanova, M., additional, Miura, T., additional, Monteiro Gil, O., additional, Montoro, A., additional, Moreno Domene, M., additional, Mrozik, A., additional, Nakayama, R., additional, O'Brien, G., additional, Oskamp, D., additional, Ostheim, P., additional, Pajic, J., additional, Pastor, N., additional, Patrono, C., additional, Pujol-Canadell, M., additional, Prieto Rodriguez, M.J., additional, Repin, M., additional, Romanyukha, A., additional, Rößler, U., additional, Sabatier, L., additional, Sakai, A., additional, Scherthan, H., additional, Schüle, S., additional, Seong, K.M., additional, Sevriukova, O., additional, Sholom, S., additional, Sommer, S., additional, Suto, Y., additional, Sypko, T., additional, Szatmári, T., additional, Takahashi-Sugai, M., additional, Takebayashi, K., additional, Testa, A., additional, Testard, I., additional, Tichy, A.ii A., additional, Triantopoulou, S., additional, Tsuyama, N., additional, Unverricht-Yeboah, M., additional, Valente, M., additional, Van Hoey, O., additional, Wilkins, R.C., additional, Wojcik, A., additional, Wojewodzka, M., additional, Younghyun, Lee, additional, Zafiropoulos, D., additional, and Abend, M., additional
- Published
- 2023
- Full Text
- View/download PDF
4. Gene Expression Changes in Irradiated Baboons: A Summary and Interpretation of a Decade of Findings
- Author
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Port, M., primary, Hérodin, F., additional, Drouet, M., additional, Valente, M., additional, Majewski, M., additional, Ostheim, P., additional, Lamkowski, A., additional, Schüle, S., additional, Forcheron, F., additional, Tichy, A., additional, Sirak, I., additional, Malkova, A., additional, Becker, B. V., additional, Veit, D. A., additional, Waldeck, S., additional, Badie, C., additional, O'Brien, G., additional, Christiansen, H., additional, Wichmann, J., additional, Beutel, G., additional, Davidkova, M., additional, Doucha-Senf, S., additional, and Abend, M., additional
- Published
- 2021
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5. Validating Baboon Ex Vivo and In Vivo Radiation-Related Gene Expression with Corresponding Human Data
- Author
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Port, M., primary, Majewski, M., additional, Herodin, F., additional, Valente, M., additional, Drouet, M., additional, Forcheron, F., additional, Tichy, A., additional, Sirak, I., additional, Zavrelova, A., additional, Malkova, A., additional, Becker, B. V., additional, Veit, D. A., additional, Waldeck, S., additional, Badie, C., additional, O'Brien, G., additional, Christiansen, H., additional, Wichmann, J., additional, Eder, M., additional, Beutel, G., additional, Vachelova, J., additional, Doucha-Senf, S., additional, and Abend, M., additional
- Published
- 2018
- Full Text
- View/download PDF
6. The influence of the CTIP Polymorphism, Q418P, on Homologous Recombination and Predisposition to Radiation-Induced Tumorigenesis (mainly rAML) in Mice
- Author
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Patel, A, Anderson, J, Kraft, D, Finnon, R, Scudamore, C, Manning, G, Bulman, R, Brown, N, Bouffler, S, O'Neill, Peter, and Badie, C
- Abstract
Exposure to ionizing radiation increases the incidence of acute myeloid leukemia (AML), which has been diagnosed in Japanese atomic bombing survivors, as well as patients treated with radiotherapy. The genetic basis for susceptibility to radiation-induced AML is not well characterized. We previously identified a candidate murine gene for susceptibility to radiation-induced AML (rAML): C-terminal binding protein (CTBP)-interacting protein (CTIP)/retinoblastoma binding protein 8 (RBBP8). This gene is essential for embryonic development, double-strand break (DSB) resection in homologous recombination (HR) and tumor suppression. In the 129S2/SvHsd mouse strain, a nonsynonymous single nucleotide polymorphism (nsSNP) in Ctip, Q418P, has been identified. We investigated the role of Q418P in radiation-induced carcinogenesis and its effect on CTIP function in HR. After whole-body exposure to 3 Gy of X rays, 11 out of 113 (9.7%) 129S2/SvHsd mice developed rAML. Furthermore, 129S2/SvHsd mouse embryonic fibroblasts (MEFs) showed lower levels of recruitment of HR factors, Rad51 and replication protein A (RPA) to radiation-induced foci, compared to CBA/H and C57BL/6 MEFs, isolated from rAML-sensitive and resistant strains, respectively. Mitomycin C and alpha particles induced lower levels of sister chromatid exchanges in 129S2/SvHsd cells compared to CBA/H and C57BL/6. Our data demonstrate that Q418P nsSNP influences the efficiency of CTIP function in HR repair of DNA DSBs in vitro and in vivo, and appears to affect susceptibility to rAML.
