Causes of evolutionary divergence in prostate cancer
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arXiv
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2025
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| author | Esenturk, Emre Sahli, Atef Haberland, Valeriia Ziuboniewicz, Aleksandra Wirth, Christopher Bova, G. Steven Bristow, Robert G Brook, Mark N Brors, Benedikt Butler, Adam Cancel-Tassin, Géraldine Cheng, Kevin CL Cooper, Colin S Corcoran, Niall M Cussenot, Olivier Eeles, Ros A Favero, Francesco Gerhauser, Clarissa Gihawi, Abraham Girma, Etsehiwot G Gnanapragasam, Vincent J Gruber, Andreas J Hamid, Anis Hayes, Vanessa M He, Housheng Hansen Hovens, Christopher M Imada, Eddie Luidy Jakobsdottir, G. Maria Jung, Chol-hee Khani, Francesca Kote-Jarai, Zsofia Lamy, Philippe Leeman, Gregory Loda, Massimo Lutsik, Pavlo Marchionni, Luigi Molania, Ramyar Papenfuss, Anthony T Pellegrina, Diogo Pope, Bernard Queiroz, Lucio R Rausch, Tobias Reimand, Jüri Robinson, Brian Schlomm, Thorsten Sørensen, Karina D Uhrig, Sebastian Weischenfeldt, Joachim Xu, Yaobo Yamaguchi, Takafumi N Zanettini, Claudio Lynch, Andy G Wedge, David C Brewer, Daniel S Woodcock, Dan J |
| author_facet | Esenturk, Emre Sahli, Atef Haberland, Valeriia Ziuboniewicz, Aleksandra Wirth, Christopher Bova, G. Steven Bristow, Robert G Brook, Mark N Brors, Benedikt Butler, Adam Cancel-Tassin, Géraldine Cheng, Kevin CL Cooper, Colin S Corcoran, Niall M Cussenot, Olivier Eeles, Ros A Favero, Francesco Gerhauser, Clarissa Gihawi, Abraham Girma, Etsehiwot G Gnanapragasam, Vincent J Gruber, Andreas J Hamid, Anis Hayes, Vanessa M He, Housheng Hansen Hovens, Christopher M Imada, Eddie Luidy Jakobsdottir, G. Maria Jung, Chol-hee Khani, Francesca Kote-Jarai, Zsofia Lamy, Philippe Leeman, Gregory Loda, Massimo Lutsik, Pavlo Marchionni, Luigi Molania, Ramyar Papenfuss, Anthony T Pellegrina, Diogo Pope, Bernard Queiroz, Lucio R Rausch, Tobias Reimand, Jüri Robinson, Brian Schlomm, Thorsten Sørensen, Karina D Uhrig, Sebastian Weischenfeldt, Joachim Xu, Yaobo Yamaguchi, Takafumi N Zanettini, Claudio Lynch, Andy G Wedge, David C Brewer, Daniel S Woodcock, Dan J |
| contents | Cancer progression involves the sequential accumulation of genetic alterations that cumulatively shape the tumour phenotype. In prostate cancer, tumours can follow divergent evolutionary trajectories that lead to distinct subtypes, but the causes of this divergence remain unclear. While causal inference could elucidate the factors involved, conventional methods are unsuitable due to the possibility of unobserved confounders and ambiguity in the direction of causality. Here, we propose a method that circumvents these issues and apply it to genomic data from 829 prostate cancer patients. We identify several genetic alterations that drive divergence as well as others that prevent this transition, locking tumours into one trajectory. Further analysis reveals that these genetic alterations may cause each other, implying a positive-feedback loop that accelerates divergence. Our findings provide insights into how cancer subtypes emerge and offer a foundation for genomic surveillance strategies aimed at monitoring the progression of prostate cancer. |
| format | Preprint |
| id |
arxiv_https___arxiv_org_abs_2503_13189 |
| institution | arXiv |
| publishDate | 2025 |
| record_format | arxiv |
| spellingShingle | Causes of evolutionary divergence in prostate cancer Esenturk, Emre Sahli, Atef Haberland, Valeriia Ziuboniewicz, Aleksandra Wirth, Christopher Bova, G. Steven Bristow, Robert G Brook, Mark N Brors, Benedikt Butler, Adam Cancel-Tassin, Géraldine Cheng, Kevin CL Cooper, Colin S Corcoran, Niall M Cussenot, Olivier Eeles, Ros A Favero, Francesco Gerhauser, Clarissa Gihawi, Abraham Girma, Etsehiwot G Gnanapragasam, Vincent J Gruber, Andreas J Hamid, Anis Hayes, Vanessa M He, Housheng Hansen Hovens, Christopher M Imada, Eddie Luidy Jakobsdottir, G. Maria Jung, Chol-hee Khani, Francesca Kote-Jarai, Zsofia Lamy, Philippe Leeman, Gregory Loda, Massimo Lutsik, Pavlo Marchionni, Luigi Molania, Ramyar Papenfuss, Anthony T Pellegrina, Diogo Pope, Bernard Queiroz, Lucio R Rausch, Tobias Reimand, Jüri Robinson, Brian Schlomm, Thorsten Sørensen, Karina D Uhrig, Sebastian Weischenfeldt, Joachim Xu, Yaobo Yamaguchi, Takafumi N Zanettini, Claudio Lynch, Andy G Wedge, David C Brewer, Daniel S Woodcock, Dan J Genomics Cancer progression involves the sequential accumulation of genetic alterations that cumulatively shape the tumour phenotype. In prostate cancer, tumours can follow divergent evolutionary trajectories that lead to distinct subtypes, but the causes of this divergence remain unclear. While causal inference could elucidate the factors involved, conventional methods are unsuitable due to the possibility of unobserved confounders and ambiguity in the direction of causality. Here, we propose a method that circumvents these issues and apply it to genomic data from 829 prostate cancer patients. We identify several genetic alterations that drive divergence as well as others that prevent this transition, locking tumours into one trajectory. Further analysis reveals that these genetic alterations may cause each other, implying a positive-feedback loop that accelerates divergence. Our findings provide insights into how cancer subtypes emerge and offer a foundation for genomic surveillance strategies aimed at monitoring the progression of prostate cancer. |
| title | Causes of evolutionary divergence in prostate cancer |
| topic | Genomics |
| url | https://arxiv.org/abs/2503.13189 |