• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.27 no.6
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• pp.519-525
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• 2001

The oral cavity has frequent contacts with many carcinogenic compounds and its soft tissue is continuously stimulated by numerous dental factors. We have examined the detailed dental factors and its correlation with oral squamous cell carcinoma, and denture-wearing effects to analyze the effect of the dental factors on the genesis of oral squamous cell carcinoma. We have studied clinical contributing factors and the dental factors in the genesis of oral squamous cell carcinoma when the effects of smoking and drinking are controlled. The study cases are 100 patients(75 males and 25 females) who were diagnosed histo-pathologically as squamous cell carcinoma at the Yonsei Medical Center. The control group was 154 patients who have no systemic malignant tumors. The effects of 6 dental factors were analyzed in this study. They were divided into the smoking group, the non smoking group, the drinking group, and the non-smoking group. The effects of dental factors were analyzed in each group. In this study, we have drawn some conclusions on the relationship between the dental factors and oral squamous cell carcinoma using $x^2$-test. 1. The repaired teeth have statistical significance on the genesis of squamous cell carcinoma. This is probably due to the combining effects of past poor oral hygiene and continuous stimulation due to poor prosthesis. 2. There is statistical significance of the lost teeth in the smoking group, and the repaired teeth and the degree of alveolar bone resorption had statistical significance in the non-smoking group. 3. Smoking and drinking by-itself have no statistical significance in the genesis of oral squamous cell carcinoma. However, in combination, they have statistical significance. In this study, dental factors had a synergistic effect with smoking and drinking. Together with avoidance of smoking and drinking, appropriate restoration and oral hygiene control are most important factors in the preventive aspects of the oral squamous cell carcinoma.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.37 no.1
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• pp.15-20
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• 2011

Introduction: The characteristics of oral tongue squamous cell carcinomas (SCC) and the treatment results were reviewed to determine the appropriate treatment strategies. Materials and Methods: The medical records of 140 patients diagnosed and treated for oral tongue SCC at Yonsei University Health System from January 1995 to December 2004 were reviewed. For statistic analysis, the survival rate was determined using the Kaplan-Meier method with SPSS version 12.0, and the difference in survival rates was evaluated using a log-rank test. Results: The mean age of the patients with oral tongue SCC patients was 55 (19-85 years old). According to the T, N and pathologic stage, the patients were distributed from a higher to a lower incidence of cases, as follows: T2 (46.4%), T1 (37.9%), T4 (8.5%), and T3 (7.1%); N0 (65%), N1 (20.7%), N2 (13.6%), and N3 (0.7%); and stage I (31.4%), stage II(25.7%), stage IV (22.2%), and stage III (20.7%). Local and regional recurrence and distant metastasis was present in 13.6%, 5% and 4.2% of patients, respectively. The five-year survival rate was 72.2%, and the prognostic factors for oral tongue SCC included neck metastasis, pathologic stage of the disease, cell differentiation, treatment modality, neck dissection as part of the treatment plan, and neck node recurrence. Discussion: It is suggested that ipsilateral neck dissection or bilateral neck dissection should be selected as a treatment of tongue SCC patients with advanced stage.

• Radiation Oncology Journal
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• v.5 no.2
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• pp.105-110
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• 1987

Fourty nine patients with squamous cell carcinoma of oral tongue were reviewed retrospectively for the evaluation of clinical manifestation and for the comparison between therapeutic modalites. The gross shape of the tumor was infiltrative in 22, ulcerative in 12, ad ulcer-oinfiltrative type in 10 patients. Direct extension of the tumor was most commonly to the floor of the mouth. The incidence of nodal metastasis generally increased with tumor stage. $55\%$ of the patients showed neck nodal metastasis at the time of diagnosis. Ipsilateral subdigastric node were most commonly involved, followed by submandibular nodes. The 5-year survival rate of patients treated with surgery and radiotherapy was $58.7\%$ in contrast to $21.6\%$ in radiation alone group. Overall 5-year survival rate was $31\%$ In radiation alone group, half of the patients in stage I, II were locally controlled. But the local control In stage III, IV was much inferior to early lesions. Especially, of 4 patients combined with implantation technique, 3 were completely controlled. 5-year survival rate of these implanted patients was $50\%,\;49.4\%$ of patients treated over 7,000cGy survived 5 years. This was significant in contrast to $6.4\%$ of the group treated below 7,000cGy. The most common sites of failures were primary sites. In early lesions primary radiotherapy with implantation would be an appropriate treatment in cancer of oral tongue, operation reserved for radiation failure. Operation and adjuvant radiotherapy is recommended in cases of advanced disease.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.30 no.6
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• pp.474-481
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• 2004

