Identification of genetic and molecular determinants associated with cardiotoxicity by anthracyclines and taxanes according to age

التفاصيل البيبلوغرافية
العنوان: Identification of genetic and molecular determinants associated with cardiotoxicity by anthracyclines and taxanes according to age
المؤلفون: Gómez-Vecino, Aurora, Corchado Cobos, Roberto, Blanco-Gómez, Adrián, Prieto, Carlos, Patino-Alonso, María Carmen, Galindo, P., Fraile, Susana, Rodrigues Teixeira, Telmo, García-Macías, Carmen, Galvis-Jiménez, Julie Milena, García Sánchez, Asunción, Isidoro-García, María, García-Cenador, Begoña, García-Criado, Francisco Javier, García-Sancha, Natalia, Holgado-Madruga, M., Sánchez-Fernández, Pedro Luis, Pérez-Losada, J.
المساهمون: Ministerio de Economía y Competitividad (España), Instituto de Salud Carlos III, Fundación Sandra Ibarra - Solidaridad Frente al Cáncer
سنة النشر: 2018
المجموعة: Digital.CSIC (Consejo Superior de Investigaciones Científicas / Spanish National Research Council)
مصطلحات موضوعية: Anthracyclines, Cardiotoxicity, Backcross
الوصف: Resumen del trabajo presentado al 5th Symposium on Biomedical Research: "Advances and Perspectives In Pharmacology, Drug Toxicity and Pharmacogenetics", celebrado en Madrid del 15 al 16 de marzo de 2018. ; [Introduction]: Cardiotoxicity due to anthracyclines (CDA) is a very common problem in cancer patients, with great repercussion on their quality of life, which limits chemotherapy treatment and has consequences in the final prognosis of the oncologic disease itself. The susceptibility and degree of cardiotoxicity by anthracyclines is very heterogeneous among patients, and who will suffer this complication is unknown. CDA is a complex trait, thus follows a model of quantitative genetics, whose polygenic component is mostly unidentified. In addition, as a complex trait, CDA heterogeneity is explained by the variability among subphenotypes that would participate in its pathogenesis. Thus, anthracyclines exert their toxicity through DNA damage, so that among these subphenotypes would be the molecular pathways involved in the response to it, and a series of signaling pathways that promote and others that protect from that heart damage anthracyclines have a pro-genotoxicity effect. Differences in these pathways with the genetic variants linked with them could contribute to different susceptibility to CDA among individuals. ; [Material and Methods]: we identified the genetic and molecular determinants of cardiotoxicity in a simplified model of controlled genetic and phenotypic heterogeneity, generated by a backcross of two mouse strains of divergent phenotypic behavior, FVB and C57BL/6. We evaluated cardiac damage at histopathological level and also quantified different subphenotypes such as signaling pathways associated with cardiac damage and protection, genotoxicity pathways, TGFβ levels, telomere length, and expression of miRNAs in the myocardium. ; [Results]: We quantified anthracycline cardiotoxicity in a heterogeneous cohort of mice with breast cancer generated by a backcross. Cardiotoxicity was higher in old ...
نوع الوثيقة: conference object
report
اللغة: English
العلاقة: #PLACEHOLDER_PARENT_METADATA_VALUE#; info:eu-repo/grantAgreement/MINECO/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/SAF2014-56989-R; info:eu-repo/grantAgreement/MINECO/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/SAF2017-88854R; https://doi.org/10.24217/2531Test- 0151.18v1s1.00026; Sí; 5th Symposium on Biomedical Research (2018); http://hdl.handle.net/10261/177623Test; http://dx.doi.org/10.13039/501100003329Test; http://dx.doi.org/10.13039/501100004587Test; http://dx.doi.org/10.13039/501100007649Test
DOI: 10.13039/501100003329
DOI: 10.13039/501100004587
DOI: 10.13039/501100007649
الإتاحة: https://doi.org/10.13039/501100003329Test
https://doi.org/10.13039/501100004587Test
https://doi.org/10.13039/501100007649Test
https://doi.org/10.24217/2531Test
http://hdl.handle.net/10261/177623Test
حقوق: none
رقم الانضمام: edsbas.9861C458
قاعدة البيانات: BASE