Oral squamous carcinoma (OSC) is the most common malignant neoplasm of the oral mucosa. Although the etiology of OSC is not fully understood, accumulated evidences indicate that the activation of proto-oncogenes and the inactivation of tumor suppressor genes underlie the disease development. An OSC cell line, YD-9 was newly established and characterized. However, the mutational analysis of p53 gene was not performed. Thus, in this study, the presence of mutation in the p53 gene was examined by amplification of exon-4 to -8 and subsequent DNA sequencing. Two point mutations were found in exon-4 and -6: A to G, resulting in amino acid change Tyr to Cys in exon-4, and C to G, resulting in amino acid change Gly to Arg in exon-6, respectively. Any mutation was not found in the exon-5, -7 and -8. The presented results would contribute to basic research to understand the biological mechanism of OSC using YD-9 cells.

Although a number of molecules have been implicated in the metastasis of oral squamous cell carcinoma (OSCC) , the precise molecular mechanisms that deterrnine the direction of rnigration and invasiveness of OSCC cells into the lymph nodes remain unclear, Chemokines are a superfarnily of small structurally related heparin- binding proteins‘ which have been identified as attractants that control the rnigration of leukocytes‘ especia lly during imrnune and inflammatory reactlOns Moreover, recent studies have demonstrated that several types 。f cancer express chemokine receptor‘s and use chemokines to metastasize to the target organ, However, there h ave been few reports on biological behaviors by downregulation 0 1' CXCR-4 in ora l cancel‘ cells We tried to screen several OSCC cell lines in order to obtain a suitable cell line model which had the cha ract eris tic of the constitutive ly expressed state of CXCR• 4 Of the several OSCC cell lines, only KOSCC-25B showed the high expression of CXCR-4 in both RT-PCR and Western blot analysis, siRNA-CXCR-4 infected subclones of KOSCC-25B(Si, 3‘ Si 1이 showed downregulation of CXCR-4 expression as expected‘ At serum-free co ndi tion‘ Si.3 s ubclone s ignif icantly decreased cell proliferations at 24 h and 48h and Si, lO subclone significant ly dec reased cell proliferations at 24 h Si ,3 clone dec reased to 67 ,4% and Si,lO clone to 65 ,5% in comparison to vector infected cells These data suggest that the downregulation of CXCR-4 expression could induce anti-rnigratory and ant i- rni g ratory effect

The human ELAV(embryonic lethal abnormal vision)-like protein HuR stabilizes a certain group of cellular mRNAs that contain AU- ri ch elements in theil‘ 3’• untranslated region, Dysregulation of mRNA s tability may be relevant in tumor biology and may lead to abnormal expression of several proteins in malignant tumors, The aim of this study is to identify the differentially expressed proteins according to the functi onal activi ty of HuR Methods : We used stabl e expression of small interfering RNA(siRNA) of HuR gene to inhibit the expression of HuR in human ora l car cinoma cell lines‘ KB cell line and YD10B cell line‘ and compared the proteomic changes between s iRNA-treated and cont rol cell line using two-dimensional gel electrophoresis , Flow cytometry caliber scan(FACS) was employed to investigate the effects of HuR on cell apoptosis and proliferation , Results: Seventeen differentially expressed proteins between the two cell lines were identified by electrospray ioruzati on quadrupole time-of- fl ight mass spectrometry(ESI-Q-TOF MS) and database searching, Among them there are eleven proteins which are significant ly up- regulated in siRNA- treated cell line, which include heat shock protein 10(influencing nucl eocytoplas rnic transpo 다， cell dedifferentiation , and inhibition of apoptosis) , keratin 19(basal cell differ ent iat ion) ‘ and nucleoside diphosphate kinase B(G protein activator), etc Enolase 1 and Ml of pyruvate kinase a re the representatives of signifi cantly down-regulated proteins in siRNA-treated cell 11l1e Conclusion : Our data suggest that HuR participate in mRNAs stability of proteins that have the counter effects in the carcinogenesis of oral ca ncer , And the functiona l proteomics a re needed to elucidate the detailed interactions between HuR and t hese molec ules

