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Evolution of the cancer genome

Evolution of the cancer genome Each tumour represents an independent evolutionary experiment, starting from almost the same point: namely, the fertilized egg. As tools for genome-wide analysis become more widely applied, commonalities and variations in the patterns of cancer evolution are emerging, and this has important implications for our understanding of cancer biology and the management of patients with tumours. Evolution may be investigated within an individual cancer through various sampling approaches, ranging from a single sample to multiple samples taken over space and/or time or even from multiple single cells. Massively parallel sequencing data from bulk tumour sampling lend themselves to mathematical approaches that permit the reconstruction of the underlying genomic architecture. Genomic technologies have identified extreme genomic heterogeneity between and even within tumour types. This suggests that evolutionary pathways underlying cancers are diverse and highlights one of the challenges for the design of cancer therapies. Intratumoural heterogeneity reflects the branching and dynamic nature of cancer evolution. When a new mutation arises in a cancer cell, the subsequent evolutionary trajectory of the cell will be influenced by the cellular ground state and any pre-existing mutations. Understanding epistatic interactions that operate within a cancer cell will contribute to our comprehension of carcinogenesis and is important for designing targeted therapeutic approaches. Emerging observations suggest that cancers do not necessarily arise gradually through multiple steps but that sudden 'crisis' events can accelerate carcinogenesis. Many of the aggressive clinical characteristics of cancer depend on the continued generation of variation. There is evidence for the existence of genomic instability in many cancer types, but it remains unclear whether it is a pre-requisite for cancer development or whether cancers can evolve in the presence of a normal mutation rate. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Reviews Genetics Springer Journals

Evolution of the cancer genome

Yates, Lucy R.; Campbell, Peter J.
Nature Reviews Genetics , Volume 13 (11) – Oct 9, 2012
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References (127)

Publisher
Springer Journals
Copyright
Copyright © 2012 by Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.
Subject
Biomedicine; Biomedicine, general; Human Genetics; Cancer Research; Agriculture; Gene Function; Animal Genetics and Genomics
ISSN
1471-0056
eISSN
1471-0064
DOI
10.1038/nrg3317
Publisher site
See Article on Publisher Site

Abstract

Each tumour represents an independent evolutionary experiment, starting from almost the same point: namely, the fertilized egg. As tools for genome-wide analysis become more widely applied, commonalities and variations in the patterns of cancer evolution are emerging, and this has important implications for our understanding of cancer biology and the management of patients with tumours. Evolution may be investigated within an individual cancer through various sampling approaches, ranging from a single sample to multiple samples taken over space and/or time or even from multiple single cells. Massively parallel sequencing data from bulk tumour sampling lend themselves to mathematical approaches that permit the reconstruction of the underlying genomic architecture. Genomic technologies have identified extreme genomic heterogeneity between and even within tumour types. This suggests that evolutionary pathways underlying cancers are diverse and highlights one of the challenges for the design of cancer therapies. Intratumoural heterogeneity reflects the branching and dynamic nature of cancer evolution. When a new mutation arises in a cancer cell, the subsequent evolutionary trajectory of the cell will be influenced by the cellular ground state and any pre-existing mutations. Understanding epistatic interactions that operate within a cancer cell will contribute to our comprehension of carcinogenesis and is important for designing targeted therapeutic approaches. Emerging observations suggest that cancers do not necessarily arise gradually through multiple steps but that sudden 'crisis' events can accelerate carcinogenesis. Many of the aggressive clinical characteristics of cancer depend on the continued generation of variation. There is evidence for the existence of genomic instability in many cancer types, but it remains unclear whether it is a pre-requisite for cancer development or whether cancers can evolve in the presence of a normal mutation rate.

Journal

Nature Reviews Genetics – Springer Journals

Published: Oct 9, 2012

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