A genetic basis for the variation in the vulnerability of cancer to DNA damage

Brian D. Yard, Drew J. Adams, Eui Kyu Chie, Pablo Tamayo, Jessica S. Battaglia, Priyanka Gopal, Kevin Rogacki, Bradley E. Pearson, James Phillips, Daniel P. Raymond, Nathan A. Pennell, Francisco Almeida, Jaime H. Cheah, Paul A. Clemons, Alykhan Shamji, Craig D. Peacock, Stuart L. Schreiber, Peter S. Hammerman and Mohamed E. Abazeed ()
Additional contact information
Brian D. Yard: Cleveland Clinic
Drew J. Adams: Case Western Reserve University
Eui Kyu Chie: Cleveland Clinic
Pablo Tamayo: Broad Institute of MIT and Harvard
Jessica S. Battaglia: Cleveland Clinic
Priyanka Gopal: Cleveland Clinic
Kevin Rogacki: Cleveland Clinic
Bradley E. Pearson: Dana-Farber Cancer Institute
James Phillips: Cleveland Clinic
Daniel P. Raymond: Cleveland Clinic
Nathan A. Pennell: Cleveland Clinic
Francisco Almeida: Cleveland Clinic
Jaime H. Cheah: Broad Institute of MIT and Harvard
Paul A. Clemons: Broad Institute of MIT and Harvard
Alykhan Shamji: Broad Institute of MIT and Harvard
Craig D. Peacock: Cleveland Clinic
Stuart L. Schreiber: Broad Institute of MIT and Harvard
Peter S. Hammerman: Broad Institute of MIT and Harvard
Mohamed E. Abazeed: Cleveland Clinic

Nature Communications, 2016, vol. 7, issue 1, 1-14

Abstract: Abstract Radiotherapy is not currently informed by the genetic composition of an individual patient’s tumour. To identify genetic features regulating survival after DNA damage, here we conduct large-scale profiling of cellular survival after exposure to radiation in a diverse collection of 533 genetically annotated human tumour cell lines. We show that sensitivity to radiation is characterized by significant variation across and within lineages. We combine results from our platform with genomic features to identify parameters that predict radiation sensitivity. We identify somatic copy number alterations, gene mutations and the basal expression of individual genes and gene sets that correlate with the radiation survival, revealing new insights into the genetic basis of tumour cellular response to DNA damage. These results demonstrate the diversity of tumour cellular response to ionizing radiation and establish multiple lines of evidence that new genetic features regulating cellular response after DNA damage can be identified.

Date: 2016
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11428

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DOI: 10.1038/ncomms11428

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