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dc.contributor.authorScott, David
dc.contributor.authorSpreadborough, Anne R
dc.contributor.authorJones, L A
dc.contributor.authorRoberts, Stephen A
dc.contributor.authorMoore, Christopher J
dc.date.accessioned2010-04-06T11:27:00Z
dc.date.available2010-04-06T11:27:00Z
dc.date.issued1996-01
dc.identifier.citationChromosomal radiosensitivity in G2-phase lymphocytes as an indicator of cancer predisposition. 1996, 145 (1):3-16 Radiat. Res.en
dc.identifier.issn0033-7587
dc.identifier.pmid8532833
dc.identifier.urihttp://hdl.handle.net/10541/95681
dc.description.abstractSanford et al. (Int. J. Radiat. Biol. 55, 963-981, 1989) have reported that G2-phase cells from many heritable cancer-prone conditions exhibit higher yields of X-ray-induced chromosome damage than those found in the majority of healthy controls. We have applied their protocol to lymphocytes of a group of control and cancer-prone individuals to see if we could confirm these observations. For control donors we observed higher aberration yields, different kinetics and more interexperiment variability than found by Sanford et al. These differences could not be attributed to unavoidable minor variations in procedures (e.g. serum batches, glassware washing methods), but the difference in X-ray qualities used in the two laboratories may have made a small contribution to the discrepancies. We attribute some of our experimental variability to the fact that, to varying extents in different experiments, centrifugation of cells prior to irradiation can slow down the progression of cells into metaphase and that cells can continue to repair during the harvesting procedure (centrifugation and hypotonic treatment). We have applied the assay to cases of ataxia telangiectasia (AT, homozygotes and heterozygotes), xeroderma pigmentosum (homozygotes and heterozygotes), familial adenomatous polyposis and the syndromes Li-Fraumeni, basal cell nevus, Down's and Fanconi's but have been unable to discriminate between these groups and controls except for AT homozygotes. By including a control sample in parallel with samples from cancer-prone groups we found a significant difference in mean aberration yields between controls and AT homozygotes and heterozygotes, but not for the other groups. Since technical features could explain the discrepancies between our laboratories, we have devised our own G2-phase assay which appears to be giving promising results.
dc.language.isoenen
dc.subjectEye Canceren
dc.subjectCanceren
dc.subjectFanconi Anaemiaen
dc.subject.meshAdenomatous Polyposis Coli
dc.subject.meshAdolescent
dc.subject.meshAtaxia Telangiectasia
dc.subject.meshBasal Cell Nevus Syndrome
dc.subject.meshChromosome Aberrations
dc.subject.meshChromosomes, Human
dc.subject.meshDisease Susceptibility
dc.subject.meshDown Syndrome
dc.subject.meshEye Neoplasms
dc.subject.meshFanconi Anemia
dc.subject.meshFemale
dc.subject.meshG2 Phase
dc.subject.meshGenetic Diseases, Inborn
dc.subject.meshHumans
dc.subject.meshInfant
dc.subject.meshKinetics
dc.subject.meshLi-Fraumeni Syndrome
dc.subject.meshLymphocytes
dc.subject.meshMale
dc.subject.meshMiddle Aged
dc.subject.meshNeoplasms
dc.subject.meshRadiation Tolerance
dc.subject.meshReference Values
dc.subject.meshRhabdomyosarcoma
dc.subject.meshTime Factors
dc.subject.meshTwins, Monozygotic
dc.subject.meshX-Rays
dc.subject.meshXeroderma Pigmentosum
dc.titleChromosomal radiosensitivity in G2-phase lymphocytes as an indicator of cancer predisposition.en
dc.typeArticleen
dc.contributor.departmentPaterson Institute for Cancer Research, Christie CRC Research Centre, Manchester, United Kingdom.en
dc.identifier.journalRadiation Researchen
html.description.abstractSanford et al. (Int. J. Radiat. Biol. 55, 963-981, 1989) have reported that G2-phase cells from many heritable cancer-prone conditions exhibit higher yields of X-ray-induced chromosome damage than those found in the majority of healthy controls. We have applied their protocol to lymphocytes of a group of control and cancer-prone individuals to see if we could confirm these observations. For control donors we observed higher aberration yields, different kinetics and more interexperiment variability than found by Sanford et al. These differences could not be attributed to unavoidable minor variations in procedures (e.g. serum batches, glassware washing methods), but the difference in X-ray qualities used in the two laboratories may have made a small contribution to the discrepancies. We attribute some of our experimental variability to the fact that, to varying extents in different experiments, centrifugation of cells prior to irradiation can slow down the progression of cells into metaphase and that cells can continue to repair during the harvesting procedure (centrifugation and hypotonic treatment). We have applied the assay to cases of ataxia telangiectasia (AT, homozygotes and heterozygotes), xeroderma pigmentosum (homozygotes and heterozygotes), familial adenomatous polyposis and the syndromes Li-Fraumeni, basal cell nevus, Down's and Fanconi's but have been unable to discriminate between these groups and controls except for AT homozygotes. By including a control sample in parallel with samples from cancer-prone groups we found a significant difference in mean aberration yields between controls and AT homozygotes and heterozygotes, but not for the other groups. Since technical features could explain the discrepancies between our laboratories, we have devised our own G2-phase assay which appears to be giving promising results.


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