• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제35권2호
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• pp.55-65
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• 2009

Purpose: We determined the therapeutic effects of blockade of epidermal growth factor(EGF) and vascular endothelial growth factor(VEGF) receptor tyrosine kinases on the growth of oral squamous cell carcinoma(OSCC) xenografted in athymic nude mice. Experimental Design: We investigated the in vivo antitumor effects of a tyrosine kinase inhibitor for EGFR and VEGFR-2, AEE788 in a mouth floor(orthotopic) tumor model. Nude mice with orthotopic tumors were randomized to receive AEE788, paclitaxel, a combination of AEE788 and paclitaxel, or control. Antitumor mechanisms of AEE788 were determined by immunohistochemical/immunofluorescent and apoptosis assays. Results: Tumors of mice treated with AEE788 demonstrated down-regulation of phosphorylated EGFR, phosphorylated VEGFR and their downstream mediators(pMAPK and pAkt), decreased proliferative index, decreased microvessel density(MVD). As a result, growth of the primary tumor and nodal metastatic potentials were inhibited by AEE788. Conclusion: These data show that EGFR and VEGFR can be molecular targets for the treatment of OSCC.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제33권3호
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• pp.263-267
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• 2007

Primary intraosseous carcinoma (PIOC) is a rare odontogenic carcinoma defined as a squamous cell carcinoma arising within a jaw having no initial connection with the oral mucosa, and probably developing from residues of the odontogenic epithelium. PIOC appears more common in male than female, especially at posterior portion of the mandible. Radiographic features of PIOC show irregular patterns of bone destruction with ill defined margins. It could be sometimes misdiagnosed as the cyst or benign tumor because it shows well defined margins. If it couldn't be done appropriate treatment initially, PIOC shows extremely aggressive involvement, extensive local destruction and spreads to the overlying soft tissue. Therefore accurate diagnosis in early state is necessary. The diagnosis criteria proposed for PIOC are : (1) absence of ulcer formation, except when caused by other factors, (2) histologic evidence of squamous cell carcinoma without a cystic component or other odontogenic tumor cell, and (3) absence of another primary tumor on chest radiograph obtained at the time of diagnosis and during a follow-up period of more than 6 month(Suei et al., 1994).

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제26권1호
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• pp.45-52
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• 2000

Nowadays, there are a lot of evidence that mutation of the p53 tumor suppressor gene is one of the most common genetic abnormalities in neoplastic progression. In this study, we analyzed 20 specimens of oral tumors(squamous cell carcinoma 14 cases, ameloblastoma 3 cases, adenoid cystic carcinoma 2 cases, malignant schwannoma 1 case)using polymerase chain reaction and direct sequencing which used an automated DNA sequencer and software for detection of mutations. Polymerase chain reactions were performed with 4 sets of primers encompassing exon 5, 6, 7, 8, and direct sequencing method was employed. The results were as followings. 1. We detected 10 point mutations out of 20 specimens (50%). 2. The genetic alterations included 7 mis-sense mutations resulting in single amino acid subtitutions, 2 silent mutations, 1 non-sense mutations encoding a stop codon. 3. Mutations were mostly in exon 7(7 out of 10 mutations, 70%) and involved codons 225, 234, 235, 236, 238, 247. 4. Therse were 4 cases of $T{\rightarrow}A$ transversion, 2 cases of $C{\rightarrow}A$ transversion, $A{\rightarrow}G$ transition, 1 case of $C{\rightarrow}G$, $T{\rightarrow}G$ transversion respectively. 5. We could find out point mutations more conveniently using PCR - Automated Direct Sequencing method.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제28권3호
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• pp.226-230
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• 2002

Carcinomas derived from ameloblastomas have been designated by a variety of terms, including malignant ameloblastoma, ameloblastic carcinoma, metastatic ameloblastoma, and primary intra-alveolar epidermoid carcinoma. The term of ameloblastic carcinoma is differentiated from the term of malignant amelblastoma and is defined as an ameloblastoma in which there is histologic evidence of malignancy in the primary tumor or the recurrent tumor(or metastasis), regardless of whether it has metastasized. The well-documented and adequately followed cases are currently lacking and this report described an instance of ameloblastic carcinoma with good result after treatment and review of literature.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제49권2호
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• pp.96-99
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• 2023

Oral spindle cell/sclerosing rhabdomyosarcoma (SCRMS) with anaplastic lymphoma kinase (ALK) expression is extremely rare, and its diagnosis is very challenging in the absence of clinical or pathological indicators. This case presented with gingival swelling and alveolar bone resorption and was suspected clinically to be periodontitis. A biopsy was performed and, due to immunoreactivity with ALK, the patient was misdiagnosed with inflammatory myofibroblastic tumor. However, based on the combined histological and immunohistochemical features, a revised diagnosis of SCRMS with ALK expression was finally concluded. We believe that this report makes a significant contribution to the precise diagnosis of this rare disease for proper treatment.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제37권6호
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• pp.530-534
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• 2011

