Putative cis-regulatory drivers in colorectal cancer

Halit Ongen (), Claus L. Andersen, Jesper B. Bramsen, Bodil Oster, Mads H. Rasmussen, Pedro G. Ferreira, Juan Sandoval, Enrique Vidal, Nicola Whiffin, Alexandra Planchon, Ismael Padioleau, Deborah Bielser, Luciana Romano, Ian Tomlinson, Richard S. Houlston, Manel Esteller, Torben F. Orntoft and Emmanouil T. Dermitzakis ()
Additional contact information
Halit Ongen: University of Geneva Medical School, 1211 Geneva, Switzerland
Claus L. Andersen: Aarhus University Hospital, 8000 Aarhus, Denmark
Jesper B. Bramsen: Aarhus University Hospital, 8000 Aarhus, Denmark
Bodil Oster: Aarhus University Hospital, 8000 Aarhus, Denmark
Mads H. Rasmussen: Aarhus University Hospital, 8000 Aarhus, Denmark
Pedro G. Ferreira: University of Geneva Medical School, 1211 Geneva, Switzerland
Juan Sandoval: Cancer Epigenetics and Biology Program (PEBC), Bellvitge Biomedical Research Institute (IDIBELL)
Enrique Vidal: Cancer Epigenetics and Biology Program (PEBC), Bellvitge Biomedical Research Institute (IDIBELL)
Nicola Whiffin: The Institute of Cancer Research
Alexandra Planchon: University of Geneva Medical School, 1211 Geneva, Switzerland
Ismael Padioleau: University of Geneva Medical School, 1211 Geneva, Switzerland
Deborah Bielser: University of Geneva Medical School, 1211 Geneva, Switzerland
Luciana Romano: University of Geneva Medical School, 1211 Geneva, Switzerland
Ian Tomlinson: Wellcome Trust Centre for Human Genetics, Roosevelt Drive, Oxford OX3 7BN, UK
Richard S. Houlston: The Institute of Cancer Research
Manel Esteller: Cancer Epigenetics and Biology Program (PEBC), Bellvitge Biomedical Research Institute (IDIBELL)
Torben F. Orntoft: Aarhus University Hospital, 8000 Aarhus, Denmark
Emmanouil T. Dermitzakis: University of Geneva Medical School, 1211 Geneva, Switzerland

Nature, 2014, vol. 512, issue 7512, 87-90

Abstract: Examination of allele-specific expression identifies 71 genes with excess somatic cis-regulatory effects in colorectal cancer (CRC), and 1,693 and 948 expression quantitative trait loci (eQTLs) in normal samples and tumours, respectively (with 36% of tumour eQTLs exclusive to CRC); tumour-specific eQTLs are more enriched for low CRC genome-wide association study P values and accumulate more somatic mutations than shared eQTLs, suggesting a role as germline-derived cancer regulatory drivers.

Date: 2014
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DOI: 10.1038/nature13602

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