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Search Results: 1 - 10 of 11407 matches for " Ruben Rene Gonzalez-Perez "
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Leptin’s Pro-Angiogenic Signature in Breast Cancer
Ruben Rene Gonzalez-Perez,Viola Lanier,Gale Newman
Cancers , 2013, DOI: 10.3390/cancers5031140
Abstract: Obesity is linked to increased incidence of breast cancer. The precise causes and mechanisms of these morbid relationships are unknown. Contradictory data on leptin angiogenic actions have been published. However, accumulating evidence would suggest that leptin’s pro-angiogenic effects in cancer play an essential role in the disease. Leptin, the main adipokine secreted by adipose tissue, is also abnormally expressed together with its receptor (OB-R) by breast cancer cells. Leptin induces proliferation and angiogenic differentiation of endothelial cells upregulates VEGF/VEGFR2 and transactivates VEGFR2 independent of VEGF. Leptin induces two angiogenic factors: IL-1 and Notch that can increase VEGF expression. Additionally, leptin induces the secretion and synthesis of proteases and adhesion molecules needed for the development of angiogenesis. Leptin’s paracrine actions can further affect stromal cells and tumor associated macrophages, which express OB-R and secrete VEGF and IL-1, respectively. A complex crosstalk between leptin, Notch and IL-1 (NILCO) that induces VEGF/VEGFR2 is found in breast cancer. Leptin actions in tumor angiogenesis could amplify, be redundant and/or compensatory to VEGF signaling. Current failure of breast cancer anti-angiogenic therapies emphasizes the necessity of targeting the contribution of other pro-angiogenic factors in breast cancer. Leptin’s impact on tumor angiogenesis could be a novel target for breast cancer, especially in obese patients. However, more research is needed to establish the importance of leptin in tumor angiogenesis. This review is focused on updated information on how leptin could contribute to tumor angiogenesis.
Notch, IL-1 and Leptin Crosstalk Outcome (NILCO) Is Critical for Leptin-Induced Proliferation, Migration and VEGF/VEGFR-2 Expression in Breast Cancer
Shanchun Guo, Ruben R. Gonzalez-Perez
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0021467
Abstract: High levels of pro-angiogenic factors, leptin, IL-1, Notch and VEGF (ligands and receptors), are found in breast cancer, which is commonly correlated with metastasis and lower survival of patients. We have previously reported that leptin induces the growth of breast cancer and the expression of VEGF/VEGFR-2 and IL-1 system. We hypothesized that Notch, IL-1 and leptin crosstalk outcome (NILCO) plays an essential role in the regulation of leptin-mediated induction of proliferation/migration and expression of pro-angiogenic molecules in breast cancer. To test this hypothesis, leptin's effects on the expression and activation of Notch signaling pathway and VEGF/VEGFR-2/IL-1 were determined in mouse (4T1, EMT6 and MMT) breast cancer cells. Remarkably, leptin up-regulated Notch1-4/JAG1/Dll-4, Notch target genes: Hey2 and survivin, together with IL-1 and VEGF/VEGFR-2. RNA knockdown and pharmacological inhibitors of leptin signaling significantly abrogated activity of reporter gene-luciferase CSL (RBP-Jk) promoter, showing that it was linked to leptin-activated JAK2/STAT3, MAPK, PI-3K/mTOR, p38 and JNK signaling pathways. Interestingly, leptin upregulatory effects on cell proliferation/migration and pro-angiogenic factors Notch, IL-1 and VEGF/VEGFR-2 were abrogated by a γ-secretase inhibitor, DAPT, as well as siRNA against CSL. In addition, blockade of IL-1R tI inhibited leptin-induced Notch, Hey2 and survivin as well as VEGF/VEGFR-2 expression. These data suggest leptin is an inducer of Notch (expression/activation) and IL-1 signaling modulates leptin effects on Notch and VEGF/VEGFR-2. We show for the first time that a novel unveiled crosstalk between Notch, IL-1 and leptin (NILCO) occurs in breast cancer. Leptin induction of proliferation/migration and upregulation of VEGF/VEGFR-2 in breast cancer cells were related to an intact Notch signaling axis. NILCO could represent the integration of developmental, pro-inflammatory and pro-angiogenic signals critical for leptin-induced cell proliferation/migration and regulation of VEGF/VEGFR-2 in breast cancer. Targeting NILCO might help to design new pharmacological strategies aimed at controlling breast cancer growth and angiogenesis.
