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Title: Molecular Subtypes in Head and Neck Cancer Exhibit Distinct Patterns of Chromosomal Gain and Loss of Canonical Cancer Genes
Authors: Walter V.
Yin X.
Wilkerson M.D.
Cabanski C.R.
Zhao N.
Du Y.
Ang M.K. 
Hayward M.C.
Salazar A.H.
Hoadley K.A.
Fritchie K.
Sailey C.G.
Weissler M.C.
Shockley W.W.
Zanation A.M.
Hackman T.
Thorne L.B.
Funkhouser W.D.
Muldrew K.L.
Olshan A.F.
Randell S.H.
Wright F.A.
Shores C.G.
Hayes D.N.
Keywords: kelch like ECH associated protein 1
protein NFE2L2
protein TP63
transcription factor Sox2
unclassified drug
cancer survival
chromosome 3q
chromosome loss
clinical feature
DNA sequence
EGFR gene
gene dosage
genetic association
genetic gain
genetic marker
genetic variability
genome analysis
head and neck cancer
lung squamous cell carcinoma
major clinical study
molecular pathology
nucleotide sequence
oxidative stress
papillomavirus infection
PIK3CA gene
recurrence free survival
Issue Date: 2013
Citation: Walter V., Yin X., Wilkerson M.D., Cabanski C.R., Zhao N., Du Y., Ang M.K., Hayward M.C., Salazar A.H., Hoadley K.A., Fritchie K., Sailey C.G., Weissler M.C., Shockley W.W., Zanation A.M., Hackman T., Thorne L.B., Funkhouser W.D., Muldrew K.L., Olshan A.F., Randell S.H., Wright F.A., Shores C.G., Hayes D.N. (2013). Molecular Subtypes in Head and Neck Cancer Exhibit Distinct Patterns of Chromosomal Gain and Loss of Canonical Cancer Genes. PLoS ONE 8 (2) : e56823. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Head and neck squamous cell carcinoma (HNSCC) is a frequently fatal heterogeneous disease. Beyond the role of human papilloma virus (HPV), no validated molecular characterization of the disease has been established. Using an integrated genomic analysis and validation methodology we confirm four molecular classes of HNSCC (basal, mesenchymal, atypical, and classical) consistent with signatures established for squamous carcinoma of the lung, including deregulation of the KEAP1/NFE2L2 oxidative stress pathway, differential utilization of the lineage markers SOX2 and TP63, and preference for the oncogenes PIK3CA and EGFR. For potential clinical use the signatures are complimentary to classification by HPV infection status as well as the putative high risk marker CCND1 copy number gain. A molecular etiology for the subtypes is suggested by statistically significant chromosomal gains and losses and differential cell of origin expression patterns. Model systems representative of each of the four subtypes are also presented. © 2013 Walter et al.
Source Title: PLoS ONE
ISSN: 19326203
DOI: 10.1371/journal.pone.0056823
Rights: Attribution 4.0 International
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