• Asian Pacific Journal of Cancer Prevention
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• 제16권4호
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• pp.1599-1603
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• 2015

Background: Epigenetic silencing of tumor suppressor genes due to promoter hypermethylation is one of the frequent mechanisms observed in cancers. Hypermethylation of several tumor suppressor genes involved in cell cycle regulation has been reported in many types of tumors including oral squamous cell carcinomas. LATS1 (Large Tumor Suppressor, isoform 1) is a novel tumor suppressor gene that regulates cell cycle progression by forming complexes with the cyclin dependent kinase, CDK1. Promoter hypermethylation of the LATS1 gene has been observed in several carcinomas and also has been linked with prognosis. However, the methylation status of LATS1 in oral squamous cell carcinomas is not known. As oral cancer is one of the most prevalent forms of cancer in India, the present study was designed to investigate the methylation status of LATS1 promoter and associate it with histopathological findings in order to determine any associations of the genetic status with stage of differentiation. Materials and Methods: Tumor chromosomal DNA isolated from biopsy tissues of thirteen oral squamous cell carcinoma biopsy tissues were subjected to digestion with methylation sensitive HpaII enzyme followed by amplification with primers flanking CCGG motifs in promoter region of LATS1 gene. The PCR amplicons were subsequently subjected to agarose gel electrophoresis along with undigested amplification control. Results: HpaII enzyme based methylation sensitive PCR identified LATS1 promoter hypermethylation in seven out of thirteen oral squamous cell carcinoma samples. Conclusions: The identification of LATS1 promoter hypermethylation in seven oral squamous cell carcinoma samples (54%), which included one sample with epithelial dysplasia, two early invasive and one moderately differentiated lesions indicates that the hypermethylation of this gene may be one of the early event during carcinogenesis. To the best of our knowledge, this is the first study to have explored and identified positive association between LATS1 promoter hypermethylation with histopathological features in oral squamous cell carcinomas.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제37권1호
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• pp.77-80
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• 2011

A calcifying epithelial odontogenic tumor (CEOT) was first described as a separate entity in 1955 by Pindborg, and has since been referred to as Pindborg tumor. CEOT is characterized by the presence of squamous-cell proliferation, calcification and amyloid deposits, and accounts for only 1% of all odontogenic tumors. CEOT is a benign, though occasional locally invasive, slow-growing neoplasm. It is located either intraosseously or extraosseously, and is usually associated with an unerupted permanent tooth. A 24 year-old female visited our clinic, presenting with a palatal swelling and intra-oral ulcer. After an incisional biopsy, the lesion was confirmed to be odontogenic tumor. A tumor resection and reconstruction surgery with tongue flap were performed.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제34권5호
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• pp.518-524
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• 2008

Chromosome 18q alteration plays a key role in colorectal tumorigenesis, and loss of heterozygosity at 18q is associated with a poor prognosis in colon cancer. DCC(Deleted in Colorectal Cancer) is a putative tumor- suppressor gene at 18q21 that encodes a transmembrane protein with structural similarity to neural cell adhesion molecule that is involved in both epithelial and neuronal cell differentiation. DCC is implicated in regulation of cell growth, survival and proliferation. Thus, tumor progression in squamous cell carcinoma, stomach cancer, colorectal cancer correlates with downregulation of DCC expression. The mechanism for DCC suppression is associated with hypermethylation of the DCC gene promoter region. Hence, the goal of this study is to identify the promoter methylation responsible for the down-regulation of DCC expression in oral squamous cell carcinoma. 12 of tissue specimens for the study are excised and gathered from 12 patients who are diagnosed as SCC in department of OMS, dental hospital, dankook university. To find expression of DCC in each tissue samples, immunohistochemical staining, RT-PCR gene analysis and methylation specific PCR are processed. The results are as follows. 1. In the DCC gene RT-PCR analysis, 5(41.6%) of 12 specimens of oral squamous cell carcinoma did not expressed DCC gene. 2. In the promoter methylation specific PCR analysis, 5(41.6%) of 12 specimens showed promoter methylation of DCC gene. 3. In the immunohistochemical staining of poor differentiated and invasive oral squamous cell carcinoma, loss of DCC expression was observed. These findings suggest that methylation of the DCC gene may play a role in loss of gene expression in invasive oral squamous cell carcinoma.

