Mitochondrial mutations drive prostate cancer aggression

Julia F. Hopkins (), Veronica Y. Sabelnykova, Joachim Weischenfeldt, Ronald Simon, Jennifer A. Aguiar, Rached Alkallas, Lawrence E. Heisler, Junyan Zhang, John D. Watson, Melvin L. K. Chua, Michael Fraser, Francesco Favero, Chris Lawerenz, Christoph Plass, Guido Sauter, John D. McPherson, Theodorus Kwast, Jan Korbel, Thorsten Schlomm, Robert G. Bristow () and Paul C. Boutros ()
Additional contact information
Julia F. Hopkins: Ontario Institute for Cancer Research
Veronica Y. Sabelnykova: Ontario Institute for Cancer Research
Joachim Weischenfeldt: European Molecular Biology Laboratory
Ronald Simon: University Medical Center Hamburg-Eppendorf
Jennifer A. Aguiar: Ontario Institute for Cancer Research
Rached Alkallas: Ontario Institute for Cancer Research
Lawrence E. Heisler: Ontario Institute for Cancer Research
Junyan Zhang: University Health Network
John D. Watson: Ontario Institute for Cancer Research
Melvin L. K. Chua: University Health Network
Michael Fraser: University Health Network
Francesco Favero: Biotech Research & Innovation Centre (BRIC) and Finsen Laboratory
Chris Lawerenz: German Cancer Research Center
Christoph Plass: German Cancer Research Center
Guido Sauter: University Medical Center Hamburg-Eppendorf
John D. McPherson: Ontario Institute for Cancer Research
Theodorus Kwast: Toronto General Hospital/University Health Network
Jan Korbel: European Molecular Biology Laboratory
Thorsten Schlomm: University Medical Center Hamburg-Eppendorf
Robert G. Bristow: University Health Network
Paul C. Boutros: Ontario Institute for Cancer Research

Nature Communications, 2017, vol. 8, issue 1, 1-8

Abstract: Abstract Nuclear mutations are well known to drive tumor incidence, aggression and response to therapy. By contrast, the frequency and roles of mutations in the maternally inherited mitochondrial genome are poorly understood. Here we sequence the mitochondrial genomes of 384 localized prostate cancer patients, and identify a median of one mitochondrial single-nucleotide variant (mtSNV) per patient. Some of these mtSNVs occur in recurrent mutational hotspots and associate with aggressive disease. Younger patients have fewer mtSNVs than those who diagnosed at an older age. We demonstrate strong links between mitochondrial and nuclear mutational profiles, with co-occurrence between specific mutations. For example, certain control region mtSNVs co-occur with gain of the MYC oncogene, and these mutations are jointly associated with patient survival. These data demonstrate frequent mitochondrial mutation in prostate cancer, and suggest interplay between nuclear and mitochondrial mutational profiles in prostate cancer.

Date: 2017
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DOI: 10.1038/s41467-017-00377-y

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