首页 | 本学科首页   官方微博 | 高级检索  
     


Molecular concepts in the pathogenesis of ameloblastoma: Implications for therapeutics
Authors:Tania Jhamb  Jill M. Kramer
Affiliation:1. Department of Oral and Maxillofacial Medicine and Diagnostic Science, Case Western Reserve University School of Dental Medicine, Cleveland, OH 44106, USA;2. Department of Oral Biology, School of Dental Medicine, University of Buffalo, The State University of New York, Buffalo, NY 14214, USA;3. Oral Diagnostic Sciences, School of Dental Medicine, University of Buffalo, The State University of New York, Buffalo, NY 14214, USA
Abstract:Ameloblastoma is a benign odontogenic neoplasm that may exhibit aggressive biological behavior as evidenced by its rapid growth and significance recurrence rates following initial surgical resection. Currently, the only therapy for ameloblastoma is surgical, and adjunctive treatment modalities are needed to mitigate tumor growth and to reduce the need for extensive and disfiguring surgeries. Many studies have identified markers expressed by ameloblastoma and these lend insight to our understanding of tumor progression. This review provides a summary of the specific molecular pathways implicated in tumor pathogenesis, including those involved in bone remodeling, apoptosis, cell signaling, and tumor suppression. Based on these data, we identify several prognostic or therapeutic markers that have been used successfully in the treatment of other neoplastic processes that may also have diagnostic and prognostic utility for ameloblastoma. Thus, it is important to determine which markers hold the greatest promise for clinical management of this benign neoplasm in order to improve treatment options, particularly in patients with aggressive forms of ameloblastoma.
Keywords:EGFR, epidermal growth factor receptor   EMT, epithelial&ndash  mesenchymal transition   ECM, extracellular matrix   ERK, extracellular signal-regulated kinase   FasL, Fas ligand   ICE, interleukin-1β converting enzyme   NF-κB, nuclear factor κB   OPG, osteoprotegerin   PI3K, phosphatidylinositol 3-kinase   PTEN, phosphatase and tensin homolog deleted on chromosome 10   RANK, receptor activator of NF-κB   RANKL, receptor activator of NF-κB Ligand   Ras/MAPK, Ras/mitogen activated protein kinase   sFas, soluble Fas   ssDNA, single stranded DNA   TCC, transitional cell carcinoma   TNF, tumor necrosis factor
本文献已被 ScienceDirect 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号