Genome stability pathways in head and neck cancers

Jenkins, Glenn, O'Byrne, Kenneth J., Panizza, Benedict and Richard, Derek J. (2013) Genome stability pathways in head and neck cancers. International Journal of Genomics, 2013 . doi:10.1155/2013/464720

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Author Jenkins, Glenn
O'Byrne, Kenneth J.
Panizza, Benedict
Richard, Derek J.
Title Genome stability pathways in head and neck cancers
Journal name International Journal of Genomics   Check publisher's open access policy
ISSN 2314-436X
2314-4378
Publication date 2013
Year available 2013
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1155/2013/464720
Open Access Status File (Publisher version)
Volume 2013
Total pages 19
Place of publication New York, United States
Publisher Hindawi Publishing Corporation
Collection year 2014
Language eng
Abstract 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.
Keyword Squamous cell carcinoma
Growth factor receptor
Nucleotide excision repair
Double strand breaks
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Official 2014 Collection
School of Medicine Publications
 
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