title: Could the PI3K canonical pathway be a common link between chronic inflammatory conditions and oral carcinogenesis?
abstract: The association between chronic inflammatory disorders and oral carcinogenesis has been both a source of interest and contention. Based upon its central importance in oral carcinogenesis, the finding that the PI3k/Akt/mTOR pathway is activated in oral lichen planus, chronic graft-versus-host disease, and chronic oral candidiasis suggests that it may provide a link between benign and malignant oral conditions. Here, we discuss a possible mechanistic rationale that addresses the activation of this important signaling pathway and its downstream events, while correlating it with the carcinogenic potential of chronic oral disorders.
authors.affiliation: Brigham and Women's Hospital and the Dana-Farber Cancer Institute and Biomodels LLC, Boston, MA, USA.
authors.forename: Stephen T
authors.initials: ST
authors.lastname: Sonis
authors.affiliation: Adjunct Professor of Oral and Maxillofacial Medicine, Department of Oral and Maxillofacial Medicine and Diagnostic Sciences, School of Dental Medicine, Case Western Reserve University, Cleveland, OH, USA.
authors.forename: Rui
authors.identifier: http://orcid.org/0000-0001-7628-8598
authors.initials: R
authors.lastname: Amaral Mendes
mesh_terms: D000818:Animals; D063646:Carcinogenesis / Q000378:metabolism*; D002908:Chronic Disease; D006801:Humans; D007249:Inflammation / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology; D009062:Mouth Neoplasms / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D019869:Phosphatidylinositol 3-Kinases
keywords: PI3K signaling pathways; candidiasis; graft-vs.-host disease; inflammation; lichen planus; oral carcinogenesis