المؤلفون: Gómez-Vecino, Aurora, Corchado Cobos, Roberto, Blanco-Gómez, Adrián, Castillo, Sonia, García-Sancha, Natalia, Martin-Garcia, Ana, Prieto, Carlos, Ruiz-Pinto, Sara, Pita, Guillermo, Velasco-Ruiz, Alejandro, Patino-Alonso, María Carmen, Galindo-Villardón, Purificación, Linarejos Vera-Pedrosa, María, Jalife, José, Macías de Plasencia, Guillermo, Castellanos-Martín, Andrés, Sáez-Freire, María del Mar, Mendiburu-Eliçabe, Marina, Fraile, Susana, Rodrigues Teixeira, Telmo, García-Macías, Carmen, Galvis-Jiménez, Julie Milena, García-Sánchez, Asunción, Isidoro-García, María, Fuentes, Manuel, García-Cenador, Begoña, García-Criado, Francisco Javier, García, Juan L., Hernández-García, María Ángeles, Cruz, Juan Jesús, Rodríguez-Sánchez, César Augusto, Martín-Ruiz, Alejandro, Pérez-López, Estefanía, Pérez-Martínez, Antonio, Gutiérrez-Larraya, Federico, Cartón, Antonio J., García-Saenz, José Ángel, Patiño-García, Ana, Martín, Miguel A., Alonso Gordoa, Teresa, Vulsteke, Christof, Croes, Lieselot, Hatse, Sigrid, Van Brussel, Thomas, Lambrechts, Diether, Wildiers, Hans, Holgado-Madruga, M., González-Neira, Ana, Sánchez, Pedro L., Pérez-Losada, J.

المساهمون: European Commission, Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Economía y Competitividad (España), Agencia Estatal de Investigación (España), Instituto de Salud Carlos III, Junta de Castilla y León, Fundación "la Caixa", Centro Nacional de Investigaciones Cardiovasculares (España), Pérez-Losada, J., Macías de Plasencia, Guillermo, Fraile, Susana, Rodrigues Teixeira, Telmo, Hernández-García, María Ángeles, Holgado-Madruga, M., González-Neira, Ana, Sánchez, Pedro L., Gómez-Vecino, Aurora, Corchado Cobos, Roberto, Blanco-Gómez, Adrián, Castillo, Sonia, García-Sancha, Natalia, Martin-Garcia, Ana, Prieto, Carlos, Ruiz-Pinto, Sara, Pita, Guillermo, Velasco-Ruiz, Alejandro, Patino-Alonso, María Carmen, Galindo-Villardón, Purificación, Linarejos Vera-Pedrosa, María, Jalife, José, Castellanos-Martín, Andrés, Sáez-Freire, María del Mar, Mendiburu-Eliçabe, Marina, García-Macías, Carmen, Galvis-Jiménez, Julie Milena, García-Sánchez, Asunción, Isidoro-García, María, Fuentes, Manuel, García-Cenador, Begoña, García-Criado, Francisco Javier, García, Juan L., Cruz, Juan Jesús, Rodríguez-Sánchez, César Augusto, Martín-Ruiz, Alejandro, Pérez-López, Estefanía, Pérez-Martínez, Antonio, Gutiérrez-Larraya, Federico, Cartón, Antonio J., García-Saenz, José Ángel, Patiño-García, Ana, Martin, Miguel, Alonso Gordoa, Teresa, Vulsteke, Christof, Croes, Lieselot, Hatse, Sigrid, Van Brussel, Thomas, Lambrechts, Diether, Wildiers, Hans

مصطلحات موضوعية: CDA, Missing heritability, Subphenotype, Pathophenotype, Complex traits

الوصف: Who produced the data? The data has been created by the authors listed above. Is the title specific enough? "Datasets related to a study aimed to identify genetic markers of CDA by subphenotypes associated with cardiotoxicity." Why has the data been created? These datasets are supplementary material with which the principal and supplementary figures and tables of our indicated work were generated. What limitations do the data have (for example, sensitive data has been deleted)? All confidential patient information is not present. We have not had access to that information, following current legal regulations. How should the data be interpreted? These data sets should not be separated from the main article in which they were utilized. Thus, to better understand their context, researchers should see them in the global scenario of our work. Are there gaps in the data, or do they give a complete picture of the topic studied? As indicated above, data should be considered and interpreted in the global context of our study. What processes have generated the data? The processes that generated the data are indicated in the summary of the data above and individually for each of them. Thus, each dataset is accompanied by a legend within the document. What does the data measure in the columns of the files? As indicated, each dataset individually shows the information contained in the legend of each dataset. What software is required to be able to read the data? The datasets are in Excel format. How should the data be quoted? Researchers should cite the data in the context of the work they belong to once it is published and free of the embargo. Can the data be reused? What use licenses are assigned to you? In principle, yes. If additional clinical information is required, these data were previously published by some of us, and the references are included in our manuscript. These data are available from the principal investigators of the references listed in our work upon reasonable request. Are there more versions of the ...