Oral squamous cel1 carcinoma(OSCC) is the most common malignancy of head neck region. Typically OSCC cells s how persist ent invasion that frequently leads to local recurrence and distant lymphatic metastasls However, molecular mechanisms of invasion of OSCC remain poorly understood. Her e we identifi ed periostin, interferon induced transmembrane protein l (IF1TM1) and wingless-type MMTV integration site family, member 5B(WNT5B) , as invasion promoting molecules in OSCC by comparing gene expression profiles between a parent OSCC cell line(MSCC-l) and its highly invasive clone(MSCC-1nvl). Overexpression of periostin, IFITMl and WNT5B mRNAs were confirmed in MSCC-1nvl by RT-PCR. Transfection of these molecules promoted invasion of OSCC cells Moreover , siRNA t r eatment of these molecules suppressed invasion of cancer cells in vitro I nter estingly, Periostin, 1F1TMl and WNT5B were highly expressed in OSCCs in comparison with nonnal tissues. 1n an orthotopic mouse model of OSCC, periostin-overexpressing cells metas tasized spontaneously to cervical lymph nodes and t o t he lung through their aggressive invasiveness. These findings suggest that peri ostin, IFITMl and WNT5B play important roles for invasion and of OSCC and can be prognostic markers and therapeutic t argets of OSCC.

Indirubin is the active ingredient 0 1' a traditional Chinese herbal medicine, Danggui Longhui Wan, used for the t reatment of chronic myelocytic leu kelma The author reports that novel indirubin derivative, 5'-nitro-indirubinox ime (5'-NIO) , has potent a nti -proliferative activity on human o1'al cancer cells , Treatment of KB cells with 5’ NIO s howed a s t rong cell growth inhibit ion during indicated time point , A typical apoptosis pattern was obtained with DNA fragmenta tion and i mmunofl uorescence analysis of annelxn-v-f!ous Western blot data revealed that p53 and p21CIP1/Waf- l level increased strongJy upon 5'-NIO treatment , The a uthor next tested whether 5'-NIO could activate apoptos is related proteins s uch as caspase-3/-7/-9, [n cells exposed to 5‘-NIO, activation of caspase-3 and -7 was observed, Interesti ngly‘ caspase-9 and cytochrome c cou ld s li ghtly activate in response to 5’-NIO. These results indicate that 5’-NIO strongly induces oral cancer cells apoptosis via a Mi tochondria-mediated cas pase cascade pathway, These observations together s uggest that 5’ NTO may have a possible therapeutic potentia[ to oral cancer

Matrix metalloproLeases(MMPs) a re a family of zinc dependent enzymes with the capacity to degrade extracellular matrix prote ins. MMPs express ion correlates with cancer cell invasiveness and metas taslS The purpose of our sωdy was t。 determine the role 0 1' stroma l fïbrob lasts in ca ncer cell invasi on by examining the expression and activity of MMP-2 and -9 We used a YD- lOB squalllous ca rcinoma cell line that was est a blished in Yonsei Univer s ity ‘ College 0 1' Dentistry. We then appli ed two types of s lrolllal fibroblastsdel‘ ived from normal gingival tissue and cancer supporting ti ss ue Morphologic examination of fïbroblas ls was carried out by rnicroscopy and doubling time was measured by MTI assay . YD-lOB cells were cultured by lh ree-d imensional culture using collagen gel with two types of flbroblasts To examine the stromal - mesenchyma l inleraclion. we used a direct co-cul tu re system between YD-IOB cells and fibroblasts. Gelatin zymography was performed to exa llline MMP-2 a ncl 9 activit ies. We found that cancer-derived fibroblasts di splay stel late-shaped cells wi th many cyLopl asmic processes. whereas normal gingi val fibroblasts were spindle shaped. The c1oubling time of bOLh lïbroblasLs was not statistically different. Three-dimensional co-culture 0 1' ca ncer cells with ca n cer- c1erived fïbroblasts induced the formation 0 1' multi - Iayered atypical cells, as compared to culturing with normal gin gival f lbrobl asts Both three-c1 imens ional culture ti ss ues inclucecl the invasive gro￦th of cancer cells into the dermal eq uival enLs . Gelatin zymography s howecl that gelatinolytic activity of MMP-2 was activaterl in both co-culture models. However , MMP-9 ac li vity was not a lterecl in YD-lOB carcinoma cells In conclusion. enhanced MMP-2 activity was inc1 uced by boLh cance r- c1eri vecl a ncl norlllal gingival fibroblasts. suggesting that the potential to invacle by stromal fibroblasts was noL l imilecl to ca ncer- c1 eri ved lïbroblasts

