Genomic instability in human cancer: molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition

Ferguson, L. R. et al. (2015) Genomic instability in human cancer: molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition. Seminars in Cancer Biology, 35(Suppl), S5-S24. (doi:10.1016/j.semcancer.2015.03.005) (PMID:25869442)

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Abstract

Genomic instability can initiate cancer, augment progression, and influence the overall prognosis of the affected patient. Genomic instability arises from many different pathways, such as telomere damage, centrosome amplification, epigenetic modifications, and DNA damage from endogenous and exogenous sources, and can be perpetuating, or limiting, through the induction of mutations or aneuploidy, both enabling and catastrophic. Many cancer treatments induce DNA damage to impair cell division on a global scale but it is accepted that personalized treatments, those that are tailored to the particular patient and type of cancer, must also be developed. In this review, we detail the mechanisms from which genomic instability arises and can lead to cancer, as well as treatments and measures that prevent genomic instability or take advantage of the cellular defects caused by genomic instability. In particular, we identify and discuss five priority targets against genomic instability: (1) prevention of DNA damage; (2) enhancement of DNA repair; (3) targeting deficient DNA repair; (4) impairing centrosome clustering; and, (5) inhibition of telomerase activity. Moreover, we highlight vitamin D and B, selenium, carotenoids, PARP inhibitors, resveratrol, and isothiocyanates as priority approaches against genomic instability. The prioritized target sites and approaches were cross validated to identify potential synergistic effects on a number of important areas of cancer biology.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Bilsland, Dr Alan and Keith, Professor Nicol
Authors: Ferguson, L. R., Chen, H., Collins, A. R., Connell, M., Damia, G., Dasgupta, S., Malhotra, M., Meeker, A. K., Amedei, A., Amin, A., Ashraf, S. S., Aquilano, K., Azmi, A. S., Bhakta, D., Bilsland, A., Boosani, C. S., Chen, S., Ciriolo, M. R., Fujii, H., Guha, G., Halicka, D., Helferich, W. G., Keith, W. N., Mohammed, S. I., Niccolai, E., Yang, X., Honoki, K., Parslow, V. R., Prakash, S., Rezazadeh, S., Shackelford, R. E., Sidransky, D., Tran, P. T., Yang, E. S., and Maxwell, C. A.
College/School:College of Medical Veterinary and Life Sciences > Institute of Cancer Sciences
Journal Name:Seminars in Cancer Biology
Publisher:Elsevier B.V.
ISSN:1044-579X
ISSN (Online):1096-3650
Copyright Holders:Copyright © 2015 The Authors
First Published:First published in Seminars in Cancer Biology 35(Suppl):S5-S24
Publisher Policy:Reproduced under a Creative Commons License

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Project CodeAward NoProject NamePrincipal InvestigatorFunder's NameFunder RefLead Dept
580721Optimisation of telomerase expression repressorsNicol KeithCancer Research UK (CAN-RES-UK)C301/A14762ICS - EXPERIMENTAL THERAPEUTICS
580722Optimisation of telomerase expression repressorsNicol KeithCancer Research UK (CAN-RES-UK)C301/A14762ICS - EXPERIMENTAL THERAPEUTICS