FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2152858728> ?p ?o ?g. }

• W2152858728 endingPage "8821" @default.
• W2152858728 startingPage "8803" @default.
• W2152858728 abstract "Glioblastoma multiforme (GBM) is the most common and malignant primary brain tumor in adults. Decades of investigations and the recent effort of the Cancer Genome Atlas (TCGA) project have mapped many molecular alterations in GBM cells. Alterations on DNAs may dysregulate gene expressions and drive malignancy of tumors. It is thus important to uncover causal and statistical dependency between ‘effector’ molecular aberrations and ‘target’ gene expressions in GBMs. A rich collection of prior studies attempted to combine copy number variation (CNV) and mRNA expression data. However, systematic methods to integrate multiple types of cancer genomic data—gene mutations, single nucleotide polymorphisms, CNVs, DNA methylations, mRNA and microRNA expressions and clinical information—are relatively scarce. We proposed an algorithm to build ‘association modules’ linking effector molecular aberrations and target gene expressions and applied the module-finding algorithm to the integrated TCGA GBM data sets. The inferred association modules were validated by six tests using external information and datasets of central nervous system tumors: (i) indication of prognostic effects among patients; (ii) coherence of target gene expressions; (iii) retention of effector–target associations in external data sets; (iv) recurrence of effector molecular aberrations in GBM; (v) functional enrichment of target genes; and (vi) co-citations between effectors and targets. Modules associated with well-known molecular aberrations of GBM—such as chromosome 7 amplifications, chromosome 10 deletions, EGFR and NF1 mutations—passed the majority of the validation tests. Furthermore, several modules associated with less well-reported molecular aberrations—such as chromosome 11 CNVs, CD40, PLXNB1 and GSTM1 methylations, and mir-21 expressions—were also validated by external information. In particular, modules constituting trans-acting effects with chromosome 11 CNVs and cis-acting effects with chromosome 10 CNVs manifested strong negative and positive associations with survival times in brain tumors. By aligning the information of association modules with the established GBM subclasses based on transcription or methylation levels, we found each subclass possessed multiple concurrent molecular aberrations. Furthermore, the joint molecular characteristics derived from 16 association modules had prognostic power not explained away by the strong biomarker of CpG island methylator phenotypes. Functional and survival analyses indicated that immune/inflammatory responses and epithelial-mesenchymal transitions were among the most important determining processes of prognosis. Finally, we demonstrated that certain molecular aberrations uniquely recurred in GBM but were relatively rare in non-GBM glioma cells. These results justify the utility of an integrative analysis on cancer genomes and provide testable characterizations of driver aberration events in GBM." @default.
• W2152858728 created "2016-06-24" @default.
• W2152858728 creator A5020953185 @default.
• W2152858728 creator A5043166309 @default.
• W2152858728 creator A5077925107 @default.
• W2152858728 date "2013-07-31" @default.
• W2152858728 modified "2023-09-26" @default.
• W2152858728 title "An integrative characterization of recurrent molecular aberrations in glioblastoma genomes" @default.
• W2152858728 cites W1501063259 @default.
• W2152858728 cites W1817561967 @default.
• W2152858728 cites W1898862743 @default.
• W2152858728 cites W1964895626 @default.
• W2152858728 cites W1968667083 @default.
• W2152858728 cites W1973978516 @default.
• W2152858728 cites W1985498551 @default.
• W2152858728 cites W2013090484 @default.
• W2152858728 cites W2025183726 @default.
• W2152858728 cites W2036010272 @default.
• W2152858728 cites W2039697049 @default.
• W2152858728 cites W2040827479 @default.
• W2152858728 cites W2047901190 @default.
• W2152858728 cites W2054035764 @default.
• W2152858728 cites W2055573510 @default.
• W2152858728 cites W2058273097 @default.
• W2152858728 cites W2060022136 @default.
• W2152858728 cites W2073254683 @default.
• W2152858728 cites W2073759231 @default.
• W2152858728 cites W2079487111 @default.
• W2152858728 cites W2084482460 @default.
• W2152858728 cites W2085458327 @default.
• W2152858728 cites W2091060185 @default.
• W2152858728 cites W2096766502 @default.
• W2152858728 cites W2100714130 @default.
• W2152858728 cites W2105528101 @default.
• W2152858728 cites W2109761160 @default.
• W2152858728 cites W2110265246 @default.
• W2152858728 cites W2113942802 @default.
• W2152858728 cites W2117007075 @default.
• W2152858728 cites W2117692326 @default.
• W2152858728 cites W2118769864 @default.
• W2152858728 cites W2121625674 @default.
• W2152858728 cites W2123879591 @default.
• W2152858728 cites W2124007301 @default.
• W2152858728 cites W2127207254 @default.
• W2152858728 cites W2127435059 @default.
• W2152858728 cites W2128813013 @default.
• W2152858728 cites W2130410032 @default.
• W2152858728 cites W2132261436 @default.
• W2152858728 cites W2134802045 @default.
• W2152858728 cites W2138217326 @default.
• W2152858728 cites W2140301591 @default.
• W2152858728 cites W2141055671 @default.
• W2152858728 cites W2141452279 @default.
• W2152858728 cites W2146206618 @default.
• W2152858728 cites W2147714160 @default.
• W2152858728 cites W2148780239 @default.
• W2152858728 cites W2152360905 @default.
• W2152858728 cites W2156276820 @default.
• W2152858728 cites W2158217645 @default.
• W2152858728 cites W2158804744 @default.
• W2152858728 cites W2161289668 @default.
• W2152858728 cites W2161409973 @default.
• W2152858728 cites W2161433585 @default.
• W2152858728 cites W2161640106 @default.
• W2152858728 cites W2164283221 @default.
• W2152858728 cites W2166079675 @default.
• W2152858728 cites W2166898290 @default.
• W2152858728 cites W2167190345 @default.
• W2152858728 doi "https://doi.org/10.1093/nar/gkt656" @default.
• W2152858728 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3799430" @default.
• W2152858728 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23907387" @default.
• W2152858728 hasPublicationYear "2013" @default.
• W2152858728 type Work @default.
• W2152858728 sameAs 2152858728 @default.
• W2152858728 citedByCount "36" @default.
• W2152858728 countsByYear W21528587282014 @default.
• W2152858728 countsByYear W21528587282015 @default.
• W2152858728 countsByYear W21528587282016 @default.
• W2152858728 countsByYear W21528587282017 @default.
• W2152858728 countsByYear W21528587282018 @default.
• W2152858728 countsByYear W21528587282019 @default.
• W2152858728 countsByYear W21528587282020 @default.
• W2152858728 countsByYear W21528587282021 @default.
• W2152858728 countsByYear W21528587282022 @default.
• W2152858728 countsByYear W21528587282023 @default.
• W2152858728 crossrefType "journal-article" @default.
• W2152858728 hasAuthorship W2152858728A5020953185 @default.
• W2152858728 hasAuthorship W2152858728A5043166309 @default.
• W2152858728 hasAuthorship W2152858728A5077925107 @default.
• W2152858728 hasBestOaLocation W21528587281 @default.
• W2152858728 hasConcept C104317684 @default.
• W2152858728 hasConcept C120821319 @default.
• W2152858728 hasConcept C141231307 @default.
• W2152858728 hasConcept C150194340 @default.
• W2152858728 hasConcept C51785407 @default.
• W2152858728 hasConcept C54355233 @default.
• W2152858728 hasConcept C55548728 @default.
• W2152858728 hasConcept C70721500 @default.

• next