Landscape of genomic alterations in cervical carcinomas View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-02

AUTHORS

Akinyemi I. Ojesina, Lee Lichtenstein, Samuel S. Freeman, Chandra Sekhar Pedamallu, Ivan Imaz-Rosshandler, Trevor J. Pugh, Andrew D. Cherniack, Lauren Ambrogio, Kristian Cibulskis, Bjørn Bertelsen, Sandra Romero-Cordoba, Victor Treviño, Karla Vazquez-Santillan, Alberto Salido Guadarrama, Alexi A. Wright, Mara W. Rosenberg, Fujiko Duke, Bethany Kaplan, Rui Wang, Elizabeth Nickerson, Heather M. Walline, Michael S. Lawrence, Chip Stewart, Scott L. Carter, Aaron McKenna, Iram P. Rodriguez-Sanchez, Magali Espinosa-Castilla, Kathrine Woie, Line Bjorge, Elisabeth Wik, Mari K. Halle, Erling A. Hoivik, Camilla Krakstad, Nayeli Belem Gabiño, Gabriela Sofia Gómez-Macías, Lezmes D. Valdez-Chapa, María Lourdes Garza-Rodríguez, German Maytorena, Jorge Vazquez, Carlos Rodea, Adrian Cravioto, Maria L. Cortes, Heidi Greulich, Christopher P. Crum, Donna S. Neuberg, Alfredo Hidalgo-Miranda, Claudia Rangel Escareno, Lars A. Akslen, Thomas E. Carey, Olav K. Vintermyr, Stacey B. Gabriel, Hugo A. Barrera-Saldaña, Jorge Melendez-Zajgla, Gad Getz, Helga B. Salvesen, Matthew Meyerson

ABSTRACT

Cervical cancer is responsible for 10-15% of cancer-related deaths in women worldwide. The aetiological role of infection with high-risk human papilloma viruses (HPVs) in cervical carcinomas is well established. Previous studies have also implicated somatic mutations in PIK3CA, PTEN, TP53, STK11 and KRAS as well as several copy-number alterations in the pathogenesis of cervical carcinomas. Here we report whole-exome sequencing analysis of 115 cervical carcinoma-normal paired samples, transcriptome sequencing of 79 cases and whole-genome sequencing of 14 tumour-normal pairs. Previously unknown somatic mutations in 79 primary squamous cell carcinomas include recurrent E322K substitutions in the MAPK1 gene (8%), inactivating mutations in the HLA-B gene (9%), and mutations in EP300 (16%), FBXW7 (15%), NFE2L2 (4%), TP53 (5%) and ERBB2 (6%). We also observe somatic ELF3 (13%) and CBFB (8%) mutations in 24 adenocarcinomas. Squamous cell carcinomas have higher frequencies of somatic nucleotide substitutions occurring at cytosines preceded by thymines (Tp*C sites) than adenocarcinomas. Gene expression levels at HPV integration sites were statistically significantly higher in tumours with HPV integration compared with expression of the same genes in tumours without viral integration at the same site. These data demonstrate several recurrent genomic alterations in cervical carcinomas that suggest new strategies to combat this disease. More... »

PAGES

371

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  • Journal

    TITLE

    Nature

    ISSUE

    7488

    VOLUME

    506

    Related Patents

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nature12881

    DOI

    http://dx.doi.org/10.1038/nature12881

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1052765735

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/24390348


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