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Review
. 2008 Dec;22(6):1099-124, vii.
doi: 10.1016/j.hoc.2008.08.007.

Molecular biology of head and neck cancer: risks and pathways

Affiliations
Review

Molecular biology of head and neck cancer: risks and pathways

Michael E Stadler et al. Hematol Oncol Clin North Am. 2008 Dec.

Abstract

Patients present with a differential baseline risk of cancer based on normal and expected variations in genes associated with cancer. The baseline risk of developing cancer is acted on throughout life as the genome of different cells interacts with the environment in the form of exposures (eg, toxins, infections). As genetic damage is incurred throughout a lifetime (directly to DNA sequences or to the epigenome), events are set in motion to progressively disrupt normal cellular pathways toward tumorigenesis. This article attempts to characterize broad categories of genetic aberrations and pathways in a manner that might be useful for the clinician to understand the risk of developing cancer, the pathways that are disrupted, and the potential for molecular-based diagnostics.

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Figures

Figure 1
Figure 1. Diversity of Head & Neck Cancer
Histopathologic diagnoses that present at the various subsites in the head and neck.
Figure 2
Figure 2. Genetic progression of HNSCC
Genetic changes associated with the histological progression of HNSCC based on loss of chromosomal material (allelic loss). Genetic alterations have been placed prior to the lesion where the frequency of the particular event plateaus. It is the accumulation and not necessarily the order of genetic events that determines the progression. A small fraction of benign squamous hyperplastic lesions contain 9p21 or 3p21 loss, suggesting that an unidentified precursor lesion (or cells) may also give rise to dysplasia. Candidate tumor suppressor genes include p16 (9p21), p53 (17p), and retinoblastoma (13q), and a candidate proto-oncogene includes cyclin D1 (11q13). (figure taken and adapted with permission from Califano.)
Figure 3
Figure 3
Molecular pathways contributing to the promotion and progression of tumorigenesis in head and neck cancer.

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