- Published
- 2016
7. Examining Radiation-Induced In Vivo and In Vitro Gene Expression Changes of the Peripheral Blood in Different Laboratories for Biodosimetry Purposes: First RENEB Gene Expression Study
- Author
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Abend, M., primary, Badie, C., additional, Quintens, R., additional, Kriehuber, R., additional, Manning, G., additional, Macaeva, E., additional, Njima, M., additional, Oskamp, D., additional, Strunz, S., additional, Moertl, S., additional, Doucha-Senf, S., additional, Dahlke, S., additional, Menzel, J., additional, and Port, M., additional
- Published
- 2016
- Full Text
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8. Time, Dose and Ataxia Telangiectasia Mutated (ATM) Status Dependency of Coding and Noncoding RNA Expression after Ionizing Radiation Exposure
- Author
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Kabacik, S., primary, Manning, G., additional, Raffy, C., additional, Bouffler, S., additional, and Badie, C., additional
- Published
- 2015
- Full Text
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9. Laboratory Intercomparison of Gene Expression Assays
- Author
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Badie, C., primary, Kabacik, S., additional, Balagurunathan, Y., additional, Bernard, N., additional, Brengues, M., additional, Faggioni, G., additional, Greither, R., additional, Lista, F., additional, Peinnequin, A., additional, Poyot, T., additional, Herodin, F., additional, Missel, A., additional, Terbrueggen, B., additional, Zenhausern, F., additional, Rothkamm, K., additional, Meineke, V., additional, Braselmann, H., additional, Beinke, C., additional, and Abend, M., additional
- Published
- 2013
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10. Comparison of Established and Emerging Biodosimetry Assays
- Author
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Rothkamm, K., primary, Beinke, C., additional, Romm, H., additional, Badie, C., additional, Balagurunathan, Y., additional, Barnard, S., additional, Bernard, N., additional, Boulay-Greene, H., additional, Brengues, M., additional, De Amicis, A., additional, De Sanctis, S., additional, Greither, R., additional, Herodin, F., additional, Jones, A., additional, Kabacik, S., additional, Knie, T., additional, Kulka, U., additional, Lista, F., additional, Martigne, P., additional, Missel, A., additional, Moquet, J., additional, Oestreicher, U., additional, Peinnequin, A., additional, Poyot, T., additional, Roessler, U., additional, Scherthan, H., additional, Terbrueggen, B., additional, Thierens, H., additional, Valente, M., additional, Vral, A., additional, Zenhausern, F., additional, Meineke, V., additional, Braselmann, H., additional, and Abend, M., additional
- Published
- 2013
- Full Text
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11. Generation of a Transcriptional Radiation Exposure Signature in Human Blood Using Long-Read Nanopore Sequencing.