It is well known that the imbalance between epithelial cell growth and inhibitor factors may cause human epithelial cancer. Over-expression of the epidermal growth factor receptor(EGFR) has been implicated in the development of oral squamous cell carcinoma. ZD1839 inhibits selectively the EGFR tyrosine kinase activity and is clinically used for cancer patients. However the mechanisms by which it exerts its anti-tumor activity remains unclear. This study attempted to determine the mechanisms underlying the effects of ZD1839 on the cellular level and to characterize the effects of ZD1839 with regard to human oral squamous cell carcinoma(OSCC) cell growth. The YD-10B and YD-38 cell lines established from OSCC in the department of Oral Pathology, Yonsei University College of Dentistry and ZD1839(Iressa) were used for this study. The inhibition of cell proliferation induced by ZD1839 was reversible and the lowest dose of ZD1839 that produced statistically significant growth inhibition in YD cell lines were 0.1 μM. The delay in cell cycle progression was induced by 0.1 μM of ZD1839 treatment after 24 hr. This reduction in cell proliferation and cell cycle delay were associated with up-regulation of the cyclin dependent kinase inhibitor(CDKI), P21CIP1/WAF1 and P27KIP1. Reduced expression of cyclin D1 was also observed after treatment with ZD 1839 to YD-38 cells but not to YD-38. The present results suggest that the antiproliferative effects of ZD1839, in vitro was associated with degradation of cyclin D1, which may be used as a possible indicator of a high cell sensitivity to ZD1839.

Epithelium maintains homeostasis by the signaling balance of growth stimulation and inhibition. Recently, loss of growth inhibitory effects of transforming growth factor-β(TGF-β) on epithelial cells is regarded as a possible mechanism of cancer. Although the genomic mutation in type I and type Ⅱ receptors of TGF-β is considered one of important mechanism of these inactivation, there might be another inactivation mechanism because the mutation rate is relatively low and inhibitory effect is not associated with the mutation. The purpose of this study is evaluating controlling mechanism type Ⅱ receptor of TGF-β by detecting effects of TGF-β on growth inhibition and on expression of cell cycle regulatory protein p21CIP1. Eight cancer cell lines derived from oral squamous cell carcinoma(OSCC) were examined. There was no growth inhibition effects by TGF-β except YD-8 cells. YD-8 cells which showed growth inhibition expresses p21CIP1 by TGF-β whether refractory cell lines, YD-9, did not. All of the tumor cells express mRNA of type Ⅱ receptor by RT-PCR and northern blot analysis, especially on YD-8 and YD-17M. From these results, most of oral cancer cell lines might loose the growth inhibitory effects by TGF-β, and the growth inhibition on YD-8 cells was mediated by expression of p21CIP1.

A novel indirubin analog, 5'-nitro-indirubinoxime inhibits cell proliferation and induces apoptosis against various human cancer cells. In this study, we performed the microarray analysis to identify genes differentially expressed in the KB oral squamous carcinoma cells after treated with 5'-nitro-indirubinoxime. Among the 10,800 genes analyzed, 1,701 genes (15.8%) showed statistically different expression level in the 5'-nitro-indirubinoxime treated cells with respect to untreated control cells. Among those, 263 genes (15.5%) were down-regulated and 220 genes (12.9%) were up-regulated more than 2-fold. Functionally related gene clusters include genes associated with signal transduction (18.1%), especially genes related with apoptosis (3.5%) and cell cycle regulation (5.8%). Our application of microarray analysis on 5'-nitro-indirubinoxime treated oral cancer cells allows the identification of candidate genes for providing novel insights into the indirubin mediated antitumor activity.

The purpose of this study was to evaluate the role of Fas, Fas-L, and FAP-1 expression in the oral squamous cell carcinomas and ameloblastomas. For this study, 10 subjects diagnosed as squamous cell carcinoma and 8 subjects of ameloblastoma referred to the Dept. of Oral Pathology, School of Dentistry, Kyung Hee University, 5 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 antibody against Fas, Fas-L, FAP-1, each was diluted at 1;100 followed by the super sensitive non- biotin horse radish peroxidase detection system with DAB as chormogen, counterstained with Gill's hematoxylin stain method , mounted. And examined under the biologic microscope with the criteria of -(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 oral mucosa on each. In normal oral epithelium, negative reaction was noted on the Fas . Fas-L stain, but on FAP-1 reaction, tumors cells with intense reaction on nuclei and cytoplasm or negative reaction on nuclei with intense reaction on cytoplasm were admixed. On Fas, Fas-1 reaction, both tumor cells of ameloblastoma and oral squamous cell carcinoma showed negative reaction on nuclei and cytoplasms. On FAP-1 reaction, tumor cells of oral squamous cell carcinomas showed more intensive response compare to that on ameloblastomas. Considering these results, the tumor cells of ameloblastoma and squamous cell carcinoma showed negative reaction on the Fas and Fas-L, but it could suggest that FAP-1 induce the development of tumors by means of inhibition of the apoptosis.