• 대한치과의사협회지
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• 제50권12호
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• pp.732-742
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• 2012

White lesions of the oral mucosa are a common clinical finding that often present first to general dentist. Some white lesion may have possibility of malignancy. Leukoplakia is the most common "potentially malignant disorder" of the oral mucosa. Leukoplakia is at present defined as "A white plaque of questionable risk having excluded (other) known disease or disorders that carry no increased risk for cancer.". Therefore, it is important for general dentist to be familiar to clinical differential diagnosis of leukoplakia from the known white lesions such as candidiasis, lichen planus, leukoedema, frictional keratosis, and so on. It is also important to decide whether such lesions require further investigation through the biopsy. As a result of biopsy, the presence of epithelial dysplasia in the leukoplakia is still the strongest predictor of future malignant transformation. In this article, oral white lesions that must be differentiated from potentially malignant disorders or early invasive squamous cell carcinoma will be reviewed together with presenting clinical cases.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제28권5호
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• pp.390-394
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• 2002

Basal cell adenocarcinoma is an epithelial neoplasm which is cytologically and histomorphologically similar to basal cell adenoma but is different because of the infilitrative growth. This tumor, a rare salivary gland tumor newly classified as basal cell adenocarcinoma by the WHO in 1991, is infiltrative, locally destructive and tends to recur but metastasis is less common. The differential diagnosis includes basal cell adenoma, adenoid cystic carcinoma, and basaloid squamous carcinoma. Nearly 90 percent of these tumors occurr in the parotid gland and can be classified into low grade carcinomas with a relative good prognosis. Basal cell adenocarcinoma of minor salivary gland is very rare and has a less favorable clinical course compared with that of the major salivary glands. This is a case of basal cell adenocarcinoma occurring at the minor salivary gland of the soft palate. We treated this patient with block excision and adjunctive radiation therapy.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제31권3호
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• pp.219-227
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• 2005

Purpose: Abnormalities in the p53 gene are regarded as the most consistent genetic abnormalities detected in head and neck squamous cell carcinogenesis. Two new members of the p53 gene family, p73 and p63 have recently been identified. They share considerable sequence homology with p53 in the transactivation, DNA binding, and oligomerization domains, indicating possible involvement in carcinogenesis. Disruption of the homeostatic balance between proliferation and apoptosis is widely believed to contribute to human oral carcinogenesis. The aim of this study was to analyze expression of p63 in squamous cell carcinogenesis and to compare with immunochemical markers representing cell proliferation and apoptosis. Materials and Methods: Using the Syrian hamster oral cancer model, the fraction of apoptotic (apoptotic index-AI), proliferating (mitotic index-MI) and p63 expressing keratinocytes were examined at normal, dysplastic and malignant oral epithelium using the TUNEL assay, PCNA and p63 immunostaining. Results: p63 significantly increased between normal and dysplastic epithelium and between dysplastic and malignant epithelium. PCNA significantly increased between normal and dysplastic epithelium and between normal and malignant epithelium. However, increase between dysplastic and malignant epithelium, though still increasing, was not statistically significant. The percentage of TUNEL positive cells increased from normal to dysplastic epithelium and returned to normal keratinocyte level in the malignant epithelium. However, differences between tissue types were not significant. The ratio of MI:AI increased significantly only in the dysplastic-malignant epithelial transition. The increase of p63 expression closely reflected the change in the MI:AI ratio during oral carcinogenesis. Conclusion: The p63 may be associated with the regulation of epithelial proliferation and apoptosis in DMBA-induced hamster buccal pouch squamous cell carcinogenesis. Further study is required to investigate which p63 isoforms are involved in hamster buccal pouch carcinogenesis.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제41권6호
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• pp.352-356
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• 2015

