Clinical significance of inflammatory mediators in the pathogenesis of oral cancer
Oral cancer has become a grave problem in many parts of the globe with two.thirds of the cases occurring in developing countries. Chronic inflammation plays a prominent role in the development of oral cancer. The rationale for molecular targeted prevention of oral cancer is promising. Therefore, the...
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Veröffentlicht in: | Journal of cancer research and therapeutics 2016-04, Vol.12 (2), p.447-457 |
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description | Oral cancer has become a grave problem in many parts of the globe with two.thirds of the cases occurring in developing countries. Chronic inflammation plays a prominent role in the development of oral cancer. The rationale for molecular targeted prevention of oral cancer is promising. Therefore, there are continued improvements to our understanding of the molecular connections between inflammation and oral cancer. The inflammatory mediators including nuclear factor kappa B, vascular endothelial growth factor, inflammatory cytokines, prostaglandin pathways, p53, reactive oxygen and nitrogen species, and microRNAs are major key players in the pathogenesis of oral cancer. Currently, visual cytology.based techniques and biopsy are used to detect dysplasia and early stage of oral squamous cell carcinoma. These approaches are limited in their ability to judge the severities of oral lesions and are useful only after the appearance of visual changes. Thus, traditional cytological and biopsy assays combined with testing of inflammatory biomarkers would be beneficial for the efficient early detection of oral dysplastic lesions and early stages of oral squamous cell carcinoma. |
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Chronic inflammation plays a prominent role in the development of oral cancer. The rationale for molecular targeted prevention of oral cancer is promising. Therefore, there are continued improvements to our understanding of the molecular connections between inflammation and oral cancer. The inflammatory mediators including nuclear factor kappa B, vascular endothelial growth factor, inflammatory cytokines, prostaglandin pathways, p53, reactive oxygen and nitrogen species, and microRNAs are major key players in the pathogenesis of oral cancer. Currently, visual cytology.based techniques and biopsy are used to detect dysplasia and early stage of oral squamous cell carcinoma. These approaches are limited in their ability to judge the severities of oral lesions and are useful only after the appearance of visual changes. 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Chronic inflammation plays a prominent role in the development of oral cancer. The rationale for molecular targeted prevention of oral cancer is promising. Therefore, there are continued improvements to our understanding of the molecular connections between inflammation and oral cancer. The inflammatory mediators including nuclear factor kappa B, vascular endothelial growth factor, inflammatory cytokines, prostaglandin pathways, p53, reactive oxygen and nitrogen species, and microRNAs are major key players in the pathogenesis of oral cancer. Currently, visual cytology.based techniques and biopsy are used to detect dysplasia and early stage of oral squamous cell carcinoma. These approaches are limited in their ability to judge the severities of oral lesions and are useful only after the appearance of visual changes. Thus, traditional cytological and biopsy assays combined with testing of inflammatory biomarkers would be beneficial for the efficient early detection of oral dysplastic lesions and early stages of oral squamous cell carcinoma.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Care and treatment</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Curcumin - pharmacology</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Development and progression</subject><subject>DNA methylation</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Inflammation - complications</subject><subject>Inflammation - metabolism</subject><subject>Inflammation Mediators - metabolism</subject><subject>Kinases</subject><subject>Mouth cancer</subject><subject>Mouth Neoplasms - etiology</subject><subject>Mouth Neoplasms - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>Nitric Oxide - metabolism</subject><subject>Properties</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Squamous cell carcinoma</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><issn>0973-1482</issn><issn>1998-4138</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkkFv3CAQhVHVqtmkvecUWeqlF2_BjA0-Jqs2qRSpUtWeEWbHGxIMG7C1yr8vziZpU604gIbvPTHzIOSU0SUwyr_QVvCSgayWDIRo6jdkwdpWlsC4fEsWL9dH5DilW0prUVXyPTmqBDSsbqsF-bly1lujXZHsxts-H73BIvSF9b3Tw6DHEB-KAdd2PqVcLsYbLLZ6vAkb9JhsmukQs8WjNn4g73rtEn582k_I729ff62uyusfl99X59elqTl3JWixxg5ajY3hspOtwB6QUmkajWuUvNPQ6I41YIyWRiA3miNyACl7bjp-Qj7vfbcx3E-YRjXYZNA57TFMSTFJRc0lB5HRT_-ht2GKPr8uU1zQumkb-pfaaIcq9x_GqM1sqs6hboGySrBMlQeoeRR5BMFjb3P5Fb88wOe1xsGagwK6F5gYUorYq220g44PilE1x67mXNWcq9rHniVnT_1NXY7qRfCccwYu9sAuuBFjunPTDqPK7J0Pu1fG5T_GCkCo5x_C_wCYmLuS</recordid><startdate>20160401</startdate><enddate>20160401</enddate><creator>Patel, Jayendrakumar</creator><creator>Shah, Franky</creator><creator>Joshi, Geeta</creator><creator>Patel, Prabhudas</creator><general>Wolters Kluwer - Medknow Publications</general><general>Medknow Publications and Media Pvt. 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Chronic inflammation plays a prominent role in the development of oral cancer. The rationale for molecular targeted prevention of oral cancer is promising. Therefore, there are continued improvements to our understanding of the molecular connections between inflammation and oral cancer. The inflammatory mediators including nuclear factor kappa B, vascular endothelial growth factor, inflammatory cytokines, prostaglandin pathways, p53, reactive oxygen and nitrogen species, and microRNAs are major key players in the pathogenesis of oral cancer. Currently, visual cytology.based techniques and biopsy are used to detect dysplasia and early stage of oral squamous cell carcinoma. These approaches are limited in their ability to judge the severities of oral lesions and are useful only after the appearance of visual changes. 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subjects | Animals Apoptosis Care and treatment Cell Transformation, Neoplastic - metabolism Curcumin - pharmacology Cytokines Cytokines - metabolism Development and progression DNA methylation Gene expression Gene Expression Regulation, Neoplastic Genetic aspects Health aspects Humans Inflammation - complications Inflammation - metabolism Inflammation Mediators - metabolism Kinases Mouth cancer Mouth Neoplasms - etiology Mouth Neoplasms - metabolism NF-kappa B - metabolism Nitric Oxide - metabolism Properties Reactive Oxygen Species - metabolism Signal Transduction - drug effects Squamous cell carcinoma Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Vascular endothelial growth factor Vascular Endothelial Growth Factor A - metabolism |
title | Clinical significance of inflammatory mediators in the pathogenesis of oral cancer |
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