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/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/RTI2018-094130-B-100; info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/SAF2017-88854-R; Sí; Gómez-Vecino, Aurora; Corchado Cobos, Roberto; Blanco-Gómez, Adrián; Castillo, Sonia; García-Sancha, Natalia; Martin-Garcia, Ana; Prieto, Carlos; Ruiz-Pinto, Sara; Pita, Guillermo; Velasco-Ruiz, Alejandro; Patino-Alonso, María Carmen; Galindo-Villardón, Purificación; Linarejos Vera-Pedrosa, María; Jalife, José; Macías de Plasencia, Guillermo; Castellanos-Martín, Andrés; Sáez-Freire, María del Mar; Mendiburu-Eliçabe, Marina; Fraile, Susana; Rodrigues Teixeira, Telmo; García-Macías, Carmen; Galvis-Jiménez, Julie Milena; García-Sánchez, Asunción; Isidoro-García, María; Fuentes, Manuel; García-Cenador, Begoña; García-Criado, Francisco Javier; García, Juan L.; Hernández-García, María Ángeles; Cruz, Juan Jesús; Rodríguez-Sánchez, César Augusto; Martín-Ruiz, Alejandro; Pérez-López, Estefanía; Pérez-Martínez, Antonio; Gutiérrez-Larraya, Federico; Cartón, Antonio J.; García-Saenz, José Ángel; Patiño-García, Ana; Martin, Miguel; Alonso Gordoa, Teresa; Vulsteke, Christof; Croes, Lieselot; Hatse, Sigrid; Van Brussel, Thomas; Lambrechts, Diether; Wildiers, Hans; Holgado-Madruga, M.; González-Neira, Ana; Sánchez, Pedro L.; Pérez-Losada, J.; 2021; Datasets related to a study aimed to identify genetic markers of CDA by subphenotypes associated with cardiotoxicity; DIGITAL.CSIC; http://dx.doi.org/10.20350/digitalCSIC/13845Test; http://hdl.handle.net/10261/239215Test; http://dx.doi.org/10.13039/501100004587Test; http://dx.doi.org/10.13039/501100011033Test; http://dx.doi.org/10.13039/501100003329Test; http://dx.doi.org/10.13039/501100000780Test; http://dx.doi.org/10.13039/501100005884Test; http://dx.doi.org/10.13039/501100014180Test

الإتاحة: https://doi.org/10.20350/digitalCSIC/13845Test
https://doi.org/10.13039/501100004587Test
https://doi.org/10.13039/501100011033Test
https://doi.org/10.13039/501100003329Test
https://doi.org/10.13039/501100000780Test
https://doi.org/10.13039/501100005884Test
https://doi.org/10.13039/501100014180Test
http://hdl.handle.net/10261/239215Test

المؤلفون: Pérez del Villar, Luis, Vicente, Belén, Blanco-Gómez, Adrián, Castellanos-Martín, Andrés, Pérez-Losada, J., Muro, Antonio

المساهمون: Fundación Ramón Areces, Junta de Castilla y León

مصطلحات موضوعية: F1B6CBA hybrid, Immunophenotypes, Experimental crosses, S. mansoni infection, Schistosomiasis susceptibility

الوصف: This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License. ; Schistosomiasis is a disease with a strong genetic component influenced by socioeconomic and ecological factors. Epidemiological studies have identified several genetic regions involved in the schistosomiasis susceptibility. However, it is not well known what physiological traits are predisposing to the disease. The study of experimental infections in inbred mouse strains with variable genetic susceptibility to the disease offers a good opportunity to tackle this question. F1B6CBA hybrid between the most divergent strains was infected in order to characterize the immunophenotypes that correlate with the susceptibility of schistosomiasis disease in mice. Complete blood counts and immunophenotype were determined at 0, 3, 6, and 9 weeks post infection. Nine weeks after cercariae exposure, animals were perfused and worm recovery was assessed. A large number of hepatic lesions, a reduction in the eosinophil and basophil count in the acute phase of infection and the decreased number of monocytes, neutrophils and B-lymphocytes are phenotypes associated with increased susceptibility to S. mansoni infection. ; The present study was supported by a grant from the Areces Foundation (2010–13) and funding of the Junta de Castilla y Leon (Orden EDU/330/2008). ; Peer Reviewed

