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DTSTART;TZID=Asia/Kolkata:20240720T103000
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SUMMARY:Journal Club with Authors #5
DESCRIPTION:Guest Author: \n\n\n\nProfessor Tiejun Li\n\n\n\nPeking University School of Stomatology\, China \n\n\n\n\n\n\n\nProf. Tiejun Li is a distinguished Peking University School of Stomatology professor. He specializes in oral pathology and has significantly contributed to the field\, particularly in studying odontogenic cysts and tumors. His research focuses on the molecular pathogenesis of these lesions and the mechanisms of bone resorption caused by aggressive odontogenic lesions. \n\n\n\nAsk Your Questions Live…\n\n\n\n\n\nAdenoid Ameloblastoma Shares Clinicopathologic\, Immunohistochemical\, and Molecular Features with Dentinogenic Ghost Cell Tumor: A Comparative Analysis\n\n\n\n\n\n\n\nXue\, Jiang\, et al. “Adenoid ameloblastoma shares clinicopathologic\, immunohistochemical\, and molecular features with dentinogenic ghost cell tumor: a comparative analysis.” The American journal of surgical pathology 47.11 (2023): 1274-1284. \n\n\n\n\n\n\n\nAbstract Summary – \n\n\n\nThe updated World Health Organization (WHO) classification of odontogenic tumors now includes adenoid ameloblastoma (AA) as a distinct entity. However\, distinguishing AA from dentinogenic ghost cell tumor (DGCT) is challenging due to their significant morphologic similarities. This study aimed to compare the clinicopathologic\, immunohistochemical\, and molecular characteristics of AA and DGCT to aid in their differentiation and understand their pathologic mechanisms. \n\n\n\nThe study analyzed 13 cases of AA\, 14 cases of DGCT (15 samples)\, 11 cases of adenomatoid odontogenic tumor (AOT)\, and 18 cases of conventional ameloblastoma (AM) for comparison. Key findings include: \n\n\n\n\nAA and DGCT share a similar long-term prognosis.\n\n\n\nImmunohistochemically\, most cytokeratins did not significantly differentiate AA and DGCT\, except for CK8/18. CK7 and CK10/13 showed significant differences between AA and AM.\n\n\n\nNuclear β-catenin accumulation was observed in all cases of AA and DGCT\, whereas AOTs and AMs exhibited cytoplasmic β-catenin.\n\n\n\nMolecularly\, CTNNB1 hotspot mutations were found in only one AA case. BRAF p.V600E mutations were present in 15% of AA\, 7% of DGCT\, and 18% of AOT cases\, compared to 94% in AM cases. KRAS mutations were found in 63% of AOT cases.\n\n\n\n\nThe study concludes that AA shares clinical\, immunohistochemical\, and molecular features with DGCT and should not be classified solely based on the presence of specific structures. Further research is necessary to explore these tumors’ pathologic mechanisms and potential therapeutic targets. \n\n\n\n\n\nHost & Moderator\n\n\n\nAssoc. Prof. Pouyan AminishakibOral and Maxillofacial PathologistVice President of the Iranian Association of Oral Pathologists \n\n\n\n\n\nGuest Moderator\n\n\n\n Prof. Merva Soluk TekkesinDepartment of Tumor PathologyInstitute of Oncology\, Istanbul University\, Turkey \n\n\n\n\n\nPresenter\n\n\n\nJiang XuePhD Candidate in Basic Oral MedicinePeking University School of Stomatology\, China \n\n\n\n\n\n\n\n\n\n\n\nJoin the Live Session or Watch Later\n\n\n\n\n\n\n\nTime converter at worldtimebuddy.comTime converter at worldtimebuddy.com\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\nFrom Our Archives:
URL:https://oralpathology360.com/event/journal-club-with-authors-5/
CATEGORIES:Journal Club
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