Supplementary data for the biological age linked to oxidative stress modifies breast cancer aggressiveness
María del Mar Sáez-Freire,
Adrián Blanco-Gómez,
Sonia Castillo-Lluva,
Aurora Gómez-Vecino,
Julie Milena Galvis-Jiménez,
Carmen Martín-Seisdedos,
María Isidoro-García,
Lourdes Hontecillas-Prieto,
María Begoña García-Cenador,
Francisco Javier García-Criado,
María Carmen Patino-Alonso,
Purificación Galindo-Villardón,
Jian-Hua Mao,
Carlos Prieto,
Andrés Castellanos-Martín,
Lars Kaderali,
Jesús Pérez-Losada
Affiliations
María del Mar Sáez-Freire
Instituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC). Universidad de Salamanca/CSIC. Salamanca, Spain; Instituto de Investigación Biosanitaria de Salamanca (IBSAL). Salamanca, Spain; Departamento de Fisiología y Farmacología. Universidad de Salamanca. Salamanca. Spain
Adrián Blanco-Gómez
Instituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC). Universidad de Salamanca/CSIC. Salamanca, Spain; Instituto de Investigación Biosanitaria de Salamanca (IBSAL). Salamanca, Spain
Sonia Castillo-Lluva
Instituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC). Universidad de Salamanca/CSIC. Salamanca, Spain; Instituto de Investigación Biosanitaria de Salamanca (IBSAL). Salamanca, Spain; Departamento de Bioquímica y Biología Molecular I. Facultad de Biología. Universidad Complutense de Madrid. Madrid, Spain
Aurora Gómez-Vecino
Instituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC). Universidad de Salamanca/CSIC. Salamanca, Spain; Instituto de Investigación Biosanitaria de Salamanca (IBSAL). Salamanca, Spain
Julie Milena Galvis-Jiménez
Instituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC). Universidad de Salamanca/CSIC. Salamanca, Spain; Instituto de Investigación Biosanitaria de Salamanca (IBSAL). Salamanca, Spain; Instituto Nacional de Cancerología, Bogotá, D.C., Colombia
Carmen Martín-Seisdedos
Instituto de Investigación Biosanitaria de Salamanca (IBSAL). Salamanca, Spain; Servicio de Bioquímica Clínica. Hospital Universitario de Salamanca. Salamanca, Spain
María Isidoro-García
Instituto de Investigación Biosanitaria de Salamanca (IBSAL). Salamanca, Spain; Servicio de Bioquímica Clínica. Hospital Universitario de Salamanca. Salamanca, Spain
Lourdes Hontecillas-Prieto
Instituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC). Universidad de Salamanca/CSIC. Salamanca, Spain; Instituto de Investigación Biosanitaria de Salamanca (IBSAL). Salamanca, Spain
María Begoña García-Cenador
Instituto de Investigación Biosanitaria de Salamanca (IBSAL). Salamanca, Spain; Departamento de Cirugía. Universidad de Salamanca. Salamanca. Spain
Francisco Javier García-Criado
Instituto de Investigación Biosanitaria de Salamanca (IBSAL). Salamanca, Spain; Departamento de Cirugía. Universidad de Salamanca. Salamanca. Spain
María Carmen Patino-Alonso
Instituto de Investigación Biosanitaria de Salamanca (IBSAL). Salamanca, Spain; Departamento de Estadística. Universidad de Salamanca. Spain
Purificación Galindo-Villardón
Instituto de Investigación Biosanitaria de Salamanca (IBSAL). Salamanca, Spain; Environmental Genomics and Systems Biology Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA; Departamento de Estadística. Universidad de Salamanca. Spain
Jian-Hua Mao
Environmental Genomics and Systems Biology Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
Carlos Prieto
Bioinformatics Service, Nucleus, University of Salamanca (USAL), Salamanca, Spain
Andrés Castellanos-Martín
Instituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC). Universidad de Salamanca/CSIC. Salamanca, Spain; Instituto de Investigación Biosanitaria de Salamanca (IBSAL). Salamanca, Spain; Corresponding authors at: Instituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC). Universidad de Salamanca/CSIC. Salamanca, Spain.
Lars Kaderali
Institute for Bioinformatics. University Medicine Greifswald. Greifswald, Germany; Co-corresponding author. Institute for Bioinformatics, University Medicine Greifswald, Greifswald, Germany
Jesús Pérez-Losada
Instituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC). Universidad de Salamanca/CSIC. Salamanca, Spain; Instituto de Investigación Biosanitaria de Salamanca (IBSAL). Salamanca, Spain; Corresponding authors at: Instituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC). Universidad de Salamanca/CSIC. Salamanca, Spain.
The data presented in this article are related to the research paper entitled “The biological age linked to oxidative stress modifies breast cancer aggressiveness” (M.M. Sáez-Freire, A. Blanco-Gómez, S. Castillo-Lluva, A. Gómez-Vecino, J.M. Galvis-Jiménez, C. Martín-Seisdedos, M. Isidoro-García, L. Hontecillas-Prieto, M.B. García-Cenador, F.J. García-Criado, M.C. Patino-Alonso, P. Galindo-Villardón, J.H. Mao, C. Prieto, A. Castellanos-Martín, L. Kaderali, J. Pérez-Losada). The data shown were obtained from a population of transgenic mice, MMTV-Erbb2/Neu, with different susceptibility to breast cancer and a mixed genetic background generated by backcrossing. It was observed that the aggressiveness of breast cancer negatively correlates with age, being lower in chronologically old mice, similar to what occurs in humans. Given that oxidative stress is associated with tumour susceptibility and the degree of aging, the association between the aggressiveness of breast cancer and multiple intermediate phenotypes directly or indirectly related to oxidative stress was studied. Using a mathematical model, we defined biological age and the degree of aging as the difference between biological and chronological ages. As a result, we observed that biologically old mice predominated among those that developed the disease early on, that is, those that were chronologically young. We then identified the specific and common genetic components of Quantitative Trait loci or QTL associated with different evolution of breast cancer, the intermediate phenotypes related to oxidative stress studied, the biological age and the degree of aging. Lastly, we showed that the expression pattern in the livers of biologically old mice were enriched in signalling pathways related to inflammation and response to infections; whereas the biologically young mice exhibited enriched pathways related to mitochondrial activity. For the explanation and discussion of these data refer to the research article cited above.