Concerns remain regarding the biocompatibility and adverse effects of dental casting alloys. The aim of this study was to understand the cytopathogenic effect of metal ions, which might be released from dental alloys, on oral squamous carcinoma(OSC) cells. The cellular morphology, viability, the type of cell death and molecular change in response to metal ion salt solutions including aluminum(Al), cobalt(Co), copper(Cu) and nickel(Ni) were examined. The values for the metal ions with the exception of AI were estimated to be between 400 and 600μM. The cells treated with the metal ions showed apoptotic change with the exception of Al ions. Metal ion-induced apoptosis was further confirmed using flow cytometric analysis. This study showed that the cytotoxicity and the mode of cell death by metal ions clearly depend on the cell type, the type of metal ion and the duration of exposure. The protein level of Rb, a tumor suppressor that affects apoptosis para-doxically, was higher in the cells treated with Co, Cu and Ni. It is believed that apoptosis and cell damage in the OSC cells treated with Co, Cu or Ni can be evoked by the regulation of Rb.

Amino acid transporters are essential for the growth and proliferation in all living cells. Among the amino acid transporters, the system L amino acid transporters are the major nutrient transport system responsible for the Na+-independent transport of neutral amino acids including several essential amino acids. The L-type amino acid transporter 1 (LAT1) is over-expressed to support cell growth in malignant tumors. The double stranded RNA-mediated RNA interference (RNAi) analysis can be in a wide variety of eukaryotes to induce the sequence-specific inhibition of gene expression. In this study, we examined the effect of LAT1 short interfering RNA (siRNA) on cell growth using siRNA of LAT1 in the KB human oral squamous cell carcinoma. In the RT-PCR analysis and western blot analysis, the siRNA of LAT1 inhibited expressions of LAT1 mRNA and protein. The uptake of [14C]L-leucine was inhibited by siRNA of LAT1. In the MTT assay, the siRNA of LAT1 inhibited the growth of the KB cells in the time-dependent manner, indicating that the growth inhibition of KB cell by the siRNA of LAT1 is induced by the blocking of neutral amino acid transport mediated by LAT1. These results suggest that the transport of neutral amino acids including several essential amino acids into the KB human oral squamous cell carcinoma is mediated mainly by LAT1. Further, the LAT1 would be a new target for the inhibition of cancer cell growth.

Epitheli a l mesenchymal interaction(EMl) is well known to be essential in eznbryonic deve]opment. wound hea]jng a nd ca rci nogenes is. Th is study was a i med to design in vi tro model for the investigation of protein analysis in epithe li al a ncl mesenchyma l i nteract ion(EMI) . This stucly usecl oral squamous cell carcinoma cell line(YD-lOB) . 1'0 investigate the clifference 0 1' protei n ex press ion of cancel‘ cells influencecl by variable in vitro conditions. three different models were des ig necl ; Collagen gel- basecl ca ncer cell culture model devoid of fibroblasts(C) , Direct coτulture moclel(M2) composed of ca ncer cells beneath co ll agen gel embeclded with Swiss 31'3 fibroblasts ‘ and Indi rect co-culture model(Ml) with collagen layer betwecn cancel‘ cells and collagen gel with f lbroblasts Two-dimensional electrophoresis was performed to compa re t he diffe r ence of protein express ion pattern of ca ncer cells aznong three znodel systems. Protein identification was done by MALDI-TOF. As res ults ‘ pl'O te in express ion pat tem of cancel' cells was quite different between znonolayer cul ture and coll agen gel based cultu re. Aclditiona ll y. protein expression was different between culture models with fi broblasts and without fibroblasts a ncl between ind irect contact and direct contact of two cell types ‘ Among differentia l prot ei n spots. catheps in D WäS iuenLifï ed by MALDl• TOF Cathepsin D exprcssion was increased from C model to 11띠 and M2 model by West em blott ing. suggest ing that cathe psi n D expression may be activated by direct and indirect stimulation of stromal fï broblas ts F' rom these resul ts ‘ these models could be appropriate for EMI study and cathepsin D mi ght be incluced by fi broblasts s timulation