- Author
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Cruz-Garcia L, O'Brien G, Sipos B, Mayes S, Love MI, Turner DJ, and Badie C
- Subjects
- Dose-Response Relationship, Radiation, Genomics, Humans, Leukocytes, Mononuclear metabolism, Leukocytes, Mononuclear radiation effects, Blood metabolism, Blood radiation effects, Nanopore Sequencing, Radiation Exposure adverse effects, Transcription, Genetic radiation effects, Transcriptome radiation effects
- Abstract
In the event of a large-scale event leading to acute ionizing radiation exposure, high-throughput methods would be required to assess individual dose estimates for triage purposes. Blood-based gene expression is a broad source of biomarkers of radiation exposure which have great potential for providing rapid dose estimates for a large population. Time is a crucial component in radiological emergencies and the shipment of blood samples to relevant laboratories presents a concern. In this study, we performed nanopore sequencing analysis to determine if the technology can be used to detect radiation-inducible genes in human peripheral blood mononuclear cells (PBMCs). The technology offers not only long-read sequencing but also a portable device which can overcome issues involving sample shipment, and provide faster results. For this goal, blood from nine healthy volunteers was 2 Gy ex vivo X irradiated. After PBMC isolation, irradiated samples were incubated along with the controls for 24 h at 37°C. RNA was extracted, poly(A)+ enriched and reverse-transcribed before sequencing. The data generated was analyzed using a Snakemake pipeline modified to handle paired samples. The sequencing analysis identified a radiation signature consisting of 46 differentially expressed genes (DEGs) which included 41 protein-coding genes, a long non-coding RNA and four pseudogenes, five of which have been identified as radiation-responsive transcripts for the first time. The genes in which transcriptional expression is most significantly modified after radiation exposure were APOBEC3H and FDXR, presenting a 25- and 28-fold change on average, respectively. These levels of transcriptional response were comparable to results we obtained by quantitative polymerase chain reaction (qPCR) analysis. In vivo exposure analyses showed a transcriptional radioresponse at 24 h postirradiation for both genes together with a strong dose-dependent response in blood irradiated ex vivo . Finally, extrapolating from the data we obtained, the minimum sequencing time required to detect an irradiated sample using APOBEC3H transcripts would be less than 3 min for a total of 50,000 reads. Future improvements, in sample processing and bioinformatic pipeline for specific radiation-responsive transcript identification, will allow the provision of a portable, rapid, real-time biodosimetry platform based on this new sequencing technology. In summary, our data show that nanopore sequencing can identify radiation-responsive genes and can also be used for identification of new transcripts.
- Published
- 2020
- Full Text
- View/download PDF
12. Dicentric Dose Estimates for Patients Undergoing Radiotherapy in the RTGene Study to Assess Blood Dosimetric Models and the New Bayesian Method for Gradient Exposure.
- Author
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Moquet J, Higueras M, Donovan E, Boyle S, Barnard S, Bricknell C, Sun M, Gothard L, O'Brien G, Cruz-Garcia L, Badie C, Ainsbury E, and Somaiah N
- Subjects
- Adult, Aged, Bayes Theorem, Biomarkers, Tumor genetics, Breast Neoplasms blood, Breast Neoplasms pathology, Breast Neoplasms radiotherapy, Chromosomes radiation effects, Dose-Response Relationship, Radiation, Female, Gastrointestinal Neoplasms blood, Gastrointestinal Neoplasms pathology, Gastrointestinal Neoplasms radiotherapy, Humans, Lung Neoplasms blood, Lung Neoplasms pathology, Lung Neoplasms radiotherapy, Male, Middle Aged, Radiation Dosage, Radiation, Ionizing, Radiometry, Urogenital Neoplasms blood, Urogenital Neoplasms pathology, Urogenital Neoplasms radiotherapy, Biomarkers, Tumor blood, Chromosome Aberrations radiation effects, Chromosomes genetics
- Abstract
The RTGene study was focused on the development and validation of new transcriptional biomarkers for prediction of individual radiotherapy patient responses to ionizing radiation. In parallel, for validation purposes, this study incorporated conventional biomarkers of radiation exposure, including the dicentric assay. Peripheral blood samples were taken with ethical approval and informed consent from a total of 20 patients undergoing external beam radiotherapy for breast, lung, gastrointestinal or genitourinary tumors. For the dicentric assay, two samples were taken from each patient: prior to radiotherapy and before the final fraction. Blood samples were set up using standard methods for the dicentric assay. All the baseline samples had dicentric frequencies consistent with the expected background for the normal population. For blood taken before the final fraction, all the samples displayed distributions of aberrations, which are indicative of partial-body exposures. Whole-body and partial-body cytogenetic doses were calculated with reference to a 250-kVp X-ray calibration curve and then compared to the dose to blood derived using two newly developed blood dosimetric models. Initial comparisons indicated that the relationship between these measures of dose appear very promising, with a correlation of 0.88 ( P = 0.001). A new Bayesian zero-inflated Poisson finite mixture method was applied to the dicentric data, and partial-body dose estimates showed no significant difference ( P > 0.999) from those calculated by the contaminated Poisson technique. The next step will be further development and validation in a larger patient group.
