BUSCADOR RECOLECTA

Oncodrive-CIS is a method aimed to identify those copy number alterations (CNAs) leading to larger in cis expression changes that may be useful in elucidating the role of these aberrations in cancer. This is based on the hypothesis that a gene driving oncogenesis through copy number changes is more prone to bias towards overexpression (or underexpression) as compared to bystanders. The effect of the gene dosage is assessed by observing expression changes not only among tumors but also taking into account normal samples data, when available./nOncodrive-CIS has several potential benefits: first, it did not examine the frequency of the CNAs across samples and therefore the detection of low-recurrent driver alterations was not impaired. Second, amplifications and deletions were evaluated separately to obtain a fair ranking of genes, because the expression change measured in deletions was lower than the one obtained from multi-copy amplifications. Third, the expression of genes in tumor samples was analyzed according to the copy number status but was also compared to normal samples, thus better revealing the gene misregulation role of CNAs in cancer cells. And finally, it should be emphasized that the relationship between expression changes and their functional impact is complex, thus Oncodrive-CIS is proposed as a method to elucidate the role of CNAs in cancer which may be complementary to analyses based on other criteria.

The aim of SVGMap is helping in the visualisation of experimental data which are associated with some graphical representation. Thus SVGMap browser allows to generate images with colored areas corresponding to the chosen data and color scale./nThe data is represented as a table and is searchable. All data as well as the generated images/figures can be exported easily through the interface./nAdditionally the tool allows to manage (add, edit or delete) experiments and configure the front-end user search appearance such as the number of images to be displayed, the scale types to use and more.

The cyclin-cdk (cyclin-dependent kinase) inhibitor p27(Kip1) (p27) has a crucial negative role on cell cycle progression. In addition to its classical role as a cyclin-cdk inhibitor, it also performs cyclin-cdk-independent functions as the regulation of cytoskeleton rearrangements and cell motility. p27 deficiency has been associated with tumor aggressiveness and poor clinical outcome, although the mechanisms underlying this participation still remain elusive. We report here a new cellular function of p27 as a transcriptional regulator in association with p130/E2F4 complexes that could be relevant for tumorigenesis. We observed that p27 associates with specific promoters of genes involved in important cellular functions as processing and splicing of RNA, mitochondrial organization and respiration, translation and cell cycle. On these promoters p27 co-localizes with p130, E2F4 and co-repressors as histone deacetylases (HDACs) and mSIN3A. p27 co-immunoprecipitates with these proteins and by affinity chromatography, we demonstrated a direct interaction of p27 with p130 and E2F4 through its carboxyl-half. We have also shown that p130 recruits p27 on the promoters, and there p27 is needed for the subsequent recruitment of HDACs and mSIN3A. Expression microarrays and luciferase assays revealed that p27 behaves as transcriptional repressor of these p27-target genes (p27-TGs). Finally, in human tumors, we established a correlation with overexpression of p27-TGs and poor survival. Thus, this new function of p27 as a transcriptional repressor could have a role in the major aggressiveness of tumors with low levels of p27.

Genome-wide analysis of the H3K4 histone demethylase RBP2 reveals a transcriptional program controlling differentiation.

Cancer gene properties.

Web tool for the selection of SNPs from the STAR project with potential functional effect. Més informació: funcSTAR (web) http://bg.upf.edu/funcSTAR/

Mutations, genes and pathways involved in tumorigenesis across 4,623 cancer genomes/exomes from 13 cancer sites. 1 SQL (Structured Query Language) file and 1 WAR (Web application ARchive) file.

Database of human genes prioritized for their probability of involvement in dominant or recessive hereditary diseases.

This database contains information on the genes identified as drivers in Rubio-Perez and Tamborero et al. (2015). It contains information on driver identification at mutational, CNA and gene fusion level. Additional ancillary information about the role and major clonality of drivers is also included. A table is also provided with the list of datasets used for mutational driver identification.

This file lists the High Confidence Drivers identified as part of the pan-cancer12 initiative, published in the paper Comprehensive identification of mutational cancer driver genes across 12 tumor types" Scientific Reports 3:2650, 2013, doi:10.1038/srep02650