العلاقة: Publisher's version; http://dx.doi.org/10.2478/s11686-014-0277-4Test; Sí; e-issn: 1896-1851; Acta Parasitologica 59(3): 529-539 (2014); http://hdl.handle.net/10261/134757Test; http://dx.doi.org/10.13039/100008054Test; http://dx.doi.org/10.13039/501100014180Test

الإتاحة: https://doi.org/10.2478/s11686-014-0277-4Test
https://doi.org/10.13039/100008054Test
https://doi.org/10.13039/501100014180Test
http://hdl.handle.net/10261/134757Test

المؤلفون: Pérez del Villar, Luis, Vicente, Belén, Galindo-Villardón, Purificación, Castellanos-Martín, Andrés, Pérez-Losada, J., Muro, Antonio

المساهمون: Universidad de Salamanca

مصطلحات موضوعية: Hematological phenotypes, Schistosoma mansoni infection, Immunological phenotypes, Mus spretus

الوصف: This is an Open Access article distributed under the terms of the Creative Commons Attribution License. ; [EN]: Most Schistosoma mansoni experimental infections are developed in several inbred strains of Mus musculus as definitive host. In contrast, Mus spretus is unexplored in Schistosoma infection studies. Mus spretus provides a high variation of immunological phenotypes being an invaluable tool for genetic studies and gene mapping. The aim of this study is to characterize hematological and immunological responses against Schistosoma mansoni infection in Mus spretus (SPRET/EiJ strain) vs. Mus musculus (CD1 strain) mice. Nine weeks after cercarial exposure, animals were perfused and the parasite burden was assessed. The parasitological data suggests that SPRET/EiJ mice tolerate higher parasite loads compared to CD1 strain. In addition, hematological parameters measured in Mus spretus group showed a significant increase in granulocytes population in early stages of infection compared to the CD1 cohort. Meanwhile, CD1 presented higher levels of lymphocytes and IgG1 in the late stages of S. mansoni experimental infection. ; [FR]: La plupart des infections expérimentales à Schistosoma mansoni sont développées chez Mus musculus comme hôte définitif. Au contraire, Mus spretus est une espèce de souris inexplorée dans les infections expérimentales á Schistosoma. Mus spretus offre une grande variation de phénotypes immunologiques, ce qui est un outil essentiel pour les études génétiques et la cartographie des gènes. L’objectif de cette étude est la caractérisation de la réponse hématologique et immunologique contre l’infection à Schistosoma mansoni chez Mus spretus (souche SPRET/EiJ) comparée à Mus musculus (souche CD1). Neuf semaines après l’exposition aux cercaires, les animaux ont été perfusés et les paramètres parasitologiques ont été obtenus. Les données parasitologiques suggèrent que la souche SPRET/EiJ tolère des charges parasitaires plus élevées que la souche CD1. Les paramètres hématologiques mesurés chez ...

العلاقة: Publisher's version; http://dx.doi.org/10.1051/parasite/2013027Test; Sí; e-issn: 1776-1042; Parasite 20: 27 (2013); http://hdl.handle.net/10261/134509Test

الإتاحة: https://doi.org/10.1051/parasite/2013027Test
http://hdl.handle.net/10261/134509Test

المؤلفون: Lu, Jing, Wen, Mingxin, Huang, Yurong, He, Xiuquan, Wang, Yunshan, Wu, Qi, Li, Zengchun, Castellanos-Martin, Andres, Abad, Mar, Cruz-Hernandez, Juan J., Rodriguez, Cesar A., Perez-Losada, Jesus, Mao, Jian-Hua, Wei, Guangwei

المصدر: Epigenetics ; volume 8, issue 6, page 571-583 ; ISSN 1559-2294 1559-2308

الإتاحة: https://doi.org/10.4161/epi.24626Test

المؤلفون: Romero Camarero, Isabel, Barajas Diego, Marcos, Castellanos Martín, Andrés, García Martín, Ángel, Varela, Gonzalo, Abad, Mar, Ludeña, María Dolores, Pérez Losada, Jesús, Sánchez García, Isidro