Social Responsibility Networks (SRN): The Role of the International Civil Society in Redressing the Negative Effects of Globalization at the Local Level Social Responsibility Networks (SRN): The Role of the International Civil Society in Redressing the Negative Effects of Globalization at the Local Level
Maria Alejandra Gonzalez-Perez
AD-minister , 2008,
Abstract: Evidencias, tanto teóricas como empíricas, indican que la globalización de laeconomía ha intensificado la exclusión social, los problemas medio ambientales y haexacerbado desigualdades en materia social y laboral. Para revertir estas situacionesse requiere de sistemas transnacionales de gobernabilidad legítimos y transparentes,que cuenten con la participación activa y reconocida de los trabajadores.Este documento se basa en una investigación empírica en la cual se presentaun modelo de participación transnacional de los actores de la sociedad civil(incluyendo los sindicatos y otras organizaciones de trabajadores), así como tambiénlas corporaciones privadas y las agencias gubernamentales. De esta manera se desarrolla una plataforma que opera como un sistema de responsabilidad socialcuyo alcance sobrepasa a la responsabilidad social empresarial (RSE). There is both theoretical and empirical evidence which indicates that the processes of globalization have intensified the onset of social exclusion and environmental problems. Globalized processes may also exacerbate inequalities that, in order to be readdressed, require transnational, transparent, accountable and participative governance systems, with an active and recognised contribution by the local community in the amelioration of these problems. This paper focuses on transnational participation of civil society actors as well as private corporations and state agencies, which together provide a platform for the development of a broader scope for corporate social responsibility (CSR).
Vascular Endothelial Growth Factor Receptor-2 Couples Cyclo-Oxygenase-2 with Pro-Angiogenic Actions of Leptin on Human Endothelial Cells
Elena Garonna,Kathleen M. Botham,Graeme M. Birdsey,Anna M. Randi,Ruben R. Gonzalez-Perez,Caroline P. D. Wheeler-Jones
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0018823
Abstract: The adipocyte-derived hormone leptin influences the behaviour of a wide range of cell types and is now recognised as a pro-angiogenic and pro-inflammatory factor. In the vasculature, these effects are mediated in part through its direct leptin receptor (ObRb)-driven actions on endothelial cells (ECs) but the mechanisms responsible for these activities have not been established. In this study we sought to more fully define the molecular links between inflammatory and angiogenic responses of leptin-stimulated human ECs.
The information content in a volatility index for Spain
Maria T. Gonzalez-Perez,Alfonso Novales
SERIEs , 2011, DOI: 10.1007/s13209-010-0031-6
Abstract: A model-free methodology is used for the first time to estimate a daily volatility index (VIBEX-NEW) for the Spanish financial market. We use a public data set of daily option prices to compute this index and show that daily changes in VIBEX-NEW display a negative, tight contemporaneous relationship with IBEX daily returns, contrary to other common volatility indicators, as an implied volatility indicator or a GARCH(1,1) conditional volatility model. This relationship is approximately symmetric to the sign on VIBEX-NEW changes and asymmetric to the IBEX-35 returns sign, which make it clearly a suitable volatility index for the Spanish stock market. We also examine the relationship between current VIBEX-NEW and future IBEX-35 volatility. Our results suggest that VIBEX-NEW can be used to produce IBEX-35 volatility forecasts at least as good as historical and conditional volatility measures. A feasible volatility correction methodology is proposed to achieve it.
Paracrine Interactions between Adipocytes and Tumor Cells Recruit and Modify Macrophages to the Mammary Tumor Microenvironment: The Role of Obesity and Inflammation in Breast Adipose Tissue
Ana M. Santander,Omar Lopez-Ocejo,Olivia Casas,Thais Agostini,Lidia Sanchez,Eduardo Lamas-Basulto,Roberto Carrio,Margot P. Cleary,Ruben R. Gonzalez-Perez,Marta Torroella-Kouri
Cancers , 2015, DOI: 10.3390/cancers7010143
Abstract: The relationship between obesity and breast cancer (BC) has focused on serum factors. However, the mammary gland contains adipose tissue (AT) which may enable the crosstalk between adipocytes and tumor cells contributing to tumor macrophage recruitment. We hypothesize that the breast AT (bAT) is inflamed in obese females and plays a major role in breast cancer development. The effects of this interplay on macrophage chemotaxis were examined in vitro, using co-cultures of mouse macrophages, mammary tumor cells and adipocytes. Macrophages were exposed to the adipocyte and tumor paracrine factors leptin, CCL2 and lauric acid (alone or in combinations). In cell supernatants Luminex identified additional molecules with chemotactic and other pro-tumor functions. Focus on the adipokine leptin, which has been shown to have a central role in breast cancer pathogenesis, indicated it modulates macrophage phenotypes and functions. In vivo experiments demonstrate that mammary tumors from obese mice are larger and that bAT from obese tumor-bearers contains higher numbers of macrophages/CLS and hypertrophic adipocytes than bAT from lean tumor-bearers, thus confirming it is more inflamed. Also, bAT distal from the tumor is more inflamed in obese than in lean mice. Our results reveal that bAT plays a role in breast cancer development in obesity.
