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dc.contributor.authorKiltie, Anne E
dc.contributor.authorBarber, James B P
dc.contributor.authorSwindell, Ric
dc.contributor.authorRyan, Anderson J
dc.contributor.authorWest, Catharine M L
dc.contributor.authorHendry, Jolyon H
dc.contributor.authorMagee, Brian
dc.date.accessioned2009-12-15T16:33:15Z
dc.date.available2009-12-15T16:33:15Z
dc.date.issued1999-02-01
dc.identifier.citationLack of correlation between residual radiation-induced DNA damage, in keratinocytes assayed directly from skin, and late radiotherapy reactions in breast cancer patients. 1999, 43 (3):481-7 Int. J. Radiat. Oncol. Biol. Phys.en
dc.identifier.issn0360-3016
dc.identifier.pmid10078626
dc.identifier.doi10.1016/S0360-3016(98)00392-7
dc.identifier.urihttp://hdl.handle.net/10541/88039
dc.description.abstractPURPOSE: To study the relationship between the severity of late reactions to radiotherapy in breast cancer patients, and the extent of residual radiation-induced DNA damage, using a rapid assay of keratinocytes obtained directly from skin biopsies. METHODS AND MATERIALS: A review was made of 32 patients with breast cancer, treated uniformly by radiotherapy between 1983 and 1988, following breast-conserving surgery. Their late radiotherapy reactions were scored (9-14 years post-radiotherapy) using a modified LENT SOMA scale, and a 5-mm buttock skin punch biopsy was obtained. Intact skin was irradiated at room temperature, and after allowing 24 h for repair, the tissue was disaggregated and the cells processed for pulsed field gel electrophoresis (PFGE). Residual DNA damage was expressed as the fraction of DNA released (FDR) following 150 Gy. RESULTS: Studies using flow cytometry on disaggregated breast skin showed that over 90% of the cells were keratinocytes. The PFGE assay was robust with low background FDRs in unirradiated skin samples (mean 3.2%) and a wide range of FDRs following irradiation from 11.5% to 26.6%. No correlation was found between the FDR at 150 Gy (FDR 150) and any of the late reaction scores or retrospective acute reaction scores. There was, however, a borderline significant correlation for family history and FDR 150 (p = 0.059). CONCLUSION: Rapid measurement of residual DNA damage in irradiated differentiated keratinocytes, the predominant cell population in skin biopsies, showed no correlation with the severity of symptomatic early or documented late reactions in a retrospectively studied group of 32 breast cancer patients.
dc.language.isoenen
dc.subjectBreast Canceren
dc.subject.meshAdult
dc.subject.meshAged
dc.subject.meshAnalysis of Variance
dc.subject.meshBiopsy
dc.subject.meshBreast
dc.subject.meshBreast Neoplasms
dc.subject.meshCarcinoma
dc.subject.meshDNA
dc.subject.meshDNA Damage
dc.subject.meshDose Fractionation
dc.subject.meshFemale
dc.subject.meshHumans
dc.subject.meshKeratinocytes
dc.subject.meshMiddle Aged
dc.subject.meshPredictive Value of Tests
dc.subject.meshRadiation Injuries
dc.subject.meshRetrospective Studies
dc.subject.meshSeverity of Illness Index
dc.subject.meshSkin
dc.titleLack of correlation between residual radiation-induced DNA damage, in keratinocytes assayed directly from skin, and late radiotherapy reactions in breast cancer patients.en
dc.typeArticleen
dc.contributor.departmentCRC Section of Genome Damage and Repair, Christie Hospital NHS Trust, Manchester, United Kingdom.en
dc.identifier.journalInternational Journal of Radiation Oncology, Biology, Physicsen
html.description.abstractPURPOSE: To study the relationship between the severity of late reactions to radiotherapy in breast cancer patients, and the extent of residual radiation-induced DNA damage, using a rapid assay of keratinocytes obtained directly from skin biopsies. METHODS AND MATERIALS: A review was made of 32 patients with breast cancer, treated uniformly by radiotherapy between 1983 and 1988, following breast-conserving surgery. Their late radiotherapy reactions were scored (9-14 years post-radiotherapy) using a modified LENT SOMA scale, and a 5-mm buttock skin punch biopsy was obtained. Intact skin was irradiated at room temperature, and after allowing 24 h for repair, the tissue was disaggregated and the cells processed for pulsed field gel electrophoresis (PFGE). Residual DNA damage was expressed as the fraction of DNA released (FDR) following 150 Gy. RESULTS: Studies using flow cytometry on disaggregated breast skin showed that over 90% of the cells were keratinocytes. The PFGE assay was robust with low background FDRs in unirradiated skin samples (mean 3.2%) and a wide range of FDRs following irradiation from 11.5% to 26.6%. No correlation was found between the FDR at 150 Gy (FDR 150) and any of the late reaction scores or retrospective acute reaction scores. There was, however, a borderline significant correlation for family history and FDR 150 (p = 0.059). CONCLUSION: Rapid measurement of residual DNA damage in irradiated differentiated keratinocytes, the predominant cell population in skin biopsies, showed no correlation with the severity of symptomatic early or documented late reactions in a retrospectively studied group of 32 breast cancer patients.


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