Oral cancer pathophysiology: Difference between revisions
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==References== | ==References== | ||
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[[Category:Oral and maxillofacial surgery]] | [[Category:Oral and maxillofacial surgery]] | ||
[[Category:Otolaryngology]] | [[Category:Otolaryngology]] | ||
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[[Category:Disease]] | [[Category:Disease]] | ||
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Revision as of 16:12, 10 September 2015
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Oral cancer Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Oral cancer pathophysiology On the Web |
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American Roentgen Ray Society Images of Oral cancer pathophysiology |
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Risk calculators and risk factors for Oral cancer pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]
Overview
Genes involved in the pathogenesis of oral cancer include tumor suppressor genes (TSGs), particularly in chromosomes 3, 9, 11, and 17.
Pathophysiology
The pathophysiology of oral cancer involves inactivated tumor suppressor genes, P16, and TP53 and overexpressed oncogenes, PRAD1.The molecular changes in oral squamous cell carcinoma in western countries (eg, United Kingdom, United States, Australia), are particularly TP53 mutations. These mutations are infrequent in eastern countries (eg, India, Southeast Asia), where the involvement of ras oncogenes is more common.