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Integrative analysis of a cancer somatic mutome
Pilar Hernández, Xavier Solé, Joan Valls, Víctor Moreno, Gabriel Capellá, Ander Urruticoechea, Miguel Pujana
Molecular Cancer , 2007, DOI: 10.1186/1476-4598-6-13
Abstract: We analyzed functional genomic data (loss of heterozygosity, copy number variation and gene expression in breast tumors) and protein binary interactions from public repositories to identify potential novel components of neoplastic processes, the functional relationships between them, and to examine their coordinated function in breast cancer pathogenesis. This analysis identified candidate tumor suppressors and oncogenes, and new genes whose expression level predicts survival rate in breast cancer patients. Mutome network modeling using different types of pathological and healthy functional relationships unveils functional modules significantly enriched in genes or proteins (genes/proteins) with related biological process Gene Ontology terms and containing known breast cancer-related genes/proteins.This study presents a comprehensive analysis of the breast somatic mutome, highlighting those genes with a higher probability of playing a determinant role in tumorigenesis and better defining molecular interactions related to the neoplastic process.Recent landmark work has described the genetic landscape of the breast and colorectal cancer genomes by identifying the collection of somatically mutated genes (cancer somatic mutome) that contributes to the neoplastic process in these cancer types [1]. Most of these genes were not previously identified as linked to human cancer and some of them encode uncharacterized proteins. A larger set of "passenger" mutations or mutations present at a frequency that is too low to determine their relationship with cancer were also identified, prompting further genetic and molecular characterization.Most biological processes involve groups of genes and proteins that behave in a coordinated way to perform a cellular function [2]. The coordinated task of genes/proteins can be represented by different types of functional relationships (e.g. gene co-expression, genetic interactions, protein binary interactions, protein complex membership) [3].
Genetic interactions: the missing links for a better understanding of cancer susceptibility, progression and treatment
Christopher A Maxwell, Víctor Moreno, Xavier Solé, Laia Gómez, Pilar Hernández, Ander Urruticoechea, Miguel Pujana
Molecular Cancer , 2008, DOI: 10.1186/1476-4598-7-4
Abstract: Most of the current knowledge of cancer susceptibility, progression and treatment has been generated by traditional approaches, in which small numbers of genes or proteins are characterized in depth to study the molecular mechanisms of neoplastic processes. With the advent of large-scale functional genomic and proteomic ("omic") methodologies, additional mechanistic insights into neoplasia have been uncovered. Whole-genome association studies for cancer risk variants and somatic mutation screening projects have completed their initial phases and will provide the "part lists" of cancer genes, both at the germline [1] and the somatic levels [2]. Transcript analyses have identified expression profiles that provide accurate prognoses for cancer patients [3]. Systematic mapping of protein-protein interactions is currently being carried out in what are referred to as 'interactome' mapping projects. This research will elucidate the wiring diagram of protein associations in cells [4,5]. These types of genes and/or protein (gene/protein) functional relationships can be modeled together to provide better understanding and predict molecular mechanisms of neoplasia [6-10].Genetic interactions are identified when the action of one gene measured through a molecular, cellular or organism phenotype is modified by one or more other genes. They provide insight into biological processes that are complementary but which frequently do not overlap with other types of gene/protein associations [11]. To date, genetic interactions remain largely unknown on a large scale in human systems. Previous reviews and assays gave excellent descriptions of the role of genetic interactions in understanding phenotypic variability [12-14]. Here, we focus our discussion on the potential of studying human genetic interactions as a means of not only better understanding cancer susceptibility and progression but also, and most importantly, developing novel anticancer treatments.The use of 'model organisms' (
Biological Convergence of Cancer Signatures
Xavier Solé, Núria Bonifaci, Núria López-Bigas, Antoni Berenguer, Pilar Hernández, Oscar Reina, Christopher A. Maxwell, Helena Aguilar, Ander Urruticoechea, Silvia de Sanjosé, Francesc Comellas, Gabriel Capellá, Víctor Moreno, Miguel Angel Pujana
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0004544
Abstract: Gene expression profiling has identified cancer prognostic and predictive signatures with superior performance to conventional histopathological or clinical parameters. Consequently, signatures are being incorporated into clinical practice and will soon influence everyday decisions in oncology. However, the slight overlap in the gene identity between signatures for the same cancer type or condition raises questions about their biological and clinical implications. To clarify these issues, better understanding of the molecular properties and possible interactions underlying apparently dissimilar signatures is needed. Here, we evaluated whether the signatures of 24 independent studies are related at the genome, transcriptome or proteome levels. Significant associations were consistently observed across these molecular layers, which suggest the existence of a common cancer cell phenotype. Convergence on cell proliferation and death supports the pivotal involvement of these processes in prognosis, metastasis and treatment response. In addition, functional and molecular associations were identified with the immune response in different cancer types and conditions that complement the contribution of cell proliferation and death. Examination of additional, independent, cancer datasets corroborated our observations. This study proposes a comprehensive strategy for interpreting cancer signatures that reveals common design principles and systems-level properties.
