<HashMap><database>biostudies-arrayexpress</database><scores/><additional><submitter>Yusuke Sato</submitter><organism>Homo sapiens</organism><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-1980</full_dataset_link><description>Gene expression in clear cell RCC was measured for 101 samples</description><repository>biostudies-arrayexpress</repository><sample_protocol>Labeling - As per manufacturer (Agilent)</sample_protocol><sample_protocol>Growth Protocol - Surgical specimens were stored in liquid nitrogen</sample_protocol><sample_protocol>Scaning - As per manufacturer (Agilent)</sample_protocol><sample_protocol>Hybridization - As per manufacturer (Agilent)</sample_protocol><sample_protocol>Nucleic Acid Extraction - Total RNA was extracted from fresh frozen tissues using RNeasy kit (Qiagen) according to the manufacturer's instructions including on-column DNase digestion. Total RNA was checked by the 2100 Agilent BioAnalyzer System (Agilent Technologies) to check for possible contamination and degradation.</sample_protocol><figure_sub>MIAME Score</figure_sub><figure_sub>Raw Data</figure_sub><figure_sub>Organization</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>Processed Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><figure_sub>Array Designs</figure_sub><data_protocol>Data Transformation - The scanned images were analyzed with Feature Extraction Software 10.5 (Agilent) using default parameters.</data_protocol><omics_type>Metabolomics</omics_type><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><pubmed_abstract>Clear-cell renal cell carcinoma (ccRCC) is the most prevalent kidney cancer and its molecular pathogenesis is incompletely understood. Here we report an integrated molecular study of ccRCC in which ≥100 ccRCC cases were fully analyzed by whole-genome and/or whole-exome and RNA sequencing as well as by array-based gene expression, copy number and/or methylation analyses. We identified a full spectrum of genetic lesions and analyzed gene expression and DNA methylation signatures and determined their impact on tumor behavior. Defective VHL-mediated proteolysis was a common feature of ccRCC, which was caused not only by VHL inactivation but also by new hotspot TCEB1 mutations, which abolished Elongin C-VHL binding, leading to HIF accumulation. Other newly identified pathways and components recurrently mutated in ccRCC included PI3K-AKT-mTOR signaling, the KEAP1-NRF2-CUL3 apparatus, DNA methylation, p53-related pathways and mRNA processing. This integrated molecular analysis unmasked new correlations between DNA methylation, gene mutation and/or gene expression and copy number profiles, enabling the stratification of clinical risks for patients with ccRCC.</pubmed_abstract><study_type>transcription profiling by array</study_type><species>Homo sapiens</species><pubmed_title>Integrated molecular analysis of clear-cell renal cell carcinoma</pubmed_title><pubmed_authors>Yusuke Sato</pubmed_authors><pubmed_authors>Sato Y, Yoshizato T, Shiraishi Y, Maekawa S, Okuno Y, Kamura T, Shimamura T, Sato-Otsubo A, Nagae G, Suzuki H, Nagata Y, Yoshida K, Kon A, Suzuki Y, Chiba K, Tanaka H, Niida A, Fujimoto A, Tsunoda T, Morikawa T, Maeda D, Kume H, Sugano S, Fukayama M, Aburatani H, Sanada M, Miyano S, Homma Y, Ogawa S.</pubmed_authors></additional><is_claimable>false</is_claimable><name>ccRCC_expression</name><description>Gene expression in clear cell RCC was measured for 101 samples</description><dates><release>2013-10-16T00:00:00Z</release><modification>2022-03-14T20:57:59.945Z</modification><creation>2022-03-14T20:57:59.945Z</creation></dates><accession>E-MTAB-1980</accession><cross_references><pubmed>23797736</pubmed><EFO>EFO_0002768</EFO></cross_references></HashMap>