Genome Stability Pathways in Head and Neck Cancers

Genomic instability underlies the transformation of host cells toward malignancy, promotes development of invasion and metastasis and shapes the response of established cancer to treatment. In this review, we discuss recent advances in our understanding of genomic stability in squamous cell carcinom...

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Main Authors: Glenn Jenkins, Kenneth J. O'Byrne, Benedict Panizza, Derek J. Richard
Format: Article
Language:English
Published: Hindawi Limited 2013-01-01
Series:International Journal of Genomics
Online Access:http://dx.doi.org/10.1155/2013/464720
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spelling doaj-22903d299c554fa19632475fd75362ce2020-11-24T23:17:52ZengHindawi LimitedInternational Journal of Genomics2314-436X2314-43782013-01-01201310.1155/2013/464720464720Genome Stability Pathways in Head and Neck CancersGlenn Jenkins0Kenneth J. O'Byrne1Benedict Panizza2Derek J. Richard3University of Queensland, Brisbane, QLD, AustraliaCancer and Ageing Research Program, Institute of Health and Biomedical Innovation at the Translational Research Institute, Queensland University of Technology, Brisbane, QLD, AustraliaUniversity of Queensland, Brisbane, QLD, AustraliaCancer and Ageing Research Program, Institute of Health and Biomedical Innovation at the Translational Research Institute, Queensland University of Technology, Brisbane, QLD, AustraliaGenomic instability underlies the transformation of host cells toward malignancy, promotes development of invasion and metastasis and shapes the response of established cancer to treatment. In this review, we discuss recent advances in our understanding of genomic stability in squamous cell carcinoma of the head and neck (HNSCC), with an emphasis on DNA repair pathways. HNSCC is characterized by distinct profiles in genome stability between similarly staged cancers that are reflected in risk, treatment response and outcomes. Defective DNA repair generates chromosomal derangement that can cause subsequent alterations in gene expression, and is a hallmark of progression toward carcinoma. Variable functionality of an increasing spectrum of repair gene polymorphisms is associated with increased cancer risk, while aetiological factors such as human papillomavirus, tobacco and alcohol induce significantly different behaviour in induced malignancy, underpinned by differences in genomic stability. Targeted inhibition of signalling receptors has proven to be a clinically-validated therapy, and protein expression of other DNA repair and signalling molecules associated with cancer behaviour could potentially provide a more refined clinical model for prognosis and treatment prediction. Development and expansion of current genomic stability models is furthering our understanding of HNSCC pathophysiology and uncovering new, promising treatment strategies.http://dx.doi.org/10.1155/2013/464720
collection DOAJ
language English
format Article
sources DOAJ
author Glenn Jenkins
Kenneth J. O'Byrne
Benedict Panizza
Derek J. Richard
spellingShingle Glenn Jenkins
Kenneth J. O'Byrne
Benedict Panizza
Derek J. Richard
Genome Stability Pathways in Head and Neck Cancers
International Journal of Genomics
author_facet Glenn Jenkins
Kenneth J. O'Byrne
Benedict Panizza
Derek J. Richard
author_sort Glenn Jenkins
title Genome Stability Pathways in Head and Neck Cancers
title_short Genome Stability Pathways in Head and Neck Cancers
title_full Genome Stability Pathways in Head and Neck Cancers
title_fullStr Genome Stability Pathways in Head and Neck Cancers
title_full_unstemmed Genome Stability Pathways in Head and Neck Cancers
title_sort genome stability pathways in head and neck cancers
publisher Hindawi Limited
series International Journal of Genomics
issn 2314-436X
2314-4378
publishDate 2013-01-01
description Genomic instability underlies the transformation of host cells toward malignancy, promotes development of invasion and metastasis and shapes the response of established cancer to treatment. In this review, we discuss recent advances in our understanding of genomic stability in squamous cell carcinoma of the head and neck (HNSCC), with an emphasis on DNA repair pathways. HNSCC is characterized by distinct profiles in genome stability between similarly staged cancers that are reflected in risk, treatment response and outcomes. Defective DNA repair generates chromosomal derangement that can cause subsequent alterations in gene expression, and is a hallmark of progression toward carcinoma. Variable functionality of an increasing spectrum of repair gene polymorphisms is associated with increased cancer risk, while aetiological factors such as human papillomavirus, tobacco and alcohol induce significantly different behaviour in induced malignancy, underpinned by differences in genomic stability. Targeted inhibition of signalling receptors has proven to be a clinically-validated therapy, and protein expression of other DNA repair and signalling molecules associated with cancer behaviour could potentially provide a more refined clinical model for prognosis and treatment prediction. Development and expansion of current genomic stability models is furthering our understanding of HNSCC pathophysiology and uncovering new, promising treatment strategies.
url http://dx.doi.org/10.1155/2013/464720
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