Publication: Molecular pathology of head and neck cancer
Authors
Crowe, D.L. ; Hacia, J.G. ; Hsieh, C.L. ; Sinha, U.K. ; Rice, D.H.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Squamous cell carcinoma of the head and
neck region (HNSCC) is the sixth most frequent cancer
worldwide, comprising almost 50% of all malignancies
in some developing nations. In the United States, 30,000
new cases and 8,000 deaths are reported each year.
Survival rates vary depending on tobacco and alcohol
consumption, age, gender, ethnic background, and
geographic area. This variability reflects the
multifactorial pathogenesis of the disease. Early
detection and diagnosis has increased survival but the
overall 5 year rate of 50% is among the lowest of the
major cancers. Differences between normal epithelium
and cancer cells of the upper aerodigestive tract arise
from specific alterations in genes controlling DNA
repair, proliferation, immortalization, apoptosis,
invasion, and angiogenesis. These proteins include both
tumor suppressors and activating oncogenes which
regulate a wide variety of intracellular signaling
pathways. Included in these pathways are growth factor
receptors, signal transducers, and transcription factors
which regulate DNA damage response, cell cycle arrest,
and programmed cell death. In head and neck cancer,
alterations of three signaling pathways occur with
sufficient frequency and produce such dramatic
phenotypic changes as to be considered the critical
transforming events of the disease. These changes
include mutation of the p53 tumor suppressor,
inactivation of the cyclin dependent kinase inhibitor p16,
and overexpression of epidermal growth factor receptor
(EGFR). This review will focus on the molecular
changes which occur in these pathways and how they
contribute to the pathogenesis of HNSCC.
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