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dc.contributor.authorVera Ramírez, Laura 
dc.contributor.authorSanchez-Rovira, Pedro
dc.contributor.authorRamírez Tortosa, María Carmen 
dc.contributor.authorRamírez Tortosa, César Luis 
dc.contributor.authorGranados Principal, Sergio 
dc.contributor.authorFernández Navarro, Mónica María
dc.contributor.authorLorente Acosta, José Antonio 
dc.contributor.authorQuiles Morales, José Luis 
dc.date.accessioned2025-01-30T09:21:02Z
dc.date.available2025-01-30T09:21:02Z
dc.date.issued2011
dc.identifier.urihttps://hdl.handle.net/10481/101126
dc.description.abstractAnti-neoplastic agents induce oxidative stress leading to lipid, carbohydrate, protein and DNA damage. We sought to explore the role of drug-induced oxidative stress on breast cancer patient’s survival. We observed that neoadjuvant patients presented a marked raise in DNA damage and protein carbonyl levels after chemotherapy, while post-chemotherapy DNA repair activity of the KU86 enzyme and total antioxidant capacity of the plasma were higher in adjuvant group. With respect to patient’s survival, we observed that increasing levels of KU86 and antioxidant capacity of the plasma during chemotherapy significantly influenced the survival rates of the patients, protecting from disease recurrence and death. Our results suggest that chemotherapy induces a certain level of systemic oxidative stress, which is maintained along successive clinical interventions and could influence the clinical outcome of the patients.es_ES
dc.language.isoenges_ES
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.titleDoes chemotherapy-induced oxidative stress improve the survival rates of breast cancer patients?es_ES
dc.typejournal articlees_ES
dc.rights.accessRightsopen accesses_ES
dc.identifier.doi10.1089/ars.2011.3993
dc.type.hasVersionAMes_ES


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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
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