The incidence of oral cancer varies widely worldwide. Its treatment often produces significant functiona l and cosmetic morbidity and its mortality continues to be high. Strategies for diagnosing, managing and preventing the disease must be based on an understanding of r isk factors and the pathogenesis of the disease locally. The World Health Organizat ion has documented that few countries have a comprehensive a pproach to the diagnosis , management and prevention of cancer at various anatomic sites. This presentation will review the United States’ experience with oral cancer and its strategies fo1' affecting incidence and prognosis . The greatest obs tacles are often political and economic, not scientific.

Chromosomal abnormality s uch as aneuploidy is one of the main factors to cause cancers This abnormality is caused by defects in centrosomal duplication‘ and most cancer cells have extra copies of centrosomes, r esulting in t he formation of multipolar spindles. Several kinases playing in mitotic phase have been implicated in regulating the centrosomal cycle‘ spindle checkpoint‘ and chromosome co ndensation and segregation. They also have Lhe ability to act as oncogenes. FOl studying the relationship between rnitotic kinase and oral cancers, the kinase activity of polo-like kinase-1, which is one of mitosis-specific kinases, is analyzed in oral carcinoma cells originated differently. Kinase activity was increased in these cancer cells compared to normal human gingival fibroblast primary cultured cells Moreover. the mitotic cell populations were a lso increased in these cell lines. Whereas the inhibition of Polo-like kinase-1 by C-terrninal domain in human gingival fibroblast cells induced multiploidy‘ the apoptotic cell population was increased in oral cancer cells overexpressed C-terminal domain 0 1' Polo- Ii ke kinase-1. These data suggested that polo-like kinase-1 might be involved in the on cogenic effect in oral cancer like other solid human carcinomas, and be target molecules for anti-cancer drug.

PDT is an establi shed cancer treatment modali ty , This can be attributed to the attractive basic concept of PDT; the combina ti on 0[' two ther a peut ic agents, a photosensitizing drug and light, which are r elatively harmless by themselves but combined ultimately ca use more 0 1' less selective tumor destruction, The bacteriochlorophyll - derivatived photosensitizers are known to be s ta ble and hi ghly efficient‘ In this s tudy, we conducted a series of experiments to develope the ligh t induced anticancer drugs against oral cancer cell ‘ We tested the cytotoxicity of the hydroxybact eriochlorine by MTT a ssay and observed the cell death pattern (apoptosis or necrosis) after PDT by hoechst 33342 and propidium iodide s taining methods , IC50 value of the hydroxybacteriochlorine was 31,3ngjm.Q, At higher doses of hydroxybacteriochlorine () 60 ng/ 뼈) ， cancer cells died exc lus ively by nec rosis after PDT By contrast, at IC50 value, h ydroxybacteri ochlorine in duced ca ncel' cell to undergo a poptotic cell death The induction begins approximately 6 hours after PDT We investigates int racellu la r localizati on of hydroxybact eri ochl orine by ora l cancer cell via confocal laser scanning microscopy, Oral can cer cells dual-stained with hydroxybactel' iochlorine and organelle-specific fluoresc ence probes (Mi totracker, Lysotracker , ER- Trac ker) revealed an int l'acellula l' flu orescence distribution restrict ed to cytoplasmic compartments with no detectable fl uoresce nce in the nucleus Confocal images of cells containing hydroxybacteriochlorine were never overlap to mi tochondria, lysosome, endoplasmic l'eticulum when digitally overlapped with the organelle-specific flu orescence probe images of the same cells , These resul ts demonstrat ed that the hydroxybacteriochlorine may have a function as a photosens it izer and cytotoxicity hydroxybactel' ioc hlorine for oral ca ncer cell is more sensitive than head & neck cancer cell or cervical cance l' cell Ther efore PDT using hydroxybact eriochlorine is suitable treatment for oral cavity car cinoma patients.

A novel indil‘ubin analog‘ 5’ nitro-indirubinoxime(Ol1) inhibits cell proliferation and induces apoptosis again st variolls hllman cancer cell s. ln this stlldy, we performed the microarray analysis to identify genes diffel'enti ally expressed in the KB oral sqllamollS carcinoma cells after treatment with 011 Of the 10‘ 800 genes a nalyzed , 1700 genes(15.7%) showed di fferent expression level in the 011-treated cells with respect to untreated control cel1s Arnong those‘ 263 genes(15, 5%) were down -reg띠 ated and 220 genes(12, 9%) were IIp-regulated more than 2-fold, Functionally related gene clllsters inclllde genes associated with signal transdllction(18, 1%) , especially genes re lated with a poptosis(3, 5%) and cell cycle reglllation(5. 8%) . Our application of microarray ar뻐ysis on 01l-treated 01'외 cancer cells al lows the identifi cati on of candidate genes for providing novel insights into the 011-mediated anti -tllmor actl Vl ty ,

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

Alterations in cell surface receptors and adhesion molecules which regulate cell-cell and cell-matrix interactions have been 뻐plicated in tumor processes. In order to investigate the effect of integrin expression on the invasiveness of oral sqllamous cell carcinoma, integ띠1 expression in the celllines such as SCC-4, SCC-9, SCC-15, and SCC-25 was analyzed, and the comparison between cell adhesion assay towards extracellular matrix proteins and in vitro invasion assay following inhibition of the functional domain of the integrins using blocking antibodies against the specific integrins 낀 nd Arg-Gly-Asp (RGD) peptide were carried out. The expression of integrin a 2, a 3, a 6 was detected in all oral squamous cell carcinoma celllines. In contrast, the expression of a vß6 integrin is detected in SCC-4 and SCC-9, not in SCC-1 5 and SCC-25. 까1e adhesion of SCC-4 cell line to collagen 1, laminin, and fibronectin was significantly reducecl by σeatment with a 3-, a 6-, and a vß6-blocking antibody, respectively (p (0.05). 꺼.1e invasion of SCC-4 cell line throllgh Matrigel was significantly reduced by treatment with v 6-blocking antibody and RGD pepticle (p(0.05). These results sllggested that specifìc integrins play an in1portant role in the process of adhesion and invasion of oral squamous cell carcinoma cells and the expression of a vß6 integrin is believed to the enhance its invasivene잃.