- Published
- 2018
- Full Text
- View/download PDF
13. Biomarkers for Uranium Risk Assessment for the Development of the CURE (Concerted Uranium Research in Europe) Molecular Epidemiological Protocol.
- Author
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Guéguen Y, Roy L, Hornhardt S, Badie C, Hall J, Baatout S, Pernot E, Tomasek L, Laurent O, Ebrahimian T, Ibanez C, Grison S, Kabacik S, Laurier D, and Gomolka M
- Subjects
- Animals, Biomarkers metabolism, Europe, Humans, Radiation Exposure, Risk Assessment, Molecular Epidemiology methods, Uranium toxicity
- Abstract
Despite substantial experimental and epidemiological research, there is limited knowledge of the uranium-induce health effects after chronic low-dose exposures in humans. Biological markers can objectively characterize pathological processes or environmental responses to uranium and confounding agents. The integration of such biological markers into a molecular epidemiological study would be a useful approach to improve and refine estimations of uranium-induced health risks. To initiate such a study, Concerted Uranium Research in Europe (CURE) was established, and involves biologists, epidemiologists and dosimetrists. The aims of the biological work package of CURE were: 1. To identify biomarkers and biological specimens relevant to uranium exposure; 2. To define standard operating procedures (SOPs); and 3. To set up a common protocol (logistic, questionnaire, ethical aspects) to perform a large-scale molecular epidemiologic study in uranium-exposed cohorts. An intensive literature review was performed and led to the identification of biomarkers related to: 1. retention organs (lungs, kidneys and bone); 2. other systems/organs with suspected effects (cardiovascular system, central nervous system and lympho-hematopoietic system); 3. target molecules (DNA damage, genomic instability); and 4. high-throughput methods for the identification of new biomarkers. To obtain high-quality biological materials, SOPs were established for the sampling and storage of different biospecimens. A questionnaire was developed to assess potential confounding factors. The proposed strategy can be adapted to other internal exposures and should improve the characterization of the biological and health effects that are relevant for risk assessment.
- Published
- 2017
- Full Text
- View/download PDF
14. The Influence of the CTIP Polymorphism, Q418P, on Homologous Recombination and Predisposition to Radiation-Induced Tumorigenesis (mainly rAML) in Mice.