Squamous cell carcinoma is the most prevalent oral cancer, which is characterized by its low survival rate, high malignancy, mortality with facial defects, and poor prognosis. Exact cause and pathogenesis of the squamous cell carcinoma is still unknown. Various routes including smoking, radiation, and viral infections predispose its genesis, and recent studies revealed that genetic defects which fail to prevent cancer proliferation play a role. Generally, a cancer develops from the decreased rate of apoptosis which is an active and voluntary cell death, and from the altered cell cycles. Anticancer effect can be obtained by recovering the apoptotic process, and by suppressing the cell cycles. Among the apoptosis related factors, bcl-2, caspase-9, and VDAC (voltage-dependent anion channel)are produced in mitochondria of the cell. Cyclosporin-A is known to induce apoptosis through its activation with VDAC. This study was to reveal the anticancer effect of Cyclosporin A to the oral squamous cell carcinoma. The inverted microscope was used to find alterations in the tissue, and sensitivity test to the anticancer cells was performed with MTT (Tetrazolium-based colorimetric) assay. Following cell line culture of primary and metastastic oral squamous cell carcinoma, electrophoresis was performed with extracted total RNA. Finally, semi-quantitative study was carried out through RT-PCR (Reverse Transcription-Polymerase Chain Reaction). The results of this study are as follows: 1. The inverted microscopic observation revealed a poorly defined cytoplasm at $2000ng{\sim}3000ng/ml$, indistinct nucleus, and apoptosis. 2. The Growth of cancer cells was decreased at 1000ng/ml of cyclosporin-A. No cancer cell growth was observed at over 2000ng/ml concentration of cyclosporin-A, and at one week, growth of cancer cells was ceased. 3. The MTT assays were decreased as cyclosporin-A concentration was increased. This means that the activation of succinyl dehydrogenase in mitochondria was decreased following administration of cyclosporin A. 4. A result of RT-PCR showed that amount of mRNA of VDAC-2 was decreased half times at a cyclosporine-A concentration of 2000ng/ml. In bcl-2, amount of mRNA was significantly decreased 1/5 times at 2000ng/ml. caspase-9, however, showed slight increase compared to the control group. From the results obtained in this study, administration of cyclosporin-A to the cell lines of oral squamous cell carcinoma induced alterations in morphology and growth of the cells as its concentration increased. Since apoptosis related factors such as VDAS-2, bcl-2, and caspase-9 also showed distinct alterations on their mRNAs, further research on cyclosporin A as an anti-cancer agent will be feasible.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.28 no.3
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• pp.193-201
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• 2006

Squamous cell carcinoma(SCC) of head and neck(SCCHN) is the sixth most common human malignant tumor. However, despite advances in prevention and treatment of SCC, the five-year survival rates for patients remain still low. To improve the outcome for patients with SCCHN, novel treatment strategies are needed. Overexpression of the epidermal growth factor(EGF) and activation of its receptor(EGFR) are associated with progressive growth of SCCHN. Vascular endothelial growth factor(VEGF) signaling molecules are related with neoangiogenesis and vascular metastasis of SCC. In this study, we determined the therapeutic effect of AEE788(Novartis Pharma AG, Basel, Switzerland), which is a dual inhibitor of EGFR/ErbB2 and VEGFR tyrosine kinases, on human oral SCC. At first, we screened the expression of EGFR, c-ErbB2(HER-2) and VEGFR-2 in a series of human oral SCC cell lines. And then we evaluated the effects of AEE788 on the phosphorylation of EGFR and VEGFR-2 in a oral SCC cell line expressing EGFR/HER-2 and VEGFR-2. We also evaluated the effects of AEE788 alone, or with paclitaxel(Taxol) on the oral SCC cell growth and apoptosis. As a result, all oral SCC cells expressed EGFR and VEGFR-2. Treatment of oral SCC cells with AEE788 led to dose-dependent inhibition of EGFR and VEGFR-2 phosphorylation, growth inhibition, and induction of apoptosis. Moreover, AEE788 sensitizes the cells to paclitaxel-mediated toxicity and apoptosis. These data mean EGFR and VEGFR-2 can be reliable targets for molecular therapy of oral SCC, and therefore warrant clinical use of EGFR/VEGFR inhibition in the treatment of patients with recurrent or metastatic oral SCC.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.32 no.2
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• pp.118-125
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• 2010

Background and Purpose: Bone metastases rarely occur in patients with oral squamous cell carcinoma (OSCC), so the molecular mechanisms of bone metastasis of OSCC remains unclear. Studies with animal models allow progresses in understanding the molecular events for bone metastasis and provide new targets for therapy. So we tried to establish a murine model for bone metastasis of oral squamous cell carcinoma. Materials and Methods: Human OSCC cells (KB cell line) were xenografted to nude mice via direct inoculation into the tibial marrow. Mice with tibial tumors were sacrificed once a week, until seven weeks after the injection of human tumor cells. Growth of tibial tumors were observed by histology. Expression of TGF-$\beta$ and CXCR-4 in bone OSCC (experimental) and subcutaneous tumor (control) was also evaluated by immunohistochemical staining. Results: Bone OSCC was successfully induced by intra-tibial injection of KB cells. Tumor mass was developed in the marrow tissues of tibia and finally invade the endosteum of tibia. Immunohistochemical staining showed higher expression of TGF-$\beta$ in bone tumors than in subcutaneous tumors. Conclusion: A murine model of bone metastasis of OSCC was suggested that imitated the clinical findings of distant vascular metastasis. This bone tumor model should facilitate understanding of the molecular pathogenesis of OSCC bone metastasis, and aid in the developement of treatment strategies against OSCC bone metastasis.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.27 no.2
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• pp.142-149
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• 2001