مصطلحات موضوعية: Cancer, Treatment, CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología

الوصف: Cancer is the subject of intense research around the world, but many questions about how the disease works remain unanswered. How exactly does cancer start and how do tumours grow? In fact, at present there are ten times more anticancer drugs being tested in clinical trials than there were 15 years ago. However, many of the new anticancer agents are predicted to show clinical benefit in only small subpopulations of patients. The cancer stem cell model could explain not only how some cancers work but also why patients suffer relapses, providing a good opportunity to gain insight into the reasons why agents work or, more commonly, don’t work, before going into a clinical trial

وصف الملف: application/pdf

العلاقة: Histology and histopathology, Vol. 27, nº 2 (2012); http://hdl.handle.net/10201/52387Test

الإتاحة: http://hdl.handle.net/10201/52387Test

المؤلفون: Liu, Yueyong, Castellanos-Martín, Andrés, Pérez-Losada, J., Kwon, Yong-Won, Abad, María del Mar, Cruz, Juan Jesús, Sun, Yinghao, Mao, Jian-Hua

المساهمون: Ministry of Science and Technology of the People's Republic of China, National Institutes of Health (US), NASA Astrobiology Institute (US), Fundación Eugenio Rodríguez Pascual, Obra Social Kutxa, Department of Energy (US), Ministerio de Ciencia e Innovación (España), National Cancer Institute (US)

الوصف: This is an open-access article distributed under the terms of the Creative Commons Attribution License.-- et al. ; FBXW7 acts as a tumor suppressor through ubiquitination and degradation of multiple oncoproteins. Loss of FBXW7 expression, which could be partially attributed by the genomic deletion or mutation of FBXW7 locus, is frequently observed in various human cancers. However, the mechanisms regulating FBXW7 expression still remain poorly understood. Here we examined the 5′ region of FBXW7 gene to investigate the regulation of FBXW7 expression. We identified seven alternative splicing (AS) 5′-UTR forms of FBXW7α that are composed of multiple novel non-coding exons. A significant difference in translational efficiency among these 5′-UTRs variants was observed by in vivo Luciferase reporter assay and Western blot. Furthermore, we found that the mRNA level of the AS form with high translational efficiency was specifically reduced in more than 80% of breast cancer cell lines and in more than 50% of human primary cancers from various tissues. In addition, we also identified mutations of FBXW7 in prostate cancers (5.6%), kidney cancers (16.7%), and bladder cancers (18.8%). Our results suggest that in addition to mutation, differential expression of FBXW7α AS forms with different translational properties may serve as a novel mechanism for inactivation of FBXW7 in human cancer. ; JPL is partially supported by FEDER and MICINN (PLE2009-119), FIS (PI10/00328) “Fundación Eugenio Rodríguez Pascual”, and Fundación Inbiomed (Instituto Oncológico Obra Social de la Caja Guipozcoa-San Sebastian, Kutxa). YS is supported by the National Basic Research Program of China (2012CB518300) and the Ministry of Science & Technology of Shanghai (08410701500). JHM is supported by the National Institutes of Health, National Cancer Institute grant R01 CA116481, the Low Dose Scientific Focus Area, Office of Biological & Environmental Research, US Department of Energy (DE-AC02-05CH11231), Laboratory Directed Research & ...

العلاقة: Publisher's version; http://dx.doi.org/10.1371/journal.pone.0049453Test; Sí; PLoS ONE 7(11): e49453 (2012); http://hdl.handle.net/10261/134252Test; http://dx.doi.org/10.13039/501100002855Test; http://dx.doi.org/10.13039/100000002Test; http://dx.doi.org/10.13039/100008055Test; http://dx.doi.org/10.13039/501100004837Test; http://dx.doi.org/10.13039/100000015Test

الإتاحة: https://doi.org/10.1371/journal.pone.0049453Test
https://doi.org/10.13039/501100002855Test
https://doi.org/10.13039/100000002Test
https://doi.org/10.13039/100008055Test
https://doi.org/10.13039/501100004837Test
https://doi.org/10.13039/100000015Test
http://hdl.handle.net/10261/134252Test