A novel inhibitor of fatty acid synthase shows activity against HER2+ breast cancer xenografts and is active in anti-HER2 drug-resistant cell lines
Teresa Puig, Helena Aguilar, Sílvia Cufí, Glòria Oliveras, Carlos Turrado, Sílvia Ortega-Gutiérrez, Bellinda Benhamú, María López-Rodríguez, Ander Urruticoechea, Ramon Colomer
Breast Cancer Research , 2011, DOI: 10.1186/bcr3077
Abstract: In a xenograft model of breast carcinoma cells that are FASN+ and HER2+, we have characterised the anticancer activity and the toxicity profile of G28UCM, the lead compound of a novel family of synthetic FASN inhibitors. In vitro, we analysed the cellular and molecular interactions of combining G28UCM with anti-HER drugs. Finally, we tested the cytotoxic ability of G28UCM on breast cancer cells resistant to trastuzumab or lapatinib, that we developed in our laboratory.In vivo, G28UCM reduced the size of 5 out of 14 established xenografts. In the responding tumours, we observed inhibition of FASN activity, cleavage of poly-ADPribose polymerase (PARP) and a decrease of p-HER2, p- protein kinase B (AKT) and p-ERK1/2, which were not observed in the nonresponding tumours. In the G28UCM-treated animals, no significant toxicities occurred, and weight loss was not observed. In vitro, G28UCM showed marked synergistic interactions with trastuzumab, lapatinib, erlotinib or gefitinib (but not with cetuximab), which correlated with increases in apoptosis and with decreases in the activation of HER2, extracellular signal-regulated kinase (ERK)1/2 and AKT. In trastuzumab-resistant and in lapatinib-resistant breast cancer cells, in which trastuzumab and lapatinib were not effective, G28UCM retained the anticancer activity observed in the parental cells.G28UCM inhibits fatty acid synthase (FASN) activity and the growth of breast carcinoma xenografts in vivo, and is active in cells with acquired resistance to anti-HER2 drugs, which make it a candidate for further pre-clinical development.Fatty acid synthase (FASN) is a multifunctional enzyme that is essential for the endogenous synthesis of long-chain fatty acids from its precursors acetyl-CoA and malonil-CoA [1]. Blocking FASN activity causes cytotoxicity in human cancer cells overexpressing FASN [2-13]. The proposed oncogenic properties of FASN seem to be the result of an increased activation of HER2 and its downstream related phos
Molecular response to aromatase inhibitor treatment in primary breast cancer
Alan Mackay, Ander Urruticoechea, J Michael Dixon, Tim Dexter, Kerry Fenwick, Alan Ashworth, Suzanne Drury, Alexey Larionov, Oliver Young, Sharon White, William R Miller, Dean B Evans, Mitch Dowsett
Breast Cancer Research , 2007, DOI: 10.1186/bcr1732
Abstract: We randomly assigned primary estrogen receptor positive breast cancer patients to treatment with anastrozole or letrozole for 2 weeks before surgery. Expression profiling using cDNA arrays was conducted on pretreatment and post-treatment biopsies. Sample pairs from 34 patients provided sufficient RNA for analysis.Profound changes in gene expression were seen with both aromatase inhibitors, including many classical estrogen-dependent genes such as TFF1, CCND1, PDZK1 and AGR2, but also many other genes that are likely to represent secondary responses; decrease in the expression of proliferation-related genes were particularly prominent. Many upregulated genes are involved in extracellular matrix remodelling, including collagens and members of the small leucine-rich proteoglycan family (LUM, DCN, and ASPN). No significant differences were seen between letrozole and anastrozole in terms of molecular effects. The gene changes were integrated into a Global Index of Dependence on Estrogen (GIDE), which enumerates the genes changing by at least twofold with therapy. The GIDE varied markedly between tumours and related significantly to