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| {{CMG}};{{AE}} {{Simrat}} | | {{CMG}};{{AE}} {{Simrat}} |
| ==Overview== | | ==Overview== |
| | Genes involved in the pathogenesis of oral cancer include tumor suppressor genes (TSGs), particularly in chromosomes 3, 9, 11, and 17. |
| ==Pathophysiology== | | ==Pathophysiology== |
| Precancerous lesions of the oropharynx include leukoplakia, erythroplakia, and mixed erythroleukoplakia.[1] Leukoplakia, the most common of the three conditions, is defined by the World Health Organization as “a white patch or plaque that cannot be characterized clinically or pathologically as any other disease.”[2] The diagnosis of leukoplakia is one of exclusion; conditions such as candidiasis, lichen planus, leukoedema, and others must be ruled out before a diagnosis of leukoplakia can be made.[1]
| | 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. |
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| The prevalence of leukoplakia in the United States is decreasing; this decline has been related to reduced tobacco consumption.[3] Although erythroplakia is not as common as leukoplakia, it is much more likely to be associated with dysplasia or carcinoma. The development of oral squamous cell carcinoma (OSCC) is a multistep process requiring the accumulation of multiple genetic alterations, influenced by a patient’s genetic predisposition as well as by environmental influences, including tobacco, alcohol, chronic inflammation, and viral infection. Tumorigenic genetic alterations consist of two major types: tumor suppressor genes, which promote tumor development when inactivated; and oncogenes, which promote tumor development when activated. Tumor suppressor genes can be inactivated through genetic events such as mutation, loss of heterozygosity, or deletion, or by epigenetic modifications such as DNA methylation or chromatin remodeling. Oncogenes can be activated through overexpression due to gene amplification, increased transcription, or changes in structure due to mutations that lead to increased transforming activity. This review focuses on the molecular mechanisms of oral carcinogenesis and the use of biologic therapy to specifically target molecules altered in OSCC. The rapid progress that has been made in our understanding of the molecular alterations contributing to the development of OSCC is leading to improvements in the early diagnosis of tumors and the refinement of biologic treatments individualized to the specific characteristics of a patient’s tumor. This review focuses on the molecular mechanisms of oral carcinogenesis and the use of biologic therapy to specifically target molecules altered in oral squamous cell carcinoma.
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| Oral squamous carcinogenesis is a multistep process in which multiple genetic events occur that alter the normal functions of oncogenes and tumour suppressor genes. This can result in increased production of growth factors or numbers of cell surface receptors, enhanced intracellular messenger signalling, and/or increased production of transcription factors. In combination with the loss of tumour suppressor activity, this leads to a cell phenotype capable of increased cell proliferation, with loss of cell cohesion, and the ability to infiltrate local tissue and spread to distant sites. Recent advances in the understanding of the molecular control of these various pathways will allow more accurate diagnosis and assessment of prognosis, and might lead the way for more novel approaches to treatment and prevention.
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| ==References=={{Reflist|2}} | | ==References=={{Reflist|2}} |
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.
==References==
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