Oncogenic drivers in 11q13 associated with prognosis and response to therapy in advanced oropharyngeal carcinomas

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorBARROS-FILHO, M. C.
dc.contributor.authorREIS-ROSA, L. A.
dc.contributor.authorHATAKEYAMA, M.
dc.contributor.authorMARCHI, F. A.
dc.contributor.authorCHULAM, T.
dc.contributor.authorSCAPULATEMPO-NETO, C.
dc.contributor.authorNICOLAU, U. R.
dc.contributor.authorCARVALHO, A. L.
dc.contributor.authorPINTO, C. A. L.
dc.contributor.authorDRIGO, S. A.
dc.contributor.authorKOWALSKI, L. P.
dc.contributor.authorROGATTO, S. R.
dc.date.accessioned2018-09-13T15:35:21Z
dc.date.available2018-09-13T15:35:21Z
dc.date.issued2018
dc.description.abstractObjectives: To identify potential molecular drivers associated with prognosis and response to treatment in advanced oropharyngeal squamous cell carcinomas (OPSCC). Materials and methods: Thirty-three OPSCC biopsies from untreated Brazilian patients were evaluated for human papilloma virus genotyping, genome wide copy number alterations and gene expression profiling. Data were integrated using CONEXIC algorithm. Validation with TCGA dataset and confirmation by RT-qPCR of candidate genes were performed. Results: High-risk HPV positive cases, detected in 55% of advanced OPSCC, were associated with better outcome. Losses of 8p11.23-p11.22, 14q11.1-q11.2 and 15q11.2, and gains of 11q13.2 and 11q13.2-q13.3 were detected as recurrent alterations. Gains of 3q26.31 and 11q13.2 and losses of 9p21.3 were exclusively detected in HPV-negative tumors. Two clusters of expression profiles were observed, being one composed mostly by HPV positive cases (83%). HPV-positive enriched cluster showed predominantly immune response-related pathways. Integrative analysis identified 10 modulators mapped in 11q13, which were frequently cancer-related. These 10 genes showed copy number gains, overexpression and an association with worse survival, further validated by TCGA database analyses. Overexpression of four genes (ORAOV1, CPT1A, SHANK2 and PPFIA1) evaluated by RT-qPCR confirmed their association with poor survival. Multivariate analysis showed that PPFIA1 overexpression and HPV status are independent prognostic markers. Moreover, SHANK2 overexpression was significantly associated with incomplete response to treatment. Conclusion: The integrative genomic and transcriptomic data revealed potential driver genes mapped in 11q13 associated with worse prognosis and response to treatment, giving fundamentals for the identification of novel therapeutic targets in OPSCC.
dc.description.indexMEDLINE
dc.description.sponsorshipNational Institute of Science and Technology in Oncogenomics [2008/57887-9, 573589/08-9]
dc.identifier.citationORAL ONCOLOGY, v.83, p.81-90, 2018
dc.identifier.doi10.1016/j.oraloncology.2018.06.010
dc.identifier.eissn1879-0593
dc.identifier.issn1368-8375
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/28512
dc.language.isoeng
dc.publisherELSEVIER SCIENCE BV
dc.relation.ispartofOral Oncology
dc.rightsrestrictedAccess
dc.rights.holderCopyright ELSEVIER SCIENCE BV
dc.subjectOropharyngeal cancer
dc.subjectDriver alterations
dc.subjectHuman papilloma virus
dc.subjectPrognostic factors
dc.subjectPredictive factors
dc.subjectTranscriptome profiling
dc.subjectArray comparative genomic hybridization
dc.subjectReverse transcriptase polymerase chain reaction
dc.subject.othersquamous-cell carcinoma
dc.subject.otherhuman-papillomavirus
dc.subject.othergenomic characterization
dc.subject.otherpoor-prognosis
dc.subject.otherneck-cancer
dc.subject.otherglobal incidence
dc.subject.otherincidence rates
dc.subject.otheroral-cavity
dc.subject.otherhead
dc.subject.othersurvival
dc.subject.wosOncology
dc.subject.wosDentistry, Oral Surgery & Medicine
dc.titleOncogenic drivers in 11q13 associated with prognosis and response to therapy in advanced oropharyngeal carcinomas
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.affiliation.countryDinamarca
hcfmusp.affiliation.countryisodk
hcfmusp.author.externalBARROS-FILHO, M. C.:AC Camargo Canc Ctr, Int Res Ctr CIPE, Sao Paulo, Brazil
hcfmusp.author.externalHATAKEYAMA, M.:AC Camargo Canc Ctr, Int Res Ctr CIPE, Sao Paulo, Brazil
hcfmusp.author.externalMARCHI, F. A.:AC Camargo Canc Ctr, Int Res Ctr CIPE, Sao Paulo, Brazil
hcfmusp.author.externalCHULAM, T.:AC Camargo Canc Ctr, Dept Head & Neck Surg & Otorhinolaryngol, Sao Paulo, Brazil
hcfmusp.author.externalSCAPULATEMPO-NETO, C.:Mol Oncol Res Ctr, Barretos, Brazil; Diagnost Amer DASA, Sao Paulo, Brazil
hcfmusp.author.externalNICOLAU, U. R.:AC Camargo Canc Ctr, Dept Oncol, Sao Paulo, Brazil
hcfmusp.author.externalCARVALHO, A. L.:Barretos Canc Hosp, Dept Head & Neck Surg, Barretos, Brazil
hcfmusp.author.externalPINTO, C. A. L.:AC Camargo Canc Ctr, Dept Pathol, Sao Paulo, Brazil
hcfmusp.author.externalDRIGO, S. A.:UNESP, Sch Med, Dept Surg & Orthoped, Botucatu, SP, Brazil; UNESP, Sch Vet Med & Anim Sci, Dept Vet Clin, Botucatu, SP, Brazil
hcfmusp.author.externalKOWALSKI, L. P.:AC Camargo Canc Ctr, Dept Head & Neck Surg & Otorhinolaryngol, Sao Paulo, Brazil; Natl Inst Sci & Technol Oncogen INCiTO, Sao Paulo, Brazil
hcfmusp.author.externalROGATTO, S. R.:Natl Inst Sci & Technol Oncogen INCiTO, Sao Paulo, Brazil; Univ Southern Denmark, Inst Reg Hlth Res, Vejle Hosp, Dept Clin Genet, Beriderbakken 4, DK-7100 Vejle, Denmark
hcfmusp.citation.scopus19
hcfmusp.contributor.author-fmusphcLUCIANA REIS ROSA SACOMAN
hcfmusp.description.beginpage81
hcfmusp.description.endpage90
hcfmusp.description.volume83
hcfmusp.origemWOS
hcfmusp.origem.pubmed30098783
hcfmusp.origem.scopus2-s2.0-85048574033
hcfmusp.origem.wosWOS:000441086600012
hcfmusp.publisher.cityAMSTERDAM
hcfmusp.publisher.countryNETHERLANDS
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