To investigate the correlation between the clinical features and the expression of p53, PCNA, and Ki-67 of the head neck squamous cell carcinoma, immunohistochemicalstaining of p53, PCNA, and Ki-67 on the paraffin embedded tissue blocks of 116 surgically removed specimens were done. The staining intensity was divided as grade 1 to grade 3 and the results were statistically analysed. 1. The positive reation rates of cell proliferation markers (PCNA and Ki-67) were higher than that of p53. There was significant correlations of the PCNA and Ki-67 expression but there was no significant correlations between p53 and PCNA or p53 and Ki-67. 2. There were no significant correlation between the expression of p53, PCNA and Ki-67 and tumor site or tumor size. 3. There was no significant differences in the positive response according to the nodal status. The node metastasis groups revealed that higher proportion of grade 3 staining of PCNA and Ki-67 than node negative group. From the above results it is concluded that p53 and cell proliferation markers PCNA and Ki-67 might have their unique mechanism involving in the growing and progression of tumor. Overexpression of p53 does not appear to represent an independent prognostic marker in head neck squamous cell carcinoma.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.36 no.2
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• pp.125-127
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• 2010

The coexistence of aspergillosis and squamous cell carcinoma (SCC) in the maxillary sinus was very rare. To our knowledge, this is the second report of coexistent SCC and aspergillosis in the maxillary sinus. A 58-year-old man underwent surgery for unilateral maxillary sinus infection with oroantral fistula. In the surgical specimen, SCC and aspergillosis were co-detected with routine and immunohistochemical stainings. Moreover, human papillomavirus 18 (HPV-18) was detected by polymerase chain reaction in the sinus specimen. The patient was re-operated with subtotal maxillectomy and has been followed up for two years without any evidence of recurrence or metastasis. Although it is not understood how aspergillosis could induce carcinoma formation, the chronic inflammation caused by prolonged fungal infection might be carcinogenic. Moreover, HPV-16 and -18 were another causative pathogens of SCC in the head and neck region. We recommend careful examination, including preoperative cytology, in patients with maxillary sinus fungal infections because of the potential for cancer development.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.33 no.1
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• pp.1-9
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• 2011

Purpose: Tumor associated angiogenesis and/or lymphangiogenesis are known to be linked by VEGFR signaling pathways. These processes are regulated by several growth factors including VEGFR-2, VEGFR-3. E7080 is an orally active inhibitor of multiple tyrosine kinases including VEGFR-2, 3. Therefore, it was proposed that E7080 may inhibit angiogenesis and lymphangiogenesis. The aim of this study was to determine the effect of E7080 in a nude mouse model of OSCC. Methods: KB cells were xenografted into the submucosal tissue of the mouth floor of athymic mice. Seven days after the xenograft, the mice were randomized into 2 groups. E7080 were administered orally to the experimental group once per day. The mice were sacrificed 3 weeks after the treatment. The tumors were examined histopathologically. Immunohistochemical assays with anti- VEGF-C, VEGFR-2, VEGFR-3, phosphorylated VEGFR-2/3 (pVEGFR-2/3), and D2-40 antibodies were then performed. Results: The transplantation of human OSCC tumor cells into the mouth floor resulted in the formation of orthotopic tumors. The experimental (E7080 treatment) group showed a slowly increased tumor volume. Moreover, immunohistochemical staining demonstrated higher levels of VEGF-C, VEGFR-2, VEGFR-3, pVEGFR-2/3 and D2-40 expression in the control group than in the experimental group. Conclusion: These results suggest that E7080 may provide therapeutic benefits in OSCC.

• The Journal of Korean Academy of Prosthodontics
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• v.54 no.2
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• pp.126-131
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• 2016

Surgical management of oral cancer results in compromised masticatory and swallowing function which affects patient in social and psychological aspects due to reduced phonetic ability and facial deformity, thus, it is imperative to provide applicable prosthetic treatment to overcome such complications. This clinical study describes rehabilitation of a patient with squamous cell carcinoma treated with marginal mandibulectomy and implantation on preserved posterior portion of mandible to provide stability and support for subsequent denture treatment. Kennedy class IV removable partial denture has provided satisfactory results in esthetics and function. Bone level stability around implants was reported to be maintained during eight months of clinical observation.