Article
Recurrent mechanisms of biallelic epigenetic inactivation reveal new putative tumour suppressor genes in prostate cancer.
Nature communications - 9 Sept 2026
Kiriy Daria, Favero Francesco, Gerhäuser Clarissa, Heilmann Jessica, Lutsik Pavlo, Gonzalez Francisco German Rodriguez, Locallo Alessio, Jespersen Jakob Schmidt, Gruber Andreas J, Olsen Andre V, Hernando Barbara, Cheng Kevin Cl, Pellegrina Diogo, Macintyre Geoff, Bova G Steven, Brewer Daniel S, Bristow Robert G, Brook Mark N, Brors Benedikt, Butler Adam, Cancel-Tassin Géraldine, Corcoran Niall M, Cussenot Olivier, Eeles Ros A, Gihawi Abraham, Girma Etsehiwot G, Gnanapragasam Vincent J, Hamid Anis, Hayes Vanessa M, He Housheng Hansen, Hovens Christopher M, Imada Eddie L, Jakobsdottir G Maria, Jung Chol-Hee, Khani Francesca, Kote-Jarai Zsofia, Lamy Philippe P, Leeman Gregory, Loda Massimo, Marchionni Luigi, Molania Ramyar, Papenfuss Anthony T, Pope Bernard, Queiroz Lucio R, Rausch Tobias, Robinson Brian, Sahli Atef, Sørensen Karina D, Uhrig Sebastian, Wedge David C, Xu Yaobo, Yamaguchi Takafumi N, Zanettini Claudio, Cooper Colin S, Schlomm Thorsten, Reimand Jüri, Weischenfeldt Joachim
Abstract excerpt
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 develop Epi2Hit, an integrative computational method that leverages whole genome sequencing, epigenomic profiling...
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