Metastatic spread to cervical lymph nodes(LNs) is a major determinant of outcome in oral squamous cell carcinoma (SCC). To provide an useful method for the detection of lymph node micrometastases, we fulfilled the histopathological examination and reverse transcriptase polymerase chain reaction(RT-PCR) using the paraffin-embedded LNs of oral SCC patients. In this study, 78 LNs from 12 patients with primary oral SCC were analyzed. Metastases in the regional LNs were evaluated by RT-PCR for squamous cell carcinoma antigen(SCCA) and cytokeratin 5(CK5). Detectability of metastatic LNs by RT-PCR was compared with histopathological examination. Of 78 LNs, CK5 and SCCA mRNA were detected in 32(41.0%) and 8(10.3%), respectively. Histopathologically, 10(12.8%) of 78 LNs were positive. CK5 mRNA was detected in all 10 histopathologically positive LNs. In contrast, SCCA mRNA was detected in 5 of 10 histopathologically positive LNs. These findings suggest that genetic diagnosis by RT-PCR based on CK5 mRNA expression may be sensitive and clinically useful technique to detect the presence of metastatic carcinoma cells in regional lymph nodes of oral SCC.

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 p16 gene encodes an inhibitor of the cyclin-dependent kinase, which inactivates cyclin-dependent kinase and contro1s the cell cycle progression, The 10ss of p16 expression or overexpression has been reported in many kinds of tumors, Both p16 and PCNA regu1ates cell cycle progression at the Gl/8 checkpoint, Although many researches about the p16 expression in ora1 cancer have been carried out, there are few studies about the corre1ation between p16 ex pression and pro1iferation of ora1 cancer cells The object of this study was to eva1uate the avai1ability of p16 as ear1y diagnostic factor and prognostic factor through corre1atión ana1ysis of p16 expression in ora1 squamous cell carcinoma and its re1ation to PCNA index and clinicopatho1ogic factors 80 we investigated p16 immunohistochemica1 expression of 83 ora1 squmaous cell carcinomas, and obtained the resu1ts as followed, 18 out of the 83 cases(21, 69%) showed p16 positive and 65 samp1es(78,31%) showed p16 negative, Whi1e the mean va1ue of PCNA indices of p16 positive cases was 65,94 ::t 18,32, that of PCNA indices at p16 negati ve ones 54,79 ::t 18, 39, This difference between them showed statistica1 sígnificance, (P=O, 030) p16 positive group was 12/60(20, 0%) of well differentiated tumors and p16 negative group was 6/23(16, 1%) of moderate1y or poor1y differentiated tumors, This difference did not show statistica1 significance. (P=O. 372) From the resu1ts above, it was suggested p16 expression is re1ated to PCNA index in ora1 squamous cell carcinomas.

Amino acid transporters play an important role in supplying organic nutrient to cells. The expression of L-type arnino acid transporter 1 (LATl) and its subunit 4F2 heavy chain (4F2hc) was evaluated to deterrnine the alterations to these transporters in oral norrnal mucosa (ONM) , oral precancerous lesion (OPL) and oral squamous cell carcinoma (OSCC). Sections from formalin-ftxed, paraffm-embedded S따nples of ONM, OPL or OSCC were exarnined using immunohistochernical staining to detect LATl and 4F2hc proteins. 까le LATl and 4F강lC expression increased progressively from ONM to hypeφ，Iastic and to dysplastic lesions and OSCC. In partiαlar， LATl rnay be a more S야dftc indicator of tumor prog~않sion than 4F2hc. 까le gradually increasing LA Tl and 4F2hc expression detected during the multistep progressive change shows that the protein rnay have an important role in the early stages of multistep oral carcinogenesis. In addition, the specific inhibition of LA Tl and 4F2hc rnight be a new rationale to suppress oral cancer progression.

Squamous cell carcinoma comprises about 95% of oral cancers. 까le gene디C 없mage in carcinogen-exposed fields is accumulated to transforrn norrnal mucosa in dysplas디c tissue and fmally invasive carcinoma through multistep process. This carcinogenic process has been a cause of the development of secondary tumors after the removal of primary carcmoma. πle improvement of therapeutic modalities of oral cancer has driven into the increase of multiple cancer occurrence in head and neck region. We experienced 3 pa디ents who had mul디ple squamous cell carcinomas in oral cavlty. π1ÎS study aimed to report multiple pr따laπ squamous cell carcinoma by clinical and pathologic examination and to discuss their molecular mechanism