- Author
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Patel A, Anderson J, Kraft D, Finnon R, Finnon P, Scudamore CL, Manning G, Bulman R, Brown N, Bouffler S, O'Neill P, and Badie C
- Subjects
- Animals, Carrier Proteins metabolism, Cell Cycle Proteins metabolism, DNA Breaks, Double-Stranded radiation effects, Genetic Predisposition to Disease, Mice, Carcinogenesis genetics, Carcinogenesis radiation effects, Carrier Proteins genetics, Cell Cycle Proteins genetics, Homologous Recombination radiation effects, Leukemia, Myeloid, Acute genetics, Leukemia, Myeloid, Acute pathology, Polymorphism, Single Nucleotide radiation effects
- Abstract
Exposure to ionizing radiation increases the incidence of acute myeloid leukemia (AML), which has been diagnosed in Japanese atomic bombing survivors, as well as patients treated with radiotherapy. The genetic basis for susceptibility to radiation-induced AML is not well characterized. We previously identified a candidate murine gene for susceptibility to radiation-induced AML (rAML): C-terminal binding protein (CTBP)-interacting protein (CTIP)/retinoblastoma binding protein 8 (RBBP8). This gene is essential for embryonic development, double-strand break (DSB) resection in homologous recombination (HR) and tumor suppression. In the 129S2/SvHsd mouse strain, a nonsynonymous single nucleotide polymorphism (nsSNP) in Ctip, Q418P, has been identified. We investigated the role of Q418P in radiation-induced carcinogenesis and its effect on CTIP function in HR. After whole-body exposure to 3 Gy of X rays, 11 out of 113 (9.7%) 129S2/SvHsd mice developed rAML. Furthermore, 129S2/SvHsd mouse embryonic fibroblasts (MEFs) showed lower levels of recruitment of HR factors, Rad51 and replication protein A (RPA) to radiation-induced foci, compared to CBA/H and C57BL/6 MEFs, isolated from rAML-sensitive and resistant strains, respectively. Mitomycin C and alpha particles induced lower levels of sister chromatid exchanges in 129S2/SvHsd cells compared to CBA/H and C57BL/6. Our data demonstrate that Q418P nsSNP influences the efficiency of CTIP function in HR repair of DNA DSBs in vitro and in vivo, and appears to affect susceptibility to rAML.
- Published
- 2016
- Full Text
- View/download PDF
15. Radiation leukemogenesis in mice: loss of PU.1 on chromosome 2 in CBA and C57BL/6 mice after irradiation with 1 GeV/nucleon 56Fe ions, X rays or gamma rays. Part I. Experimental observations.
- Author
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Peng Y, Brown N, Finnon R, Warner CL, Liu X, Genik PC, Callan MA, Ray FA, Borak TB, Badie C, Bouffler SD, Ullrich RL, Bedford JS, and Weil MM
- Subjects
- Animals, Chromosomes, Chromosomes, Artificial, Bacterial metabolism, Dose-Response Relationship, Radiation, Gamma Rays, Male, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, X-Rays, Gene Expression Regulation, Leukemic, Iron, Leukemia etiology, Leukemia metabolism, Neoplasms, Radiation-Induced etiology, Neoplasms, Radiation-Induced metabolism, Proto-Oncogene Proteins metabolism, Trans-Activators metabolism
- Abstract
Since deletion of the PU.1 gene on chromosome 2 is a crucial acute myeloid leukemia (AML) initiating step in the mouse model, we quantified PU.1 deleted cells in the bone marrow of gamma-, X- and 56Fe-ion-irradiated mice at various times postirradiation. Although 56Fe ions were initially some two to three times more effective than X or gamma rays in inducing PU.1 deletions, by 1 month postirradiation, the proportions of cells with PU.1 deletions were similar for the HZE particles and the sparsely ionizing radiations. These results indicate that while 56Fe ions are more effective in inducing PU.1 deletions, they are also more effective in causing collateral damage that removes hit cells from the bone marrow. After X, gamma or 56Fe-ion irradiation, AML-resistant C57BL/6 mice have fewer cells with PU.1 deletions than CBA mice, and those cells do not persist in the bone marrow of the C57B6/6 mice. Our findings suggest that quantification of PU.1 deleted bone marrow cells 1 month postirradiation can be used as surrogate for the incidence of radiation-induced AML measured in large-scale mouse studies. If so, PU.1 loss could be used to systematically assess the potential leukemogenic effects of other ions and energies in the space radiation environment.
