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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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | International Journal of Genomics |
| Online Access: | http://dx.doi.org/10.1155/2013/464720 |
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| _version_ | 1832565358178861056 |
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| author | Glenn Jenkins Kenneth J. O'Byrne Benedict Panizza Derek J. Richard |
| author_facet | Glenn Jenkins Kenneth J. O'Byrne Benedict Panizza Derek J. Richard |
| author_sort | Glenn Jenkins |
| collection | DOAJ |
| 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. |
| format | Article |
| id | doaj-art-22903d299c554fa19632475fd75362ce |
| institution | Kabale University |
| issn | 2314-436X 2314-4378 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Genomics |
| spelling | doaj-art-22903d299c554fa19632475fd75362ce2025-02-03T01:07:52ZengWileyInternational 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 |
| spellingShingle | Glenn Jenkins Kenneth J. O'Byrne Benedict Panizza Derek J. Richard Genome Stability Pathways in Head and Neck Cancers International Journal of Genomics |
| title | 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_short | Genome Stability Pathways in Head and Neck Cancers |
| title_sort | genome stability pathways in head and neck cancers |
| url | http://dx.doi.org/10.1155/2013/464720 |
| work_keys_str_mv | AT glennjenkins genomestabilitypathwaysinheadandneckcancers AT kennethjobyrne genomestabilitypathwaysinheadandneckcancers AT benedictpanizza genomestabilitypathwaysinheadandneckcancers AT derekjrichard genomestabilitypathwaysinheadandneckcancers |