Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/9009
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dc.contributor.authorPinar, Beatrizen_US
dc.contributor.authorHenríquez Hernández, Luis Albertoen_US
dc.contributor.authorLara Jiménez, Pedro Carlosen_US
dc.contributor.authorBordón, Elisaen_US
dc.contributor.authorRodríguez-Gallego, Carlosen_US
dc.contributor.authorLloret Saez-Bravo, Martaen_US
dc.contributor.authorNúñez, María Isabelen_US
dc.contributor.authorRuiz de Almodóvar, Marianoen_US
dc.date.accessioned2012-11-14T09:50:28Z-
dc.date.accessioned2018-04-25T13:59:21Z-
dc.date.available2012-11-14T09:50:28Z-
dc.date.available2018-04-25T13:59:21Z-
dc.date.issued2010en_US
dc.identifier.issn1748-717Xen_US
dc.identifier.otherScopus-
dc.identifier.urihttp://hdl.handle.net/10553/9009-
dc.description.abstractBackground: DNA-damage assays, quantifying the initial number of DNA double-strand breaks induced by radiation, have been proposed as a predictive test for radiation-induced toxicity. Determination of radiation-induced apoptosis in peripheral blood lymphocytes by flow cytometry analysis has also been proposed as an approach for predicting normal tissue responses following radiotherapy. The aim of the present study was to explore the association between initial DNA damage, estimated by the number of double-strand breaks induced by a given radiation dose, and the radio-induced apoptosis rates observed. Methods: Peripheral blood lymphocytes were taken from 26 consecutive patients with locally advanced breast carcinoma. Radiosensitivity of lymphocytes was quantified as the initial number of DNA double-strand breaks induced per Gy and per DNA unit (200 Mbp). Radio-induced apoptosis at 1, 2 and 8 Gy was measured by flow cytometry using annexin V/propidium iodide. Results: Radiation-induced apoptosis increased in order to radiation dose and data fitted to a semi logarithmic mathematical model. A positive correlation was found among radio-induced apoptosis values at different radiation doses: 1, 2 and 8 Gy (p < 0.0001 in all cases). Mean DSB/Gy/DNA unit obtained was 1.70 ± 0.83 (range 0.63-4.08; median, 1.46). A statistically significant inverse correlation was found between initial damage to DNA and radio-induced apoptosis at 1 Gy (p = 0.034). A trend toward 2 Gy (p = 0.057) and 8 Gy (p = 0.067) was observed after 24 hours of incubation. Conclusions: An inverse association was observed for the first time between these variables, both considered as predictive factors to radiation toxicity.en_US
dc.languagespaen_US
dc.relation.ispartofRadiation Oncologyen_US
dc.sourceRadiation Oncology 2010, [ISSN 1748-717X], 5:85en_US
dc.subject320101 Oncologíaen_US
dc.subject.otherRadio-Induced Apoptosisen_US
dc.subject.otherPeripheral-Blood Lymphocytesen_US
dc.subject.otherDouble-Strand Breaksen_US
dc.subject.otherLate Skin Reactionsen_US
dc.subject.otherRadiotherapy Patientsen_US
dc.subject.otherClinical Toxicityen_US
dc.subject.otherRadiosensitivityen_US
dc.subject.otherPredictionen_US
dc.subject.otherIndividualizationen_US
dc.subject.otherRepairen_US
dc.titleRadiation induced apoptosis and initial DNA damage are inversely related in locally advanced breast cancer patientsen_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1186/1748-717X-5-85en_US
dc.identifier.scopus2-s2.0-77956940176-
dc.identifier.isi000283255900001-
dc.date.updated2012-11-12T18:49:01Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066en-
dc.rights.holderBeatriz Pinar et al.; licensee BioMed Central Ltd.-
dc.compliance.driver1-
dc.contributor.authorscopusid6507421079-
dc.contributor.authorscopusid15829708200-
dc.contributor.authorscopusid7004374085-
dc.contributor.authorscopusid24402677200-
dc.contributor.authorscopusid6602114379-
dc.contributor.authorscopusid7003855087-
dc.contributor.authorscopusid7202233396-
dc.contributor.authorscopusid16309121200-
dc.identifier.crisid21987;12688;325;-;-;9308;-;--
dc.identifier.eissn1748-717X-
dc.identifier.issue1-
dc.relation.volume5en_US
dc.investigacionCiencias de la Saluden_US
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess-
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess-
dc.type2Artículoen_US
dc.contributor.daisngid1285881-
dc.contributor.daisngid465624-
dc.contributor.daisngid591076-
dc.contributor.daisngid2045042-
dc.contributor.daisngid603384-
dc.contributor.daisngid802813-
dc.contributor.daisngid439080-
dc.contributor.daisngid1522433-
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:Pinar, B-
dc.contributor.wosstandardWOS:Henriquez-Hernandez, LA-
dc.contributor.wosstandardWOS:Lara, PC-
dc.contributor.wosstandardWOS:Bordon, E-
dc.contributor.wosstandardWOS:Rodriguez-Gallego, C-
dc.contributor.wosstandardWOS:Lloret, M-
dc.contributor.wosstandardWOS:Nunez, MI-
dc.contributor.wosstandardWOS:De Almodovar, MR-
dc.date.coverdateSeptiembre 2010en_US
dc.identifier.supplement21987;12688;325;-;-;9308;-;--
dc.identifier.ulpgces
dc.description.jcr2,409
dc.description.jcrqQ2
dc.description.scieSCIE
item.grantfulltextopen-
item.fulltextCon texto completo-
crisitem.author.deptDepartamento de Ciencias Clínicas-
crisitem.author.deptGIR IUIBS: Medio Ambiente y Salud-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Clínicas-
crisitem.author.deptGIR IUIBS: Farmacología Molecular y Traslacional-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Médicas y Quirúrgicas-
crisitem.author.deptDepartamento de Ciencias Clínicas-
crisitem.author.orcid0000-0003-3237-0316-
crisitem.author.orcid0000-0002-4344-8644-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNamePinar Sedeño, María Beatriz-
crisitem.author.fullNameHenríquez Hernández, Luis Alberto-
crisitem.author.fullNameLara Jiménez, Pedro Carlos-
crisitem.author.fullNameBordón Rodríguez, Elisa de los Reyes-
crisitem.author.fullNameRodríguez Gallego, José Carlos-
crisitem.author.fullNameLloret Sáez-Bravo, Marta-
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