Matrix metalloproteinases(MMPs) are involved in the degradation of extracellular matrix, which is re lated to infiltrative growth and metastasis of tumor and are regulated by tisslle inhibitor of metalloproteinases(TIMPs) or cell adhesion molecllles such as E-cadherin and epidermal growth factor receptor (EGFR). The aim of this study is to evaluate the relationship between MMP-2, MMP-9 expressions and clinico-pathologic factors, 끼MP-1 ， TIMP-2, EGFR and E-cadherin expressions. lmmunohistochemical stains were perfom1ed on 55 cases of squamous cell carcinoma of the ordl cavity and the results were as follows. MMP-2 and MMP-9 expressions were noted in 30(54.5%) and 22(40.0%) of 55 cases, TIMP-1 and πMP-2 in 21(38.2%) and 33(60.0%), and E-cadherin and EGFR expressions in 35(63.6%) and 26(47.3%) of 55 cases, respectively. MMP-2 expression rdte was slightly higher 띠 cases without recurrence, and 끼MP- 2 expression rate was slightly higher in cases showing more inftltrative growth pattem. 까1e expression rate of EGFR was higher in cases with well differentiation(p=0.OO47), but no posi디ve relationship between the expression rate of Ecadherin and histologic grade was found. Cases with positive reaction for MMP-9 showed an increasing tendency of nega디ve reaction for TIMP-1. π1e expression rate of MMP-2 was higher in cases with positive reaction for E-cadherin and EGFR with no statistical significance. 까1e expression rate of MMP-9 was significantly higher in cases with positive reaction for E-cadherin(p=0.022l). These results suggest that MMP-2, MMP-9, TIMP-1 and TIMP-2 expressions are involved in the development of oral squamous cell carcinomas, but MMP-2, MMP-9, 끼MP-1 ， and 끼MP-2 expressions might not seem to be a useful prognostic factors because there were no significant relationship between clinicopathologic parameters. EGFR expression showed positive correlation with low histologic grade, so EGFR expression could be regarded as a good prognostic factor. In the progression of sqllamous cell

까le purpose of this study was to evaluate the role of EGF(Epidermal Growth Factor) , EGFR(Epidemlal Growth Factor Receptor), aFGF(acidic Fibroblast Growth Factor, FGF-1), bFGF(basic Fibroblast Growth Factor, FGF-2), FGFR(Fibroblast Growth Factor Receptor), and VEGF(Vascular Endothelial Growth Factor) 띠 the development of the oral squamous cell carcinoma. For this study 6 subjects, diagnosed as squamous cell carcinoma refelTed to the Dept. of Oral Path. College of Dentistry, Kyung Hee University, 2 subjects of normal 이띠 mucosa with any inflammatolY changes were used as expelimental, control groups respectively. AlI the 디ssu es ; expe디me nta l and control group were fixed in 100;ú neutral fOlmalin solution and embeclded in paraffìn , seIial tissue section were made 511m in thickness ancl processecl in the standard way for immunohistochemical methocl, using primary ancl seconclalY antibodies, for EGF(Antirabbit Ig G, rabbit kit at 1:100 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 써t at 1:100 dilution), FGFR(Antimouse Ig G, mouse kit at 1:100 dilution), ancl VEGF(Antirabbit Ig G, rabbit kit at 1:100 clilution), all BioGenex U.S.A. macle, followed by the Stre ptavidin - Horse Radish Peroxidase(InnoGenex, Human-avidin kit) application, counter stained with Mayer’s hematoxylin stain method. And examined under the biologic microscope, -(no epithelial stain), +(weak or focal epithelial stain), ++(mode rate or focal intensive epithelial stain), +++(intense generalized epithelial staining) for the epithelial, and connective tissue component in squamous cell carcinoma and in nomlal mucosal epithelium on each. Attained results as follows ; 1. It is noted that more intensed reactio n EGF, EGFR, aFGF, bFGF, FGFR, and VEGF on experimental group compare to that on the control group. 2. Increased reaction is noted on the tumor components compare to that in the stromal tissues. 3. Intensed reaction is noted on the basement membrane adjacent to cancer nest to EGF, EGFR, aFGF, bFGF, FGFR, and VEGF 4. It is noted that intensed positive reaction on cancer pearls, cancer components with hyperactivities, in cancer nest. And at the peIiphelY of cancer nest, diffuse moclerate reaction to EGF, EGFR, aFGF, bFGF, FGFR, and VEGF is notecl This results suggest that EGF, EGFR, aFGF, bFGF, FGFR, and VEGF mJy be effectecl to the growth ancl clevelopment of the squamous cell carcinoma.