المؤلفون: Pérez-Losada, J., Castellanos-Martín, Andrés, Mao, Jian-Hua

الوصف: El pdf del artículo es la versión de autor. ; Cancer susceptibility is due to interactions between inherited genetic factors and exposure to environmental carcinogens. The genetic component is constituted mainly by weakly acting low-penetrance genetic variants that interact among themselves, as well as with the environment. These low susceptibility genes can be categorized into two main groups: one includes those that control intrinsic tumor cell activities (i.e. apoptosis, proliferation or DNA repair), and the other contains those that modulate the function of extrinsic tumor cell compartments (i.e. stroma, angiogenesis, or endocrine and immune systems). Genome-Wide Association Studies (GWAS) of human populations have identified numerous genetic loci linked with cancer risk and behavior, but nevertheless the major component of cancer heritability remains to be explained. One reason may be that GWAS cannot readily capture gene–gene or gene–environment interactions. Mouse model approaches offer an alternative or complementary strategy, because of our ability to control both the genetic and environmental components of risk. Recently developed genetic tools, including high-throughput technologies such as SNP, CGH and gene expression microarrays, have led to more powerful strategies for refining quantitative trait loci (QTL) and identifying the critical genes. In particular, the cross-species approaches will help to refine locations of QTLs, and reveal their genetic and environmental interactions. The identification of human tumor susceptibility genes and discovery of their roles in carcinogenesis will ultimately be important for the development of methods for prediction of risk, diagnosis, prevention and therapy for human cancers. ; J. H. Mao is supported by Office of Biological & Environmental Research, of the U.S. Department of Energy under Contract No. DE-AC02-05CH11231, by Laboratory Downloaded on 20 February 2012 Published on 24 January 2011 on http://pubs.rsc.orgTest | doi:10.1039/C0IB00094A View Online This ...

العلاقة: http://dx.doi.org/10.1039/C0IB00094ATest; Integrative Biology 3: 316-328 (2011); http://hdl.handle.net/10261/45892Test

الإتاحة: https://doi.org/10.1039/C0IB00094ATest
http://hdl.handle.net/10261/45892Test

المؤلفون: Liu, Yueyong, Ren, Shancheng, Castellanos-Martin, Andres, Perez-Losada, Jesus, Kwon, Yong-Won, Huang, Yurong, Wang, Zeran, Abad, Mar, Cruz-Hernandez, Juan J., Rodriguez, Cesar A., Sun, Yinghao, Mao, Jian-Hua

مصطلحات موضوعية: 59 BASIC BIOLOGICAL SCIENCES

الوصف: BXW7 acts as a tumor suppressor through ubiquitination and degradation of multiple oncoproteins. Loss of FBXW7 expression, which could be partially attributed by the genomic deletion or mutation of FBXW7 locus, is frequently observed in various human cancers. However, the mechanisms regulating FBXW7 expression still remain poorly understood. Here we examined the 59 region of FBXW7 gene to investigate the regulation of FBXW7 expression. We identified seven alternative splicing (AS) 59-UTR forms of FBXW7a that are composed of multiple novel non-coding exons. A significant difference in translational efficiency among these 59-UTRs variants was observed by in vivo Luciferase reporter assay and Western blot. Furthermore, we found that the mRNA level of the AS form with high translational efficiency was specifically reduced in more than 80% of breast cancer cell lines and in more than 50% of human primary cancers from various tissues. In addition, we also identified mutations of FBXW7 in prostate cancers (5.6%), kidney cancers (16.7%), and bladder cancers (18.8%). Our results suggest that in addition to mutation, differential expression of FBXW7a AS forms with different translational properties may serve as a novel mechanism for inactivation of FBXW7 in human cancer.

وصف الملف: application/pdf

العلاقة: http://www.osti.gov/servlets/purl/1627560Test; https://www.osti.gov/biblio/1627560Test; https://doi.org/10.1371/journal.pone.0049453Test

الإتاحة: https://doi.org/10.1371/journal.pone.0049453Test
http://www.osti.gov/servlets/purl/1627560Test
https://www.osti.gov/biblio/1627560Test

المؤلفون: Castellanos-Martín, Andrés, Castillo-Lluva, Sonia, Sáez-Freire, María del Mar, Blanco-Gómez, Adrián, Hontecillas-Prieto, Lourdes, Patino-Alonso, Carmen, Galindo-Villardon, Purificación, Pérez del Villar, Luis, Martín-Seisdedos, Carmen, Isidoro-Garcia, María, Abad-Hernández, María del Mar, Cruz-Hernández, Juan Jesús, Rodríguez-Sánchez, César Augusto, González-Sarmiento, Rogelio, Alonso-López, Diego, De Las Rivas, Javier, García-Cenador, Begoña, García-Criado, Javier, Lee, Do Yup, Bowen, Benjamin, Reindl, Wolfgang, Northen, Trent, Mao, Jian-Hua, Pérez-Losada, Jesús

