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dc.contributor.authorZampetti-Bosseler, Fen
dc.contributor.authorScott, Daviden
dc.date.accessioned2011-06-29T12:59:01Z
dc.date.available2011-06-29T12:59:01Z
dc.date.issued1981-05
dc.identifier.citationCell death, chromosome damage and mitotic delay in normal human, ataxia telangiectasia and retinoblastoma fibroblasts after x-irradiation. 1981, 39 (5):547-58 Int J Radiat Biol Relat Stud Phys Chem Meden
dc.identifier.issn0020-7616
dc.identifier.pmid6972365
dc.identifier.doi10.1080/09553008114550651
dc.identifier.urihttp://hdl.handle.net/10541/134850
dc.description.abstractWe recently showed (Scott and Zampetti-Bosseler 1980) that X-ray sensitive mouse lymphoma cells sustain more chromosome damage, mitotic delay and spindle defects than X-ray resistant cells. We proposed that (a) chromosome aberrations contribute much more to lethality than spindle defects, and (b) that DNA lesions are less effectively repaired in the sensitive cells and give rise to more G2 mitotic delay and chromosome aberrations. Our present results on human fibroblasts with reported differential sensitivity to ionizing radiation (i.e. normal donors and patients with ataxia telangiectasia and retinoblastoma) support the first hypothesis since we observed a positive correlation between chromosome aberration frequencies and cell killing and no induced spindle defects. Our second hypothesis is however not substantiated since X-ray sensitive fibroblasts from the ataxia patient suffered less mitotic delay than cells from normal donors. A common lesion for mitotic delay and chromosome aberrations can still be assumed by adopting the hypothesis of Painter and Young (1981) that the defect in ataxia cells is not in repair but in a failure of DNA damage to initiate mitotic delay. In contrast to other reports, we found the retinoblastoma cells to be of normal radiation sensitivity (cell killing and aberration).
dc.language.isoenen
dc.subject.meshAdolescent
dc.subject.meshAdult
dc.subject.meshAtaxia Telangiectasia
dc.subject.meshCell Survival
dc.subject.meshChild, Preschool
dc.subject.meshChromosome Aberrations
dc.subject.meshDose-Response Relationship, Radiation
dc.subject.meshFemale
dc.subject.meshFibroblasts
dc.subject.meshHumans
dc.subject.meshMale
dc.subject.meshMitosis
dc.subject.meshMitotic Index
dc.subject.meshRetinoblastoma
dc.subject.meshTime Factors
dc.titleCell death, chromosome damage and mitotic delay in normal human, ataxia telangiectasia and retinoblastoma fibroblasts after x-irradiation.en
dc.typeArticleen
dc.contributor.departmentPaterson Laboratories, Christie Hospital & Holt Radium Institute, Manchester, M20 9BX, U.K.en
dc.identifier.journalInternational Journal of Radiation Biology and Related Studies in Physics, Chemistry, and Medicineen
html.description.abstractWe recently showed (Scott and Zampetti-Bosseler 1980) that X-ray sensitive mouse lymphoma cells sustain more chromosome damage, mitotic delay and spindle defects than X-ray resistant cells. We proposed that (a) chromosome aberrations contribute much more to lethality than spindle defects, and (b) that DNA lesions are less effectively repaired in the sensitive cells and give rise to more G2 mitotic delay and chromosome aberrations. Our present results on human fibroblasts with reported differential sensitivity to ionizing radiation (i.e. normal donors and patients with ataxia telangiectasia and retinoblastoma) support the first hypothesis since we observed a positive correlation between chromosome aberration frequencies and cell killing and no induced spindle defects. Our second hypothesis is however not substantiated since X-ray sensitive fibroblasts from the ataxia patient suffered less mitotic delay than cells from normal donors. A common lesion for mitotic delay and chromosome aberrations can still be assumed by adopting the hypothesis of Painter and Young (1981) that the defect in ataxia cells is not in repair but in a failure of DNA damage to initiate mitotic delay. In contrast to other reports, we found the retinoblastoma cells to be of normal radiation sensitivity (cell killing and aberration).


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