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Unraveling the Drivers of Tumorigenesis in the Context of Evolution: Theoretical Models and Bioinformatics Tools

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Abstract

Cancer originates from somatic cells that have accumulated mutations. These mutations alter the phenotype of the cells, allowing them to escape homeostatic regulation that maintains normal cell numbers. The emergence of malignancies is an evolutionary process in which the random accumulation of somatic mutations and sequential selection of dominant clones cause cancer cells to proliferate. The development of technologies such as high-throughput sequencing has provided a powerful means to measure subclonal evolutionary dynamics across space and time. Here, we review the patterns that may be observed in cancer evolution and the methods available for quantifying the evolutionary dynamics of cancer. An improved understanding of the evolutionary trajectories of cancer will enable us to explore the molecular mechanism of tumorigenesis and to design tailored treatment strategies.

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Acknowledgements

This work was supported by the National Natural Science Foundation of China [Grant No. 31971371]. We thank the Information Technology Center and State Key Lab of CAD&CG Zhejiang University, and Alibaba Cloud for the support of computing resources.

Funding

Funding was provided by the National Natural Science Foundation of China [Grant No. 31971371].

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Correspondence to Zhan Zhou or Xun Gu.

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Handling editor: Konstantinos Voskarides.

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Zhu, X., Zhao, W., Zhou, Z. et al. Unraveling the Drivers of Tumorigenesis in the Context of Evolution: Theoretical Models and Bioinformatics Tools. J Mol Evol 91, 405–423 (2023). https://doi.org/10.1007/s00239-023-10117-0

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  • DOI: https://doi.org/10.1007/s00239-023-10117-0

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