title: Transcriptional profiling by sequencing of oropharyngeal cancer.
abstract: OBJECTIVE
  To compare full transcriptome expression levels of matched tumor and normal samples from patients with oropharyngeal carcinoma stratified by known tumor etiologic factors.
  
  
  METHODS
  Full transcriptome sequencing was analyzed for 10 matched tumor and normal tissue samples from patients with previously untreated oropharyngeal carcinoma. Transcriptomes were analyzed using massively parallel messenger RNA sequencing and validated using the NanoString nCounter system. Global gene expression levels were compared in samples grouped by smoking status and human papillomavirus status. This study was completed between June 10, 2010, and June 30, 2011.
  
  
  RESULTS
  Global gene expression analysis indicated tumor tissue from former smokers grouped more closely to the never smokers than the current smokers. Pathway analysis revealed alterations in the expression of genes involved in the p53 DNA damage-repair pathway, including CHEK2 and ATR, which display patterns of increased expression that is associated with human papillomavirus-negative current smokers rather than former or never smokers.
  
  
  CONCLUSIONS
  These findings support the application of messenger RNA sequencing technology as an important clinical tool for more accurately stratifying patients based on individual tumor biology with the goal of improving our understanding of tumor prognosis and treatment response, ultimately leading to individualized patient care strategies.
authors.affiliation: Division of Experimental Pathology and Laboratory Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
authors.forename: Rebecca R
authors.initials: RR
authors.lastname: Laborde
authors.forename: Vivian W
authors.initials: VW
authors.lastname: Wang
authors.forename: Todd M
authors.initials: TM
authors.lastname: Smith
authors.forename: N Eric
authors.initials: NE
authors.lastname: Olson
authors.forename: Steven M
authors.initials: SM
authors.lastname: Olsen
authors.forename: Joaquín J
authors.initials: JJ
authors.lastname: García
authors.forename: Kerry D
authors.initials: KD
authors.lastname: Olsen
authors.forename: Eric J
authors.initials: EJ
authors.lastname: Moore
authors.forename: Jan L
authors.initials: JL
authors.lastname: Kasperbauer
authors.forename: Nicole M
authors.initials: NM
authors.lastname: Tombers
authors.forename: David I
authors.initials: DI
authors.lastname: Smith
mesh_terms: D000368:Aged; D064007:Ataxia Telangiectasia Mutated Proteins; D018797:Cell Cycle Proteins / Q000235:genetics; D064447:Checkpoint Kinase 2; D004249:DNA Damage / Q000235:genetics; D004260:DNA Repair / Q000235:genetics; D005260:Female; D020869:Gene Expression Profiling; D016158:Genes, p53 / Q000235:genetics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009959:Oropharyngeal Neoplasms / Q000209:etiology / Q000235:genetics*; D030361:Papillomavirus Infections / Q000150:complications; D017346:Protein Serine-Threonine Kinases / Q000235:genetics; D012334:RNA, Neoplasm / Q000235:genetics; D015398:Signal Transduction / Q000235:genetics; D012907:Smoking / Q000009:adverse effects
chemical_list: D018797:Cell Cycle Proteins; D012334:RNA, Neoplasm; D064447:Checkpoint Kinase 2; C576597:ATR protein, human; D064007:Ataxia Telangiectasia Mutated Proteins; C578634:CHEK2 protein, human; D017346:Protein Serine-Threonine Kinases