The Mutational Landscape of Prostate Cancer
(2013) In European Urology 64(4). p.567-576- Abstract
- Context: Prostate cancer (PCa) is a clinically heterogeneous disease with marked variability in patient outcomes. Molecular characterization has revealed striking mutational heterogeneity that may underlie the variable clinical course of the disease. Objective: In this review, we discuss the common genomic alterations that form the molecular basis of PCa, their functional significance, and the potential to translate this knowledge into patient care. Evidence acquisition: We reviewed the relevant literature, with a particular focus on recent studies on somatic alterations in PCa. Evidence synthesis: Advances in sequencing technology have resulted in an explosion of data regarding the mutational events underlying the development and... (More)
- Context: Prostate cancer (PCa) is a clinically heterogeneous disease with marked variability in patient outcomes. Molecular characterization has revealed striking mutational heterogeneity that may underlie the variable clinical course of the disease. Objective: In this review, we discuss the common genomic alterations that form the molecular basis of PCa, their functional significance, and the potential to translate this knowledge into patient care. Evidence acquisition: We reviewed the relevant literature, with a particular focus on recent studies on somatic alterations in PCa. Evidence synthesis: Advances in sequencing technology have resulted in an explosion of data regarding the mutational events underlying the development and progression of PCa. Heterogeneity is the norm; few abnormalities in specific genes are highly recurrent, but alterations in certain signaling pathways do predominate. These alterations include those in pathways known to affect tumorigenesis in a wide spectrum of tissues, such as the phosphoinositide 3-kinase/phosphatase and tensin homolog/Akt pathway, cell cycle regulation, and chromatin regulation. Alterations more specific to PCa are also observed, particularly gene fusions of ETS transcription factors and alterations in androgen signaling. Mounting data suggest that PCa can be subdivided based on a molecular profile of genetic alterations. Conclusions: Major advances have been made in cataloging the genomic alterations in PCa and understanding the molecular mechanisms underlying the disease. These findings raise the possibility that PCa could soon transition from being a poorly understood, heterogeneous disease with a variable clinical course to being a collection of homogenous subtypes identifiable by molecular criteria, associated with distinct risk profiles, and perhaps amenable to specific management strategies or targeted therapies. (C) 2013 European Association of Urology. Published by Elsevier B.V. All rights reserved. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4061412
- author
- Barbieri, Christopher E. ; Bangma, Chris H. ; Bjartell, Anders LU ; Catto, James W. F. ; Culig, Zoran ; Gronberg, Henrik ; Luo, Jun ; Visakorpi, Tapio and Rubin, Mark A.
- organization
- publishing date
- 2013
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Sequencing, Genomics, Copy number aberrations, Oncogene, Tumor, suppressor
- in
- European Urology
- volume
- 64
- issue
- 4
- pages
- 567 - 576
- publisher
- Elsevier
- external identifiers
-
- wos:000323939900017
- scopus:84883823918
- pmid:23759327
- ISSN
- 1873-7560
- DOI
- 10.1016/j.eururo.2013.05.029
- language
- English
- LU publication?
- yes
- id
- 8a66f1a0-050e-4398-89d6-608a012df207 (old id 4061412)
- date added to LUP
- 2016-04-01 13:07:26
- date last changed
- 2022-04-21 19:51:05
@article{8a66f1a0-050e-4398-89d6-608a012df207,
abstract = {{Context: Prostate cancer (PCa) is a clinically heterogeneous disease with marked variability in patient outcomes. Molecular characterization has revealed striking mutational heterogeneity that may underlie the variable clinical course of the disease. Objective: In this review, we discuss the common genomic alterations that form the molecular basis of PCa, their functional significance, and the potential to translate this knowledge into patient care. Evidence acquisition: We reviewed the relevant literature, with a particular focus on recent studies on somatic alterations in PCa. Evidence synthesis: Advances in sequencing technology have resulted in an explosion of data regarding the mutational events underlying the development and progression of PCa. Heterogeneity is the norm; few abnormalities in specific genes are highly recurrent, but alterations in certain signaling pathways do predominate. These alterations include those in pathways known to affect tumorigenesis in a wide spectrum of tissues, such as the phosphoinositide 3-kinase/phosphatase and tensin homolog/Akt pathway, cell cycle regulation, and chromatin regulation. Alterations more specific to PCa are also observed, particularly gene fusions of ETS transcription factors and alterations in androgen signaling. Mounting data suggest that PCa can be subdivided based on a molecular profile of genetic alterations. Conclusions: Major advances have been made in cataloging the genomic alterations in PCa and understanding the molecular mechanisms underlying the disease. These findings raise the possibility that PCa could soon transition from being a poorly understood, heterogeneous disease with a variable clinical course to being a collection of homogenous subtypes identifiable by molecular criteria, associated with distinct risk profiles, and perhaps amenable to specific management strategies or targeted therapies. (C) 2013 European Association of Urology. Published by Elsevier B.V. All rights reserved.}},
author = {{Barbieri, Christopher E. and Bangma, Chris H. and Bjartell, Anders and Catto, James W. F. and Culig, Zoran and Gronberg, Henrik and Luo, Jun and Visakorpi, Tapio and Rubin, Mark A.}},
issn = {{1873-7560}},
keywords = {{Sequencing; Genomics; Copy number aberrations; Oncogene; Tumor; suppressor}},
language = {{eng}},
number = {{4}},
pages = {{567--576}},
publisher = {{Elsevier}},
series = {{European Urology}},
title = {{The Mutational Landscape of Prostate Cancer}},
url = {{http://dx.doi.org/10.1016/j.eururo.2013.05.029}},
doi = {{10.1016/j.eururo.2013.05.029}},
volume = {{64}},
year = {{2013}},
}