Nature Communications (Aug 2017)
Synthetic lethality between androgen receptor signalling and the PARP pathway in prostate cancer
- Mohammad Asim,
- Firas Tarish,
- Heather I. Zecchini,
- Kumar Sanjiv,
- Eleni Gelali,
- Charles E. Massie,
- Ajoeb Baridi,
- Anne Y. Warren,
- Wanfeng Zhao,
- Christoph Ogris,
- Leigh-Anne McDuffus,
- Patrice Mascalchi,
- Greg Shaw,
- Harveer Dev,
- Karan Wadhwa,
- Paul Wijnhoven,
- Josep V. Forment,
- Scott R. Lyons,
- Andy G. Lynch,
- Cormac O’Neill,
- Vincent R. Zecchini,
- Paul S. Rennie,
- Aria Baniahmad,
- Simon Tavaré,
- Ian G. Mills,
- Yaron Galanty,
- Nicola Crosetto,
- Niklas Schultz,
- David Neal,
- Thomas Helleday
Affiliations
- Mohammad Asim
- Cancer Research UK Institute, University of Cambridge
- Firas Tarish
- Science for Life Laboratory, Division of Translational Medicine and Chemical Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet
- Heather I. Zecchini
- Cancer Research UK Institute, University of Cambridge
- Kumar Sanjiv
- Science for Life Laboratory, Division of Translational Medicine and Chemical Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet
- Eleni Gelali
- Science for Life Laboratory, Division of Translational Medicine and Chemical Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet
- Charles E. Massie
- Cancer Research UK Institute, University of Cambridge
- Ajoeb Baridi
- Cancer Research UK Institute, University of Cambridge
- Anne Y. Warren
- Department of Pathology, Addenbrooke’s Cambridge University Hospital
- Wanfeng Zhao
- Department of Pathology, Addenbrooke’s Cambridge University Hospital
- Christoph Ogris
- Science for Life Laboratory, Division of Translational Medicine and Chemical Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet
- Leigh-Anne McDuffus
- Cancer Research UK Institute, University of Cambridge
- Patrice Mascalchi
- Cancer Research UK Institute, University of Cambridge
- Greg Shaw
- Cancer Research UK Institute, University of Cambridge
- Harveer Dev
- Cancer Research UK Institute, University of Cambridge
- Karan Wadhwa
- Cancer Research UK Institute, University of Cambridge
- Paul Wijnhoven
- The Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge
- Josep V. Forment
- The Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge
- Scott R. Lyons
- Cancer Research UK Institute, University of Cambridge
- Andy G. Lynch
- Cancer Research UK Institute, University of Cambridge
- Cormac O’Neill
- Cancer Research UK Institute, University of Cambridge
- Vincent R. Zecchini
- Cancer Research UK Institute, University of Cambridge
- Paul S. Rennie
- The Vancouver Prostate Centre, Department of Urologic Sciences, University of British Columbia
- Aria Baniahmad
- Institute of Human Genetics, Jena University Hospital
- Simon Tavaré
- Cancer Research UK Institute, University of Cambridge
- Ian G. Mills
- Centre for Molecular Medicine Norway, Nordic European Molecular Biology Laboratory Partnership, University of Oslo
- Yaron Galanty
- The Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge
- Nicola Crosetto
- Science for Life Laboratory, Division of Translational Medicine and Chemical Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet
- Niklas Schultz
- Science for Life Laboratory, Division of Translational Medicine and Chemical Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet
- David Neal
- Cancer Research UK Institute, University of Cambridge
- Thomas Helleday
- Science for Life Laboratory, Division of Translational Medicine and Chemical Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet
- DOI
- https://doi.org/10.1038/s41467-017-00393-y
- Journal volume & issue
-
Vol. 8,
no. 1
pp. 1 – 10
Abstract
Tumours with homologous recombination (HR) defects become sensitive to PARPi. Here, the authors show that androgen receptor (AR) regulates HR and AR inhibition activates the PARP pathway in vivo, thus inhibition of both AR and PARP is required for effective treatment of high risk prostate cancer.
