Molecular concepts in the pathogenesis of ameloblastoma: Implications for therapeutics |
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Authors: | Tania Jhamb Jill M. Kramer |
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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 |
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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. |
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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 |
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