Genomic instability in human cancer

Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition

Lynnette R. Ferguson, Helen Chen, Andrew R. Collins, Marisa Connell, Giovanna Damia, Santanu Dasgupta, Meenakshi Malhotra, Alan Keith Meeker, Amedeo Amedei, Amr Amin, S. Salman Ashraf, Katia Aquilano, Asfar S. Azmi, Dipita Bhakta, Alan Bilsland, Chandra S. Boosani, Sophie Chen, Maria Rosa Ciriolo, Hiromasa Fujii, Gunjan Guha & 15 others Dorota Halicka, William G. Helferich, W. Nicol Keith, Sulma I. Mohammed, Elena Niccolai, Xujuan Yang, Kanya Honoki, Virginia R. Parslow, Satya Prakash, Sarallah Rezazadeh, Rodney E. Shackelford, David Sidransky, Phuoc T Tran, Eddy S. Yang, Christopher A. Maxwell

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
JournalSeminars in Cancer Biology
DOIs
StateAccepted/In press - 2015

Fingerprint

Genomic Instability
Diet
Neoplasms
DNA Damage
Centrosome
Therapeutics
DNA Repair-Deficiency Disorders
Isothiocyanates
Telomerase
Telomere
Aneuploidy
Carotenoids
Selenium
Epigenomics
Vitamin D
DNA Repair
Cell Division
Cluster Analysis
Mutation

Keywords

  • Cancer prevention
  • Cancer therapy
  • DNA damage
  • Genomic instability
  • Nutraceutical

ASJC Scopus subject areas

  • Cancer Research

Cite this

Genomic instability in human cancer : Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition. / Ferguson, Lynnette R.; Chen, Helen; Collins, Andrew R.; Connell, Marisa; Damia, Giovanna; Dasgupta, Santanu; Malhotra, Meenakshi; Meeker, Alan Keith; Amedei, Amedeo; Amin, Amr; Ashraf, S. Salman; Aquilano, Katia; Azmi, Asfar S.; Bhakta, Dipita; Bilsland, Alan; Boosani, Chandra S.; Chen, Sophie; Ciriolo, Maria Rosa; Fujii, Hiromasa; Guha, Gunjan; Halicka, Dorota; Helferich, William G.; Keith, W. Nicol; Mohammed, Sulma I.; Niccolai, Elena; Yang, Xujuan; Honoki, Kanya; Parslow, Virginia R.; Prakash, Satya; Rezazadeh, Sarallah; Shackelford, Rodney E.; Sidransky, David; Tran, Phuoc T; Yang, Eddy S.; Maxwell, Christopher A.

In: Seminars in Cancer Biology, 2015.

Research output: Contribution to journalArticle

Ferguson, LR, Chen, H, Collins, AR, Connell, M, Damia, G, Dasgupta, S, Malhotra, M, Meeker, AK, Amedei, A, Amin, A, Ashraf, SS, Aquilano, K, Azmi, AS, Bhakta, D, Bilsland, A, Boosani, CS, Chen, S, Ciriolo, MR, Fujii, H, Guha, G, Halicka, D, Helferich, WG, Keith, WN, Mohammed, SI, Niccolai, E, Yang, X, Honoki, K, Parslow, VR, Prakash, S, Rezazadeh, S, Shackelford, RE, Sidransky, D, Tran, PT, Yang, ES & Maxwell, CA 2015, 'Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition', Seminars in Cancer Biology. https://doi.org/10.1016/j.semcancer.2015.03.005
Ferguson, Lynnette R. ; Chen, Helen ; Collins, Andrew R. ; Connell, Marisa ; Damia, Giovanna ; Dasgupta, Santanu ; Malhotra, Meenakshi ; Meeker, Alan Keith ; Amedei, Amedeo ; Amin, Amr ; Ashraf, S. Salman ; Aquilano, Katia ; Azmi, Asfar S. ; Bhakta, Dipita ; Bilsland, Alan ; Boosani, Chandra S. ; Chen, Sophie ; Ciriolo, Maria Rosa ; Fujii, Hiromasa ; Guha, Gunjan ; Halicka, Dorota ; Helferich, William G. ; Keith, W. Nicol ; Mohammed, Sulma I. ; Niccolai, Elena ; Yang, Xujuan ; Honoki, Kanya ; Parslow, Virginia R. ; Prakash, Satya ; Rezazadeh, Sarallah ; Shackelford, Rodney E. ; Sidransky, David ; Tran, Phuoc T ; Yang, Eddy S. ; Maxwell, Christopher A. / Genomic instability in human cancer : Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition. In: Seminars in Cancer Biology. 2015.
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T2 - Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition

AU - Ferguson, Lynnette R.

AU - Chen, Helen

AU - Collins, Andrew R.

AU - Connell, Marisa

AU - Damia, Giovanna

AU - Dasgupta, Santanu

AU - Malhotra, Meenakshi

AU - Meeker, Alan Keith

AU - Amedei, Amedeo

AU - Amin, Amr

AU - Ashraf, S. Salman

AU - Aquilano, Katia

AU - Azmi, Asfar S.

AU - Bhakta, Dipita

AU - Bilsland, Alan

AU - Boosani, Chandra S.

AU - Chen, Sophie

AU - Ciriolo, Maria Rosa

AU - Fujii, Hiromasa

AU - Guha, Gunjan

AU - Halicka, Dorota

AU - Helferich, William G.

AU - Keith, W. Nicol

AU - Mohammed, Sulma I.

AU - Niccolai, Elena

AU - Yang, Xujuan

AU - Honoki, Kanya

AU - Parslow, Virginia R.

AU - Prakash, Satya

AU - Rezazadeh, Sarallah

AU - Shackelford, Rodney E.

AU - Sidransky, David

AU - Tran, Phuoc T

AU - Yang, Eddy S.

AU - Maxwell, Christopher A.

PY - 2015

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N2 - 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.

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