Several recent studies have detected genetic and cytogenetic alterations in epithelial odontogenic tumors. However, the detailed mechanisms of oncogenesis, cytodifferention, and tumor progression remain unknown. p63 as p53 homolog gene has been identified at loci 3q27-29. The p53 signaling cascade has an important role in oncogenesis or cyto- differentiation of odontogenic epithelium. Recently, several syndromes associated with p63 gene mutations have shown to include various tooth abnormalities of both the primary and permanent dentition. But little is known about p63 expression in odontogenic tumors, especially ameloblastomas. The purpose of this study were to examine various expression of p63 in ameloblastomas by immunohistochemistry and to clarify the possible biological role of p63 in ameloblastomas. 15 specimens including 6 follicular, 4 plexiform, 3 acanthomatous, and 2 granular cell types were fixed in 10% neutral formalin. 4um thick sections were used for routine H&E and immunohistochemical examinations. After immuno- histochemical satining, they were examined at a final magnification of 400X. For each case a minimum of 1000 nuclei located in the central and peripheral layers were counted in up to 10 consecutive microscopic fields per case. The immunoreactive cells were evaluated semiquantitatively. Immunoreactivity for p63 in all the types of ameloblastomas was higher in peripheral neoplastic cells than in central neoplastic cells. Keratinizing cells in acanthomatous ameloblastoma and granular cells in granular cell ameloblastoma showed markedly decreased reactivity for p63 in acanthomatous and granular cell ameloblastoma. Labelling index of acanthomatous, plexiform, and granular cell type was 86±11%, 81±17% and 83±15% in peripheral area while 88±14%, 82±11% and 76±10% in central area, respectively. Labelling index of follicular type was 17±4% in peripheral area while 21±3% in central area. There was no significant relationship between plexiform, acanthomaous, and granular cell type, while significant relationships between follicular and acanthomatous type, between plexiform and follicular type, and between granular cell and follicular type, respectively. It suggested that p63 expression could paly an important role in the pathogenesis of ameloblastomas. Morever plexiform, acanthomatous, and granular cell type would show more aggressive proliferative potentiality than follicular type.

Ameloblastomas are benign odontogenic tumor and the most common neoplasm in jaws and they have locally invasive property and high recurrence rate. Four typical subtypes ameloblastomas are plexiform, follicular, granular cell and acanthomatous type, but their developmental states during tumorigenesis are uncertain. And thus authors studied about developing states of four types of ameloblastomas by immunohistochemical staining for cytokeratin 8/18 which was an intermediate filament of epithelial cell origin and for vimentin which was an intermediate filament of mesenchymal cell origin, and then by comparative analyses of the results. Authors selected seven cases for every four types of ameloblastomas, and then performed immunohistochemcial staining for cytkeratin 8/18 and vimentin to all selected specimen by using monoclonal antibodies about cytoleratin 8/18 and vimentin, LSAB(Labelled StreptoAvidin Biotin) reactant and HRP(Horse Radish Peroxidase) system. Labelling indices of cytokeratin 8/18 of plexiform and follicular types of ameloblastomas were significantly high values in the group of ameloblast-like cells and labelling indices of cytokeratin 8/18 of all types of ameloblastoma were high values in the group of transformed cells, but their differences were not significant. Labelling index of vimentin of plexiform ameloblastoma was significantly high value in the group of ameloblast-like cells and others showed comparatively lower values. Labelling index of vimentin of granular cell type of ameloblastoma in the group of transformed cells was significantly high value and others showed comparatively lower values. Consequently the most primitive form of ameloblastoma was plexiform, and more differenciated form was follicular type and granular cell type and acanthomatous type were most differenciated form of ameloblastomas