مصطلحات موضوعية: 59 BASIC BIOLOGICAL SCIENCES

الوصف: Background: An essential question in cancer is why individuals with the same disease have different clinical outcomes. Progress toward a more personalized medicine in cancer patients requires taking into account the underlying heterogeneity at different molecular levels. Results: Here, we present a model in which there are complex interactions at different cellular and systemic levels that account for the heterogeneity of susceptibility to and evolution of ERBB2-positive breast cancers. Our model is based on our analyses of a cohort of mice that are characterized by heterogeneous susceptibility to ERBB2-positive breast cancers. Our analysis reveals that there are similarities between ERBB2 tumors in humans and those of backcross mice at clinical, genomic, expression, and signaling levels. We also show that mice that have tumors with intrinsically high levels of active AKT and ERK are more resistant to tumor metastasis. Our findings suggest for the first time that a site-specific phosphorylation at the serine 473 residue of AKT1 modifies the capacity for tumors to disseminate. Finally, we present two predictive models that can explain the heterogeneous behavior of the disease in the mouse population when we consider simultaneously certain genetic markers, liver cell signaling and serum biomarkers that are identified before the onset of the disease. Conclusions: Considering simultaneously tumor pathophenotypes and several molecular levels, we show the heterogeneous behavior of ERBB2-positive breast cancer in terms of disease progression. This and similar studies should help to better understand disease variability in patient populations.

وصف الملف: application/pdf

العلاقة: http://www.osti.gov/servlets/purl/1626930Test; https://www.osti.gov/biblio/1626930Test; https://doi.org/10.1186/s13059-015-0599-zTest

الإتاحة: https://doi.org/10.1186/s13059-015-0599-zTest
http://www.osti.gov/servlets/purl/1626930Test
https://www.osti.gov/biblio/1626930Test

المؤلفون: Sáez-Freire, María del Mar, Blanco-Gómez, Adrián, Castillo-Lluva, Sonia, Gómez-Vecino, Aurora, Galvis-Jiménez, Julie Milena, Martín-Seisdedos, Carmen, Isidoro-García, María, Hontecillas-Prieto, Lourdes, García-Cenador, María Begoña, García-Criado, Francisco Javier, Patino-Alonso, María Carmen, Galindo-Villardón, Purificación, Mao, Jian-Hua, Prieto, Carlos, Castellanos-Martín, Andrés, Kaderali, Lars, Pérez-Losada, Jesús

الوصف: The incidence of breast cancer increases with age until menopause, and breast cancer is more aggressive in younger women. The existence of epidemiological links between breast cancer and aging indicates that both processes share some common mechanisms of development. Oxidative stress is associated with both cancer susceptibility and aging. Here we observed that ERBB2-positive breast cancer, which developed in genetically heterogeneous ERBB2-positive transgenic mice generated by a backcross, is more aggressive in chronologically younger than in older mice (differentiated by the median survival of the cohort that was 79 weeks), similar to what occurs in humans. In this cohort, we estimated the oxidative biological age using a mathematical model that integrated several subphenotypes directly or indirectly related to oxidative stress. The model selected the serum levels of HDL-cholesterol and magnesium and total AKT1 and glutathione concentrations in the liver. The grade of aging was calculated as the difference between the predicted biological age and the chronological age. This comparison permitted the identification of biologically younger and older mice compared with their chronological age. Interestingly, biologically older mice developed more aggressive breast cancer than the biologically younger mice. Genomic regions on chromosomes 2 and 15 linked to the grade of oxidative aging were identified. The levels of expression of Zbp1 located on chromosome 2, a gene related to necroptosis and inflammation, positively correlated with the grade of aging and tumour aggressiveness. Moreover, the pattern of gene expression of genes linked to the inflammation and the response to infection pathways was enriched in the livers of biologically old mice. This study shows part of the complex interactions between breast cancer and aging.

وصف الملف: application/pdf

العلاقة: http://www.osti.gov/servlets/purl/1629214Test; https://www.osti.gov/biblio/1629214Test; https://doi.org/10.1016/j.dib.2018.03.132Test

الإتاحة: https://doi.org/10.1016/j.dib.2018.03.132Test
http://www.osti.gov/servlets/purl/1629214Test
https://www.osti.gov/biblio/1629214Test