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dc.contributor.authorScott, David
dc.contributor.authorSpreadborough, Anne R
dc.contributor.authorRoberts, Stephen A
dc.date.accessioned2009-09-22T15:05:01Z
dc.date.available2009-09-22T15:05:01Z
dc.date.issued2003-06
dc.identifier.citationLess G(2) arrest in irradiated cells of breast cancer patients than in female controls: a contribution to their enhanced chromosomal radiosensitivity? 2003, 79 (6):405-11 Int. J. Radiat. Biol.en
dc.identifier.issn0955-3002
dc.identifier.pmid12963542
dc.identifier.doi10.1080/0955300031000150602
dc.identifier.urihttp://hdl.handle.net/10541/82124
dc.description.abstractPURPOSE: To determine if the efficacy of G(2) checkpoint control (measured as the degree of mitotic inhibition) was reduced in breast cancer patients (n=129) compared with healthy controls (n=105) after exposure of lymphocytes to X-rays. We had previously shown that the average level of radiation-induced chromosome damage was higher in G(2) lymphocytes of these patients than in the controls, and it was proposed that this was a marker of low penetrance predisposition to cancer. MATERIALS AND METHODS: Proliferating lymphocytes were X-irradiated (50 cGy) and sampled at 90 min post-irradiation, which was the time of maximum mitotic inhibition of G(2) cells, expressed as the extent of reduction in the mitotic index in irradiated compared with unirradiated cells. RESULTS: Repeated measurements on 28 controls showed that there were reproducible differences in mitotic inhibition between individuals. Inhibition was significantly greater in female than in male controls (p=0.014), but less in patients than in female controls (p=0.009). There was a weak inverse correlation between the extent of inhibition and the amount of chromosome damage in all females (r=-0.15, p=0.043). CONCLUSIONS: The lesser mitotic inhibition in patients than in female controls might contribute to their greater mean G(2) chromosomal radiosensitivity. However, this hypothesis is not easily reconciled with other observations that (1) the significant difference in inhibition between the sexes in controls was not accompanied by any gender difference in radiosensitivity and (2) there was an inverse correlation between inhibition and age in controls, yet no age-related increase in radiosensitivity. There might, therefore, be no causal relationship between G(2) mitotic inhibition and chromosomal radiosensitivity.
dc.language.isoenen
dc.subjectBreast Canceren
dc.subject.meshAdult
dc.subject.meshAge Factors
dc.subject.meshAged
dc.subject.meshBreast Neoplasms
dc.subject.meshCase-Control Studies
dc.subject.meshCell Division
dc.subject.meshChromosome Aberrations
dc.subject.meshChromosomes, Human
dc.subject.meshDNA Damage
dc.subject.meshFemale
dc.subject.meshG2 Phase
dc.subject.meshHumans
dc.subject.meshLymphocytes
dc.subject.meshMale
dc.subject.meshMiddle Aged
dc.subject.meshMitosis
dc.subject.meshSex Factors
dc.subject.meshX-Rays
dc.titleLess G(2) arrest in irradiated cells of breast cancer patients than in female controls: a contribution to their enhanced chromosomal radiosensitivity?en
dc.typeArticleen
dc.contributor.departmentPaterson Institute for Cancer Research, Christie Hospital NHS Trust, Manchester M20 4BX, UK. dscott@picr.man.ac.uken
dc.identifier.journalInternational Journal of Radiation Biologyen
html.description.abstractPURPOSE: To determine if the efficacy of G(2) checkpoint control (measured as the degree of mitotic inhibition) was reduced in breast cancer patients (n=129) compared with healthy controls (n=105) after exposure of lymphocytes to X-rays. We had previously shown that the average level of radiation-induced chromosome damage was higher in G(2) lymphocytes of these patients than in the controls, and it was proposed that this was a marker of low penetrance predisposition to cancer. MATERIALS AND METHODS: Proliferating lymphocytes were X-irradiated (50 cGy) and sampled at 90 min post-irradiation, which was the time of maximum mitotic inhibition of G(2) cells, expressed as the extent of reduction in the mitotic index in irradiated compared with unirradiated cells. RESULTS: Repeated measurements on 28 controls showed that there were reproducible differences in mitotic inhibition between individuals. Inhibition was significantly greater in female than in male controls (p=0.014), but less in patients than in female controls (p=0.009). There was a weak inverse correlation between the extent of inhibition and the amount of chromosome damage in all females (r=-0.15, p=0.043). CONCLUSIONS: The lesser mitotic inhibition in patients than in female controls might contribute to their greater mean G(2) chromosomal radiosensitivity. However, this hypothesis is not easily reconciled with other observations that (1) the significant difference in inhibition between the sexes in controls was not accompanied by any gender difference in radiosensitivity and (2) there was an inverse correlation between inhibition and age in controls, yet no age-related increase in radiosensitivity. There might, therefore, be no causal relationship between G(2) mitotic inhibition and chromosomal radiosensitivity.


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