Elevated expression of survivin is strongly associated with tumorigenesis and even in human common cancers. The purpose of this study is to confirm whether survivin is associated with odontogenic tumor expecially in the development and growth in ameloblastomas. For the control group; 3 specimens obtained from normal oral mucosa without any inflammatory reaction were used. For the experimental group, specimens obtained from 17 subjects of ameloblastomas; follicular type, plexiform type, granular cell type, acantomatous type and unicystic ameloblastoma. All the specimens were embedded in paraffin, sectioned 5μm or more in thickness, and stained with hematoxylin- eosin stain method. For immunostain, the specimens were incubated with 1:200 diluted primary antibody, followed by the secondary antibody. The bound antibodies were visualized by addition of diaminobenzidine tetrahydrochloride (DAB) for 30 minutes at room temperature. The specimens were counterstained with Gill’s Hematoxylin and mounted. Intensity of survivin immunoreactivity specimens was quantitatively scaled using under the light microscope with the following criteria; Intensive reaction; +++, Moderate reaction; ++, Minimal reaction; +. Using the image analyzer (Korea Optical System), immunoreactivity of the tumor cells in various fields was measured and statistically analyzed with SPSS 17.0 Program. In control group, moderate positive reaction was noted in the cytoplasm of cells in the basal and spinous layer, but negative reaction was revealed in the nucleus. Expression of survivin was significantly increased in the cytoplasm of ameloblastomas as compared to that of control group (p<0.05). Expression of survivin in the nucleus and the cytoplasm of the tumor cells between subtype of ameloblastoma was not significantly different. These results suggest that expression of survivin is closely associated with the development, and growth of the ameloblastomas. However it is unlikely that survivin can be used as a marker for cellular malignancy.

The purpose of this study was to evaluate the role of integrin α3 and integrin β1 in the ameloblastomas. For this study, 10 specimens diagnosed as amoblastomas referred to the Department of Oral Pathology, School of Dentistry, Kyung Hee University, and 5 specimens of normal oral mucosa without any inflammatory changes were used as experimental and control groups, respectively. The ameloblastomas devided into follicular type, plexiform type, acanthomatous type, and granular cell type. All specimens; experimental and control group were fixed in 10% neutral formalin solution and embedded in paraffin, and then the serial tissue sections were made 5㎛ in thickness and processed for immunohistochemical observation. The specimens were incubated with primary antibody against integrin α3 or integrin β1, each was diluted at 1 : 100, followed by the Supersensitive non-biotin horse radish peroxidase detection system with DAB as chromogen. After counterstaining with Gill's hematoxylin stain method and mounted, and examined under the light microscope. Based on the intensity of the immunoreactivity, intensity of the immunity was scored no epithelial stain, weak or focal epithelial stain, moderate or focal intensive epithelial stain, intense generalized epithelial staining for the epithelial, and connective tissue component in ameloblastomas, and normal oral mucosa on each. Attained results as follows. Expression of integrin α3 in the oral mucosa, weak reaction was noted on the all layers of epithelium, and submucosa. Expression of integrin β1 in the oral mucosa, intense reaction on the superficial layer, moderate reaction in basal layer were shown. Expression of integrin α3 in ameloblastomas, it was noted that weak reaction on the ameloblast like cells in the all types and rarely in basement membrane. Expression of integrin β1 in ameloblastomas, intense reaction on the tumor cell ,and partly in the nuclei in follicular type was noted, And moderate reaction on the tumor cell in plexiform , acathomatous types, but weak reaction in granular cell type was shown. This results result suggest that integrin α3 may influenced negligibly, but the integrin β1 influenced significantly the development of the ameloblastomas considering the response is increased on the region with highly cellular activities