This paper reports two cases of schwannomas arising from the oral cavity. One is an intraoral ancient schwannoma located at the left cheek, which evolved over a period of 13 years. The tumor was a well-demarcated buccal mass, which was located in the left lower first premolar area, with an obliterated the buccal vestibule, leaving the overlying mucosa intact. The second case was a central intraosseous schwannoma located from the left lower 1st molar periapical area to the left 3rd molar periapical area. Pathologically, the first mass was composed of the spindle shaped tumor cells with wavy nuclei beneath the fibroconnective tissue of the gingiva but second case mass was not. Occasional nuclear pleomorphism was observed but mitosis or necrosis was absent. There were Antoni A and B areas along with strong, diffuse staining with the S-100 protein. Ancient schwannomas were diagnosed. Schwannoma is a slow-growing benign tumor, and an ancient schwannoma that shows cellular atypism is a variant of a schwannoma caused by purely degenerative changes. To date, only limited cases of ancient schwannomas in the oral cavity have been reported.

• Maxillofacial Plastic and Reconstructive Surgery
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• 제34권6호
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• pp.498-504
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• 2012

The odontogenic keratocyst (OKC) was originally classified as a developmental cyst, and OKC is histologically divided into orthokeratic and parakeratic types. According to revised histopathological classification of odontogenic tumors by the World Health Organization (2005), the term, keratocystic odontogenic tumor (KCOT) has been adopted to describe parakeratic OKC. The KCOT is noted for its capacity to recur after treatment. The aggressive, or potentially aggressive, nature of KCOT has led to alternative treatments. Among the treatments is noted the use of Carnoy's solution as adjunctive intralesional therapy having a low rate of recurrence. This study suggests a possible benefit of Carnoy's solution against recurrence of KCOT.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제27권6호
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• pp.483-490
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• 2001

There were many controversies in the cause and progress of tumorigenesis. Recently, studies on the mutation of genes related to the tumor have extensively been performed due to development of molecular biology. Structural and morphological changes of chromosomes, which are related to the abnormal activation of oncogenes or inactivation of tumor suppression genes, transform the normal cells into the tumor cells. p53 and Rb are well known tumor suppressor genes, while oncogenes include c-myc, bcl-2 and ras, etc. When exposed to cell damaging agents, p53 inhibits cell growth by inducing transcription of p21. Especially p73, which is homo-logy of p53, frequently deleted in melanoma, neuroblastoma, colon cancer, and breast cancer, when over produced, p73 activates the transcription of p21, bax-1 and inhibits cell growth by inducing apoptosis. For study on mRNA expression of p21 and p73, normal oral keratinocytes, and cell lines of primary and metastatic oral squamous cell carcinoma were cultured and then electrophoresis and RT-PCR(reverse transcription-polymerase chain reaction) were performed. 1. The mRNA of p21 and p73 in normal oral keratinocyte expressed lower than that of primary squamous cell carcinoma. 2. The mRNA of p21 in metastatic oral squamous carcinoma cell lines was expressed as various patterns compared with that of normal oral keratinocyte. 3. In the metastatic oral squamous cell lines, the mRNA of HN8 expressed higher than that of HN12 or HN19. 4. The mRNA of p73 in primary oral squamous cell lines expressed 4-5 times higher than that of normal keratinocyte. 5. In metastatic oral squamous cell lines, there was no significant expression of p73 mRNA compared with that of normal oral keratinocyte. From the results obtained in this study, mRNA expression of p73 in primary oral squamous cell lines was remarkable, while mRNA expression of p21 and p73 in metastatic oral squamous cell lines were statistically insignificant.

• Maxillofacial Plastic and Reconstructive Surgery
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• 제32권2호
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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.

• Maxillofacial Plastic and Reconstructive Surgery
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• 제34권4호
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• pp.239-245
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• 2012

Purpose: Vascular endothelial growth factor (VEGF) plays a key role in tumor angiogenesis and lymphangiogenesis including induction of endothelial cell proliferation, migration and capillary tube formation. E7080 (S1164, Selleck chemical, Houston, TX, USA) is a muti-targeted kinase inhibitor, which targets VEGF receptor-2, 3 (VEGFR-2, 3) and inhibits survival and proliferation of tumor cell. The purpose of this study was to determine the anti-tumor effect of E7080 on oral squamous cell carcinoma. Methods: An oral squamous cell carcinoma cell line, SCC-9 was used in this study. E7080 was applied to SCC-9 cells by 3 different concentrations (1, 5, 10 ${\mu}g/mL$). Control means no application of E7080. The cellular growth was evaluated by real-time cell electronic sensing and MTT assay. The signal transduction was evaluated by Western blotting. Results: In experimental group, SCC-9 cell proliferation was decreased and the VEGFR-3 downstream pathways were inhibited compared with control. Furthermore, increasing the concentration of E7080, the ability of E7080 to disturbance of SCC-9 cell proliferation was increased. Conclusion: Proliferation of SCC-9 cells was inhibited by E7080, which was through by inhibition of VEGFR-3 downstream pathway. In vivo study with E7080 will be required to provide therapeutic benefits in oral squamous cell carcinoma.