Abstract
Cancer, the unregulated growth of cells, has been a major area of focus of research for years due to its impact on human health. Cancer development can be traced back to aberrant modifications in genetic and epigenetic mechanisms within the body over time. Given time and cost implications of human genome experimentation, computational modeling is increasingly being employed to improve understanding of mechanisms which determine cancer initiation and progression. Here, we introduce a network-based model for genetic and epigenetic signals in colorectal cancer, with the focus on the gene level and tumor pathways. The current framework also considers the influence of ageing for micromolecular events in cancer development.
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Notes
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The addition of a methyl group to cytosine ring.
- 2.
Histones are the proteins that pack DNA in nucleosomes. They are grouped into two categories: the core histones (H2A, H2B, H3, H4) and the linker histones (H1 and H5).
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Acknowledgements
This project acknowledges financial support from CIESCI ERA-Net Complexity Project, (EU/IRCSET). Access to the StatEpigen database is also gratefully acknowledged.
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Roznovăţ, I.A., Ruskin, H.J. (2013). Modelling the Genetic and Epigenetic Signals in Colon Cancer Using a Bayesian Network. In: Gilbert, T., Kirkilionis, M., Nicolis, G. (eds) Proceedings of the European Conference on Complex Systems 2012. Springer Proceedings in Complexity. Springer, Cham. https://doi.org/10.1007/978-3-319-00395-5_126
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DOI: https://doi.org/10.1007/978-3-319-00395-5_126
Publisher Name: Springer, Cham
Print ISBN: 978-3-319-00394-8
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