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Recurrent mechanisms of biallelic epigenetic inactivation reveal new putative tumour suppressor genes in prostate cancer.

Daria Kiriy, Francesco Favero, Clarissa Gerhäuser, Jessica Heilmann, Pavlo Lutsik, Francisco German Rodriguez Gonzalez, Alessio Locallo, Jakob Schmidt Jespersen, Andreas J Gruber, Andre V Olsen, Barbara Hernando, Kevin Cl Cheng, Diogo Pellegrina, Geoff Macintyre, G Steven Bova, Daniel S Brewer, Robert G Bristow, Mark N Brook, Benedikt Brors, Adam Butler, Géraldine Cancel-Tassin, Niall M Corcoran, Olivier Cussenot, Ros A Eeles, Abraham Gihawi, Etsehiwot G Girma, Vincent J Gnanapragasam, Anis Hamid, Vanessa M Hayes, Housheng Hansen He, Christopher M Hovens, Eddie L Imada, G Maria Jakobsdottir, Chol-Hee Jung, Francesca Khani, Zsofia Kote-Jarai, Philippe P Lamy, Gregory Leeman, Massimo Loda, Luigi Marchionni, Ramyar Molania, Anthony T Papenfuss, Bernard Pope, Lucio R Queiroz, Tobias Rausch, Brian Robinson, Atef Sahli, Karina D Sørensen, Sebastian Uhrig, David C Wedge, Yaobo Xu, Takafumi N Yamaguchi, Claudio Zanettini, Pan Prostate Cancer Group (PPCG), Colin S Cooper, Thorsten Schlomm, Jüri Reimand, Joachim Weischenfeldt

Nature communicationsSep 9, 2026PMID 42716948doi:10.1038/s41467-026-72182-5 Journal ArticlepubmedProvenance
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PubMed
Retrieved
Sep 11, 2026
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normalized (units and labels harmonized; values unchanged)
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ING-PUBMED-20260911-000001
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The inactivation of tumour suppressor genes is a key step in cancer development, and is usually achieved by homozygous loss. In prostate cancer, however, large genomic regions are often hemizygously lost, which complicates the identification of putative tumour suppressors in these regions. Here, we…

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