BACKGROUND: Ameloblastoma (AB) is a locally invasive neoplasm with a potentially destructive behavior. The molecular mechanisms that regulate its cell growth are not yet fully understood. Intervention between G1 cell cycle regulatory proteins could participate in its pathogenesis. P53 gene status implied that p53 mutation might play a role in its tumorigensis; though few mutated genes were perceived. In the absence of p53 mutations, downregulation of p21 could be suggested. Moreover, apoptotic pathways including Bcl2 were also reported to be involved in its progressive growth. Deregulation of these cell cycle regulatory proteins may be reflected on its proliferative potential. Immunohistochemical detection of PCNA represents a useful marker for the proliferating cellular fraction of AB. PURPOSE: To determine whether cell cycle alteration plays a role in oncogenesis of plexiform ameloblastoma (PAB). MATERIAL AND METHODS: A panel of cell cycle-related antibodies, including p53, p21, Bcl2 and proliferation marker PCNA, were examined immunohistochemically in 18 cases of PAB; three of them were recurred ones. Immunoexpression was scored using a semi-quantitative scale and statistically analyzed. RESULTS: The investigation revealed decreased immunoreactivity for p21 compared to intense immunoexpression for p53 and Bcl2. As regards to the proliferative potential, majority of cells exhibited immunolabeling for PCNA particularly at the periphery of the neoplastic odontogenic strands as well as in the endothelial cell lining of the stromal blood vessels. CONCLUSIONS: Abnormalities in components of the cell-cycle regulatory machinery might play a role in the development of PAB. Furthermore, the peripheral cell layer is the port for these deregulations; hence it is thought to maintain the proliferating fraction that in turn expanding the neoplastic strands. KEY WORDS: Plexiform ameloblastoma - p53 - p21 - Bcl2 - PCNA.
BACKGROUND:Ameloblastoma (AB) is a locally invasive neoplasm with a potentially destructive behavior. The molecular mechanisms that regulate its cell growth are not yet fully understood. Intervention between G1 cell cycle regulatory proteins could participate in its pathogenesis. P53 gene status implied that p53 mutation might play a role in its tumorigensis; though few mutated genes were perceived. In the absence of p53 mutations, downregulation of p21 could be suggested. Moreover, apoptotic pathways including Bcl2 were also reported to be involved in its progressive growth. Deregulation of these cell cycle regulatory proteins may be reflected on its proliferative potential. Immunohistochemical detection of PCNA represents a useful marker for the proliferating cellular fraction of AB. PURPOSE: To determine whether cell cycle alteration plays a role in oncogenesis of plexiform ameloblastoma (PAB). MATERIAL AND METHODS: A panel of cell cycle-related antibodies, including p53, p21, Bcl2 and proliferation marker PCNA, were examined immunohistochemically in 18 cases of PAB; three of them were recurred ones. Immunoexpression was scored using a semi-quantitative scale and statistically analyzed. RESULTS: The investigation revealed decreased immunoreactivity for p21 compared to intense immunoexpression for p53 and Bcl2. As regards to the proliferative potential, majority of cells exhibited immunolabeling for PCNA particularly at the periphery of the neoplastic odontogenic strands as well as in the endothelial cell lining of the stromal blood vessels. CONCLUSIONS: Abnormalities in components of the cell-cycle regulatory machinery might play a role in the development of PAB. Furthermore, the peripheral cell layer is the port for these deregulations; hence it is thought to maintain the proliferating fraction that in turn expanding the neoplastic strands. KEY WORDS: Plexiform ameloblastoma - p53 - p21 - Bcl2 - PCNA.
Authors: Eliane Macedo Sobrinho Santos; Hércules Otacílio Santos; Ivoneth Dos Santos Dias; Sérgio Henrique Santos; Alfredo Maurício Batista de Paula; John David Feltenberger; André Luiz Sena Guimarães; Lucyana Conceição Farias Journal: Int J Mol Cell Med Date: 2016-12-06