- Published
- 2009
- Full Text
- View/download PDF
16. A new model describing the curves for repair of both DNA double-strand breaks and chromosome damage.
- Author
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Foray N, Badie C, Alsbeih G, Fertil B, and Malaise EP
- Subjects
- Cell Line, Humans, Models, Biological, Chromosome Aberrations, DNA Damage, DNA Repair
- Abstract
A review of reports dealing with fittings of the data for repair of DNA double-strand breaks (DSBs) and excess chromosome fragments (ECFs) shows that several models are used to fit the repair curves. Since DSBs and ECFs are correlated, it is worth developing a model describing both phenomena. The curve-fitting models used most extensively, the two repair half-times model for DSBs and the monoexponential plus residual model for ECFs, appear to be too inflexible to describe the repair curves for both DSBs and ECFs. We have therefore developed a new concept based on a variable repair half-time. According to this concept, the repair curve is continuously bending and dependent on time and probably reflects a continuous spectrum of damage repairability. The fits of the curves for DSB repair to the variable repair half-time and the variable repair half-time plus residual models were compared to those obtained with the two half-times plus residual and two half-times models. Similarly, the fits of the curves for ECF repair to the variable repair half-time and variable half-time plus residual models were compared to that obtained with the monoexponential plus residual model. The quality of fit and the dependence of adjustable parameters on the portion of the curve fitted were used as comparison criteria. We found that: (a) It is useful to postulate the existence of a residual term for unrepairable lesions, regardless of the model adopted. (b) With the two cell lines tested (a normal and a hypersensitive one), data for both DSBs and ECFs are best fitted to the variable repair half-time plus residual model, whatever the repair time range.
- Published
- 1996
17. Induction and rejoining of DNA double-strand breaks and interphase chromosome breaks after exposure to X rays in one normal and two hypersensitive human fibroblast cell lines.
- Author
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Badie C, Iliakis G, Foray N, Alsbeih G, Cedervall B, Chavaudra N, Pantelias G, Arlett C, and Malaise EP
- Subjects
- Cell Line, Fibroblasts radiation effects, Humans, Interphase, Male, X-Rays, Chromosome Aberrations, DNA radiation effects, DNA Damage, DNA Repair
- Abstract
The aim of this work was to measure simultaneously and in a quantitative manner double-strand breaks (DSBs), interphase chromosome breaks and cell lethality either immediately after irradiation, or at various times thereafter (up to 24 h), in cells of three nontransformed human fibroblast cell lines of widely different intrinsic radiosensitivity. We wished to assess initial damage, repair kinetics and residual damage at the DNA and the chromosome level, and to correlate these parameters with cell killing. We employed HF19 cells, a normal fibroblast cell line, AT2 cells, a radiosensitive cell line from a patient suffering from ataxia telangiectasia (AT), and 180BR cells, a radiosensitive cell line from a patient with no clinical symptoms of AT. AT2 and 180BR cells, in addition to being radiosensitive, also display a reduced ability to repair potentially lethal damage compared to HF19 cells. The yield of DSBs, as measured by pulsed-field gel electrophoresis, is similar in all three cell lines (slopes correspond to 1.6-1.7% Gy-1 of DNA-associated radioactivity released from the gel well into the lane). In contrast, residual DSBs measured 24 h after irradiation are almost zero for HF19 cells (0.1% confidence interval = 0-1.4%), but are 12.5% (+/- 2.3%) and 43.8% (+/- 1.2%) of those measured immediately after irradiation in AT2 and 180BR cells, respectively. Residual interphase chromosome breaks are 11.6% (+/- 1.6%), 29.7% (+/- 5.7%) and 41.4% (+/- 2.2%) of those measured immediately after irradiation in HF19, AT2 and 180BR cells, respectively. Neither the initial yield of DSBs nor that of excess interphase chromosome breaks can explain the differences in radiosensitivity between the three cell lines; however, there is a correlation between residual DSBs, rate of DSB rejoining at 24 h, residual interphase chromosome breaks on the one hand and cell survival on the other hand.
- Published
- 1995
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