Journal
SEMINARS IN CANCER BIOLOGY
Volume 35, Issue -, Pages S5-S24Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcancer.2015.03.005
Keywords
Genomic instability; Cancer therapy; Cancer prevention; DNA damage; Nutraceutical
Categories
Funding
- Italian Ministry of University and Research
- University of Florence
- Terry Fox Foundation
- UAEU Program for Advanced Research
- Al-Jalila Foundation
- Zayed Center for Health Sciences
- Italia Ministry of Education, University and Research- Miur [PRIN 20125S38FA_002]
- University of Glasgow
- Child and Family Research Institute PhD studentship
- Michael Cuccione childhood cancer research foundation fellowship
- Ovarian Prostate Cancer Research Trust Laboratory
- University of Oslo
- Italian Association for Cancer Research [AIRC IG 10636]
- Elsa U Pardee Foundation
- Auckland Cancer Society Research Centre, University of Auckland
- National Institutes of Health
- Ministry of Education, Culture, Sports, Science and Technology, Japan [24590493]
- CIHR
- Avon Foundation for Women [OBC 134038]
- NIH/NCI [RO1CA172380, P30CA006973, RCI RFA0D09009, 5R01 CA132996-03]
- DOD [W81WH1210545, W81XWH12PCRPTIA]
- Italian Ministry of University
- University of Italy
- CIHR [MOP 64308]
- Department of Biology, University of Rochester
- Patrick C. Walsh Prostate Cancer Research Fund
- Department of Defense [W81XWH-11-1-0272, W81XWH-13-1-0182]
- Commonwealth Foundation
- Uniting Against Lung Cancer
- Sidney Kimmel Translational Scholar award [SKF-13-021]
- ACS Scholar award [122688-RSG-12-196-01-TBG]
- NIH [1R01CA166348]
- Susan G. Komen Foundation
- AACR
- Gabrielle's Angel Foundation
- Eli Lilly
- Bristol Myers Squibb
- Beatson Oncology Centre Fund
- CRUK grant [C301/A14762]
Ask authors/readers for more resources
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. (C) 2015 The Authors. Published by Elsevier Ltd.
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