pretreatment levels of HER2 and changes in immunohistochemically detected Ki67.Our findings identify the transcriptional signatures associated with aromatase inhibitor treatment of primary breast tumours. Larger datasets using this approach should enable identification of estrogen-dependent molecular changes, which are the determinants of benefit or resistance to endocrine therapy.Approaching 80% of human breast carcinomas express estrogen receptor (ER)-α protein at clinically significant levels and are considered ER positive. Estrogen deprivation, or antagonism, is an effective treatment for many but not all patients with such tumours. The selective ER modifier tamoxifen has been the predominant treatment for the past two decades and improves survival in ER-positive patients receiving this as adjuvant therapy after surgery [1]. However, in po
Strategies for Human Adipose Tissue Repair and Regeneration  [PDF]
Asun Monfort, Ander Izeta
Journal of Cosmetics, Dermatological Sciences and Applications (JCDSA) , 2012, DOI: 10.4236/jcdsa.2012.222021
Abstract: In plastic and reconstructive surgery there is an increasing demand for malleable implants to repair soft tissue congenital defects, or those resulting from aging, traumatic injury and tumour resection. However, currently available methods present a number of limitations such as volume loss over time and eventual resorption of the graft. Tissue engineering techniques provide promising therapeutic solutions to these inconveniences through development of engineered equivalents that best imitate adipose tissue, both structurally and functionally. Here we review the latest achievements in the human adipose tissue engineering field, with a focus on its regenerative potential for a number of clinical applications.
Etniker Bizkaia. Publicación del Departamento de Etnografía del Instituto Labayru-Bilbao
Manterola, Ander
Revista de Dialectología y Tradiciones Populares , 2002,
Abstract: One of the products of José Miguel de Barandiarán's teaching and popularization of Basque ethnography, the journal Etniker Bizkaia contains the field studies and methodological guides of the research team who works in Biscay as part of a project aiming for the Ethnographic Atlas of the Basque Country. Uno de los productos de la labor docente y divulgadora de la etnografía vasca, llevada a cabo por José Miguel de Barandiarán, es la revista Etniker Bizkaia que recoge los trabajos de campo y las guías metodológicas creadas por los miembros del equipo investigador que trabaja en la zona de Vizcaya, dentro del proyecto del Atlas Etnográfico de Vasconia.
La Partición de la Casa en Instituciones Consuetudinarias.
Ander Manterola
Munibe Antropologia-Arkeologia , 1990,
Abstract: El trabajo estudia el papel que ha desempe ado la casa tradicional en la estructura de dos instituciones: la Cofradía y el Municipio, tal como se manifiestan en el área interior de Bizcaia, País Vasco. En ambas se utiliza un antiguo sinónimo de casa, Foguera, en acepción jurídica, para expresar que es precisamente la casa una unidad de participación, tanto en la antigua institución pública, como en las actuales instituciones consuetudinarias.
Gurrutxaga, Ander
Arbor : Ciencia, Pensamiento y Cultura , 2011,
Politiques publiques, entre action et autorité.
Ander Audikana
EspacesTemps.net , 2008,
Abstract: Après celle de 2003, cette deuxième édition vient confirmer que l’objectif pédagogique (p. 1) de l’ouvrage de Gilles Massardier a été atteint. La critique souvent adressée à ce type d’exercice de mise au point d’une discipline particulière est qu’il hésite entre la simplification excessive et le caractère encyclopédique. Il y aurait trop peu ou bien beaucoup trop. Les autres manuels fran ais dans le champ de l’analyse des politiques publiques sont d’abord ...
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