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dc.contributor.authorMartin, Lynn M
dc.contributor.authorMarples, Brian
dc.contributor.authorDavies, Anthony M
dc.contributor.authorAtzberger, Ann
dc.contributor.authorEdwards, Connla
dc.contributor.authorLynch, Thomas H
dc.contributor.authorHollywood, Donal
dc.contributor.authorMarignol, Laure
dc.date.accessioned2014-07-17T09:31:59Z
dc.date.available2014-07-17T09:31:59Z
dc.date.issued2013-07-10
dc.identifier.citationMartin LM et al. DNA mismatch repair protein MSH2 dictates cellular survival in response to low dose radiation in endometrial carcinoma cells. 2013, 335 (1):19-25 Cancer Lett.en_GB
dc.identifier.issn1872-7980
dc.identifier.pmid23376256
dc.identifier.doi10.1016/j.canlet.2013.01.046
dc.identifier.urihttp://hdl.handle.net/10147/323264
dc.description.abstractDNA repair and G2-phase cell cycle checkpoint responses are involved in the manifestation of hyper-radiosensitivity (HRS). The low-dose radioresponse of MSH2 isogenic endometrial carcinoma cell lines was examined. Defects in cell cycle checkpoint activation and the DNA damage response in irradiated cells (0.2 Gy) were evaluated. HRS was expressed solely in MSH2+ cells and was associated with efficient activation of the early G2-phase cell cycle checkpoint. Maintenance of the arrest was associated with persistent MRE11, γH2AX, RAD51 foci at 2 h after irradiation. Persistent MRE11 and RAD51 foci were also evident 24 h after 0.2 Gy. MSH2 significantly enhances cell radiosensitivity to low dose IR.
dc.language.isoenen
dc.publisherElsevier Ireland Ltden_GB
dc.rightsArchived with thanks to Cancer lettersen_GB
dc.subjectCANCERen_GB
dc.subject.meshCarcinoma
dc.subject.meshCell Line, Tumor
dc.subject.meshCell Nucleus
dc.subject.meshCell Survival
dc.subject.meshDNA Mismatch Repair
dc.subject.meshDNA-Binding Proteins
dc.subject.meshEndometrial Neoplasms
dc.subject.meshFemale
dc.subject.meshG2 Phase Cell Cycle Checkpoints
dc.subject.meshGene Expression
dc.subject.meshHistones
dc.subject.meshHumans
dc.subject.meshMutS Homolog 2 Protein
dc.subject.meshRadiation Tolerance
dc.subject.meshRecombinational DNA Repair
dc.subject.otherCELL BIOLOGYen_GB
dc.titleDNA mismatch repair protein MSH2 dictates cellular survival in response to low dose radiation in endometrial carcinoma cells.en_GB
dc.typeArticleen
dc.contributor.departmentRadiation and Urologic Oncology, Prostate Molecular Oncology Research Group, Academic Unit of Clinical and Molecular Oncology, Institute of Molecular Medicine, Trinity College Dublin, Dublin 8, Ireland.en_GB
dc.identifier.journalCancer lettersen_GB
dc.description.fundingNo fundingen
dc.description.provinceLeinsteren
dc.description.peer-reviewpeer-reviewen
html.description.abstractDNA repair and G2-phase cell cycle checkpoint responses are involved in the manifestation of hyper-radiosensitivity (HRS). The low-dose radioresponse of MSH2 isogenic endometrial carcinoma cell lines was examined. Defects in cell cycle checkpoint activation and the DNA damage response in irradiated cells (0.2 Gy) were evaluated. HRS was expressed solely in MSH2+ cells and was associated with efficient activation of the early G2-phase cell cycle checkpoint. Maintenance of the arrest was associated with persistent MRE11, γH2AX, RAD51 foci at 2 h after irradiation. Persistent MRE11 and RAD51 foci were also evident 24 h after 0.2 Gy. MSH2 significantly enhances cell radiosensitivity to low dose IR.


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