Oncodrive-CIS: A Method to Reveal Likely Driver Genes Based on the Impact of Their Copy Number Changes on Expression
David Tamborero, Nuria Lopez-Bigas, Abel Gonzalez-Perez
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0055489
Abstract: A well-established approach for detecting genes involved in tumorigenesis due to copy number alterations (CNAs) is to assess the recurrence of the alteration across multiple samples. Expression data can be used to filter this list of candidates by assessing whether the gene expression significantly differs between tumors depending on the copy number status. A drawback of this approach is that it may fail to detect low-recurrent drivers. Furthermore, this analysis does not provide information about expression changes for each gene as compared to the whole data set and does not take into consideration the expression of normal samples. Here we describe a novel method (Oncodrive-CIS) aimed at ranking genes according to the expression impact caused by the CNAs. The rationale of Oncodrive-CIS is based on the hypothesis that genes involved in cancer due to copy number changes are more biased towards misregulation than are bystanders. Moreover, to gain insight into the expression changes caused by gene dosage, the expression of samples with CNAs is compared to that of tumor samples with diploid genotype and also to that of normal samples. Oncodrive-CIS demonstrated better performance in detecting putative associations between copy-number and expression in simulated data sets as compared to other methods aimed to this purpose, and picked up genes likely to be related with tumorigenesis when applied to real cancer samples. In summary, Oncodrive-CIS provides a statistical framework to evaluate the in cis effect of CNAs that may be useful to elucidate the role of these aberrations in driving oncogenesis. An implementation of this method and the corresponding user guide are freely available at http://bg.upf.edu/oncodrivecis.
Colour gradients within SDSS DR7 galaxies: hints of recent evolution
V. Gonzalez-Perez,F. J. Castander,G. Kauffmann
Physics , 2010, DOI: 10.1111/j.1365-2966.2010.17744.x
Abstract: The evolutionary path followed by a galaxy shapes its internal structure, and, in particular, its internal colour variation. We present a study of the internal colour variation within galaxies from the Seventh Data Release of the Sloan Digital Sky Survey (SDSS DR7). We statistically study the connection between the internal colour variation and global galactic properties, looking for hints of the recent galactic evolution. Considering only galaxies with good photometry and spectral measurements, we define four luminosity-threshold samples within the redshift range 0.01
Visualizing multidimensional cancer genomics data
Michael P Schroeder, Abel Gonzalez-Perez, Nuria Lopez-Bigas
Genome Medicine , 2013, DOI: 10.1186/gm413
Abstract: Cancer genomics benefits from high-throughput technologies that allow the comparison of the genomic sequences, epigenomic profiles, and transcriptomes of tumor cells with those of normal cells. These technologies often characterize different types of somatic alterations (or variations) in a tumor cell population that are absent from normal cells - including copy number alterations (CNAs), mutations, gene expression changes and methylation changes [1-4]. Together, these somatic alterations constitute multidimensional oncogenomics datasets that describe the variations that coexist in common elements (for example, the genes) of the genome (or transcriptome) of a particular cohort of tumor cells. Such data are currently being used to identify cancer-driver genes and pathways, to discover molecular targets for new therapies, and to define molecular profiles that characterize clinically meaningful patient categories. An array of analytical methods are currently used to exploit the information contained within this multidimensional layout [5-12].Along with computational and statistical methodologies, effective visual exploration by experts is crucial to successful extraction of knowledge from oncogenomics data. For example, this step might be key to unraveling rare genomic events, verifying data quality at maximum resolution or identifying key players in cancer development. Thus, researchers need intuitive tools that allow the visual integration and simultaneous exploration of both different types of alterations and clinical information. Many data visualization tools have been developed in recent years to support genomic studies. In this review, we revisit the most common ways in which these data are visualized, and present selected tools that allow researchers to visualize multidimensional oncogenomics datasets effectively (Table 1).To aid our review of the tools, we describe four case studies that illustrate their use: the visual exploration of 1) alterations in cancer-d
Improving the prediction of the functional impact of cancer mutations by baseline tolerance transformation
Abel Gonzalez-Perez, Jordi Deu-Pons, Nuria Lopez-Bigas
Genome Medicine , 2012, DOI: 10.1186/gm390
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