TY - JOUR AU - Woodcock, Dan J. AU - Sahli, Atef AU - Teslo, Ruxandra AU - Bhandari, Vinayak AU - Gruber, Andreas J. AU - Ziubroniewicz, Aleksandra AU - Gundem, Gunes AU - Xu, Yaobo AU - Butler, Adam AU - Anokian, Ezequiel AU - Pope, Bernard J. AU - Jung, Chol-Hee AU - Tarabichi, Maxime AU - Dentro, Stefan AU - Farmery, J. Henry R. AU - Van Loo, Peter AU - Warren, Anne Y. AU - Gnanapragasam, Vincent AU - Hamdy, Freddie C. AU - Bova, G. Steven AU - Foster, Christopher S. AU - Neal, David E. AU - Lu, Yong-Jie AU - Kote-Jarai, Zsofia AU - Fraser, Michael AU - Bristow, Robert G. AU - Boutros, Paul C. AU - Costello, Anthony J. AU - Corcoran, Niall M. AU - Hovens, Christopher M. AU - Massie, Charlie E. AU - Lynch, Andy G. AU - Brewer, Daniel S. AU - Eeles, Rosalind A. AU - Cooper, Colin S. AU - Wedge, David C. TI - Genomic evolution shapes prostate cancer disease type JO - Cell genomics VL - 4 IS - 3 SN - 2666-979X CY - Amsterdam PB - Elsevier M1 - DKFZ-2024-02503 SP - 100511 - PY - 2024 AB - The development of cancer is an evolutionary process involving the sequential acquisition of genetic alterations that disrupt normal biological processes, enabling tumor cells to rapidly proliferate and eventually invade and metastasize to other tissues. We investigated the genomic evolution of prostate cancer through the application of three separate classification methods, each designed to investigate a different aspect of tumor evolution. Integrating the results revealed the existence of two distinct types of prostate cancer that arise from divergent evolutionary trajectories, designated as the Canonical and Alternative evolutionary disease types. We therefore propose the evotype model for prostate cancer evolution wherein Alternative-evotype tumors diverge from those of the Canonical-evotype through the stochastic accumulation of genetic alterations associated with disruptions to androgen receptor DNA binding. Our model unifies many previous molecular observations, providing a powerful new framework to investigate prostate cancer disease progression.Keywords: AR binding; cancer evolution; evotype model; evotypes; ordering; prostate cancer. LB - PUB:(DE-HGF)16 DO - DOI:10.1016/j.xgen.2024.100511 UR - https://inrepo02.dkfz.de/record/294791 ER -