BackgroundIn recent years, increasing amounts of genomic and clinical cancer data have become publically available through large-scale collaborative projects such as The Cancer Genome Atlas (TCGA). However, as long as these datasets are difficult to access and interpret, they are essentially useless for a major part of the research community and their scientific potential will not be fully realized. To address these issues we developed MEXPRESS, a straightforward and easy-to-use web tool for the integration and visualization of the expression, DNA methylation and clinical TCGA data on a single-gene level (http://mexpress.be).ResultsIn comparison to existing tools, MEXPRESS allows researchers to quickly visualize and interpret the different TCGA datasets and their relationships for a single gene, as demonstrated for GSTP1 in prostate adenocarcinoma. We also used MEXPRESS to reveal the differences in the DNA methylation status of the PAM50 marker gene MLPH between the breast cancer subtypes and how these differences were linked to the expression of MPLH.ConclusionsWe have created a user-friendly tool for the visualization and interpretation of TCGA data, offering clinical researchers a simple way to evaluate the TCGA data for their genes or candidate biomarkers of interest.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-015-1847-z) contains supplementary material, which is available to authorized users.

The recent growth in the number of publicly available cancer omics databases has been accompanied by the development of various tools that allow researchers to visually explore these data. In 2015, we built MEXPRESS, an online tool for the integration and visualization of gene expression, DNA methylation and clinical data from The Cancer Genome Atlas (TCGA), a large collection of publicly available multi-omics cancer data. MEXPRESS addresses the need for an easy-to-use, interactive application that allows researchers to identify dysregulated genes and their clinical relevance in cancer. Furthermore, while other tools typically do not support integrated visualization of expression and DNA methylation data in combination with the precise genomic location of the methylation, MEXPRESS is unique in how it depicts these diverse data types together. Motivated by the large number of users MEXPRESS has managed to attract over the past 3 years and the recent migration of all TCGA data to a new data portal, we developed a new version of MEXPRESS (https://mexpress.be). It contains the latest TCGA data, additional types of omics and clinical data and extra functionality, allowing users to explore mechanisms of gene dysregulation beyond expression and DNA methylation.

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Purpose: The importance of genetic and epigenetic alterations maybe in their aggregate role in altering core pathways in tumorigenesis.Experimental Design: Merging genome-wide genomic and epigenomic alterations, we identify key genes and pathways altered in colorectal cancers (CRC). DNA methylation analysis was tested for predicting survival in CRC patients using Cox proportional hazard model.Results: We identified 29 low frequency-mutated genes that are also inactivated by epigenetic mechanisms in CRC. Pathway analysis showed the extracellular matrix (ECM) remodeling pathway is silenced in CRC. Six ECM pathway genes were tested for their prognostic potential in large CRC cohorts (n ¼ 777). DNA methylation of IGFBP3 and EVL predicted for poor survival (IGFBP3: HR ¼ 2.58, 95% CI: 1.37-4.87, P ¼ 0.004; EVL: HR ¼ 2.48, 95% CI: 1.07-5.74, P ¼ 0.034) and simultaneous methylation of multiple genes predicted significantly worse survival (HR ¼ 8.61, 95% CI: 2.16-34.36, P < 0.001 for methylation of IGFBP3, EVL, CD109, and FLNC). DNA methylation of IGFBP3 and EVL was validated as a prognostic marker in an independent contemporary-matched cohort (IGFBP3 HR ¼ 2.06, 95% CI: 1.04-4.09, P ¼ 0.038; EVL HR ¼ 2.23, 95% CI: 1.00-5.0, P ¼ 0.05) and EVL DNA methylation remained significant in a secondary historical validation cohort (HR ¼ 1.41, 95% CI: 1.05-1.89, P ¼ 0.022). Moreover, DNA methylation of selected ECM genes helps to stratify the high-risk stage 2 colon cancers patients who would benefit from adjuvant chemotherapy (HR: 5.85, 95% CI: 2.03-16.83, P ¼ 0.001 for simultaneous methylation of IGFBP3, EVL, and CD109).Conclusions: CRC that have silenced genes in ECM pathway components show worse survival suggesting that our finding provides novel prognostic biomarkers for CRC and reflects the high importance of integrative analyses linking genetic and epigenetic abnormalities with pathway disruption in cancer. Clin Cancer Res; 17(6); 1535-45. Ó2011 AACR.