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http://purl.uniprot.org/citations/15983384http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15983384http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15983384http://www.w3.org/2000/01/rdf-schema#comment"Lung cancer is the leading cause of cancer mortality worldwide, yet there exists a limited view of the genetic lesions driving this disease. In this study, an integrated high-resolution survey of regional amplifications and deletions, coupled with gene-expression profiling of non-small-cell lung cancer subtypes, adenocarcinoma and squamous-cell carcinoma (SCC), identified 93 focal copy-number alterations, of which 21 span <0.5 megabases and contain a median of five genes. Whereas all known lung cancer genes/loci are contained in the dataset, most of these recurrent copy-number alterations are previously uncharacterized and include high-amplitude amplifications and homozygous deletions. Notably, despite their distinct histopathological phenotypes, adenocarcinoma and SCC genomic profiles showed a nearly complete overlap, with only one clear SCC-specific amplicon. Among the few genes residing within this amplicon and showing consistent overexpression in SCC is p63, a known regulator of squamous-cell differentiation. Furthermore, intersection with the published pancreatic cancer comparative genomic hybridization dataset yielded, among others, two focal amplicons on 8p12 and 20q11 common to both cancer types. Integrated DNA-RNA analyses identified WHSC1L1 and TPX2 as two candidates likely targeted for amplification in both pancreatic ductal adenocarcinoma and non-small-cell lung cancer."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.org/dc/terms/identifier"doi:10.1073/pnas.0504126102"xsd:string
http://purl.uniprot.org/citations/15983384http://purl.org/dc/terms/identifier"doi:10.1073/pnas.0504126102"xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Zhang Y."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Zhang Y."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Yang Z."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Yang Z."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Wong K.-K."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Wong K.-K."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Depinho R.A."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Depinho R.A."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Feng B."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Feng B."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Ji H."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Ji H."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Chin L."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Chin L."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Protopopov A."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Protopopov A."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"You M.J."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"You M.J."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Tonon G."xsd:string
http://purl.uniprot.org/citations/15983384http://purl.uniprot.org/core/author"Tonon G."xsd:string