Basal cell adenoma (BCA) is a rare, benign neoplasm that most frequently arises in the parotid gland. We treated a 54-year-old female patient with BCA that had developed in the deep portion of the left parotid gland. The patient presented with gradual facial swelling with no other symptoms. We performed a total parotidectomy to excise the mass, but we preserved the facial nerve. Histopathology revealed a well-encapsulated mass. The tumor was composed of islands of comparatively uniform, small, dark, basaloid epithelial cells in the stroma. Histologic and immunohistochemical studies concluded that the BCA tumors were mostly trabecular. Postoperatively, there was no facial nerve weakness, and the tumor did not recur during the 24-month follow-up period.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제33권3호
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• pp.211-220
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• 2007

Objective: In organotypic culture of immortalized human oral keratinocytes (IHOK), the change of the growth and differentiation was investigated according to the fibroblast type and the involvement of mitogen-activated protein (MAP) kinase. Materials & Methods: IHOK was cultured three dimensionally with gingival fibroblast (GF), dermal fibroblast (DF) and immortalized gingival fibroblast (IGF). We characterized biologic properties of three dimensionally reconstructed IHOK by histological, immunohistochemical, and Western blot analysis. We also investigated whether MAP kinase pathway was involved in epithelial-mesenchymal interaction by Western blot analysis. Results: The best condition of three dimensionally cultured IHOK was the dermal equivalent consisting of type I collagen and IGF. IGF increased the expression of more proliferating cell nuclear antigen (PCNA), involucrin than GF and DF in response to co-culture with IHOK. Extracellularly regulated kinase (ERK) pathway was activated in organotypic co-culture with IGF. Conclusion: The organotypic co-culture of IHOK with dermal equivalent consisting of type I collagen and IGF resulted in excellent morphologic and immunohistochemical characteristics and involved ERK pathway. The epithelial-mesenchymal interaction was activated according to the fibroblast type.

• 대한치과의사협회지
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• 제12권1호
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• pp.21-28
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• 1974

The author has observed the distribution of the tissue mast cells in 67 various tumors and precancerous lesions which occurred in the oral cavity. The specimcns ware obtained from the department of oral pathology, college of dentistry, Seoul National University, from Jan. 1970 to June, 1973. The results are as follows: 1) The number of the tissue mast cell was decrease predominantly in malignant tumors, especially in squamous cell carcinomas and in sarcomas. 2) The number of the tissue mast cell distirbution in adenocarcinomas one of malignant group was sligtly increased in with healthy oral mucosa. 3) The number of tissue mast cells in ameloblastomas one of benign group of the tumor of epithelial originwas more decreased than that in healthy oral mucosa. 4) The number of tissue mast cells in fibromas was more than that in healthy oral mucosa. 5) The number of the tissue mast cells in mixed tumors was increased one and a half times as many as that in healthy oral mucosa. 6) The number of the tissue mast cells in mixed tumors was increased one and a half times as many as that in healthy oral mucosa. 7) The tissue mast cell distribution can be observed more densly in the stroma of tumors than in the parenchyme of tumors.

• Journal of Oral Medicine and Pain
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• 제7권1호
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• pp.27-31
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• 1982

This study was undertaken in order to get biomorphometric significance of oral candidiasis as a diagnostic method. Specimen was collected from 23 oral candidiasis outpatients(10 male and 13 female) of dental infirmary of U.C.L.A. Health Center from Sept. 1,1981 to Aug. 1,1982. The results were as follows : 1. The male-female ratio on oral candidiasis was 5/6.5. 2. The mean age of male was 42.8 and the mean age of female was 60.1. 3. The nucleocytoplasmic ratio of outmost epithelial cell layer was 0.60 ane (the nuclecytoplasmic ratio of)basal cell layer was 0.87. The difference was significant.