Genome stability pathways in head and neck cancers

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

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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. © 2013 Glenn Jenkins et al.

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ID Code: 67774
Item Type: Journal Article
Refereed: Yes
Keywords: cetuximab, cisplatin, epidermal growth factor receptor, gefitinib, mismatch repair protein, nicotinamide adenine dinucleotide adenosine diphosphate ribosyltransferase 1, nicotinamide adenine dinucleotide adenosine diphosphate ribosyltransferase 2, phosphatidylinositol 3 kinase, replication factor A, transforming growth factor alpha, alkylation, breast cancer, cancer radiotherapy, cancer survival, cause specific survival, chromosome 7, chromosome aberration, disease free survival, DNA adduct, DNA damage, DNA end joining repair, DNA repair, double stranded DNA break, excision repair, external beam radiotherapy, Fanconi anemia, gene mutation, genomic instability, genotype, head and neck cancer, head and neck squamous cell carcinoma, homologous recombination, human, Human papillomavirus type 16, ionizing radiation, lymph node metastasis, meta analysis (topic), microsatellite instability, mismatch repair, mouth cancer, nucleic acid base substitution, overall survival, oxidative stress, perineural invasion, phase 2 clinical trial (topic), phenotype, precancer, predictive value, priority journal, protein expression, protein phosphorylation, radiation protection, recurrence free survival, review, single nucleotide polymorphism, somatic mutation, tumor suppressor gene, ultraviolet radiation, upregulation, xeroderma pigmentosum
DOI: 10.1155/2013/464720
ISSN: 2314436X
Subjects: Australian and New Zealand Standard Research Classification > MEDICAL AND HEALTH SCIENCES (110000) > ONCOLOGY AND CARCINOGENESIS (111200)
Divisions: Current > Schools > School of Biomedical Sciences
Current > QUT Faculties and Divisions > Faculty of Health
Current > Institutes > Institute of Health and Biomedical Innovation
Copyright Owner: Copyright 2013 Glenn Jenkins et al.
Copyright Statement: This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Deposited On: 24 Feb 2014 23:44
Last Modified: 26 Feb 2014 22:53

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