The purpose of this study was to evaluate the role of c-fos and c-jun expression in the oral squamous cell carcinoma and ameloblastomas. For this study, 12 subjects diagnosed as squamous cell carcinoma and 7 subjects of ameloblastomas referred to the Dept. of Oral Path. School of Dentistry, Kyung Hee University, 2 subjects of normal oral mucosa without any inflammatory changes were used as experimental, control groups respectively. All the tissues ; experimental and control group were fixed in neutral formalin solution and embedded in paraffin, serial tissue section were made 5㎛ in thickness and processed in the standard way for immunohistochemical method, using primary and secondary antibodies, for c-fos (Anti-c-fos protein, rabbit polyclonal kit at 1:100 dilution), c-jun( anti-c-jun protein, rabbit polyclonal at 1:100 dilution), all BioGenex U.S.A. made, followed by the Streptavidin - Horse Radish Peroxidase(InnoGenex, Human-Avidin kit) application, counter stained with Mayer's hematoxylin stain method, mounted. And examined under the biologic microscope, with the criteria-(no epithelial stain), +(weak or focal epithelial stain), ++(moderate or focal intensive epithelial stain), +++(intense generalized epithelial staining) for the epithelial, and connective tissue component in squamous cell carcinomas, ameloblastomas and normal mucosal epithelium on each. Attained results as follows ; 1. In oral mucosa, c-fos and c-jun intensely expressed on the all cell layers except on the basal layer. Intense reaction is noted in the c-jun than in the c-fos. and a few cells with positive cytoplasm, negative nuclear are scattered in all layer. 2. The response to c-fos in ameloblastomas, is various according to the histological type, but intense resposes are nodted in nuclear and cytoplasm on the tall columnar cells at the periphery of the follicles compare to that on the stellate cells. 3. The respone to c-fos in squamous cell carcinoma, intense reaction is noted in cytoplasm and nuclei of the tumor cells in well differentiated, poorly differentiated type. 4. The response to c-jun in ameloblastoma, it is noted that moderate respone in nuclear and cytoplasm, at the tall columnar cells at the periphery of follicular or plexiform type but intense respone was notes on the columnar cells, and stellate cell in cytoplasm and nuclear of acanthomatous type. 5. The respon to c-jun in squamous cell carcinoma, it is noted that intensive responses only in cytoplasm in well differentiated type, but intensive responses in nuclei and cytoplasm in the poorly differentiated type are revealed. Intensive responses on c-fos, c-jun were noted on the high atypical cells. This results suggest that c-fos and c-jun may be affected to the reactivation on growth and development of the squamous cell carcinoma.

The puφose of this study was to evaluate the role of EGF(Epidermal Growth Factor), EGFR(Epidermal Growth Factor Receptor), aFGF(acidic Fibroblast Growth Factor or FGF-1), bFGF(basic Fibroblast Growth Factor or FGF-2), FGFR(Fibroblast Growth Faαor Receptor), and VEGF(Vascular Endothelial Growth Factor) in the development of the human ameloblastomas For this study 9 subjects, diagnosed as ameloblastomas referred to the Dept. of Oral Path. College of Dentistry, Kyung Hee University, 2 subjeαs of normal oral mucosa with any inflammatory changes were used as experimental, control groups respectively. All the tissues ; experimental and control group were fixed in 10% neutral formalin solution and embedded in paraffm, serial tissue section were made 하1m in thickness and processed in the standard way for immunohistochemical method, using primary and secondary antibodies, for EGF(Antirabbit Ig G, rabbit kit at }:1oo dilution), EGFR(Antimouse Ig G, mouse kit at 1:100 dilution), aFGF(Antirabbit Ig G, rabbit kit at 1:100 dilution), bFGF(Antirabbit Ig G, rabbit kit at 1:100 dilution), FGFR(Antimouse Ig G, mouse kit at 1:100 dilution) , and VEGF(Antirabbit Ig G, rabbit kit at 1:100 dilution), all BioGenex U.S. A. made, followed by the Streptavidin - Horse Radish Peroxidase(InnoGenex, Human-avidin kit) appli때on ， counter stained with Mayer’s hematoxylin stain method. And examined under the biologic microscope, graded -(no epithelial stain), +(weak or focal epithelial stain), ++(moderate or focal intensive epithelial stain), +++(intense generalized epithelial staining) for the epithelial, and connective 따sue component in ameloblastomas and in normal mucosal epithelium on each. Attained results as follows ; 1. EGF, EGFR, aFGF, bFGF, FGFR, and VEGF showed more intense stainability on experimental group compare t，。 that on the control group. 2. EGF, EGFR, aFGF, bFGF, FGFR, and VEGF showed more intense stainability in epithelial component and more intensely stained on the peripheral ce11s of the ameloblastomas. 3. EGF, EGFR, aFGF, bFGF, FGFR, and VEGF showed positive stainability on the stromal tissues but its level is lower compare to that on the epithelial components. Those results suggested that those growth factors take a role in development and progression on the amelob비las와tomas