• Imaging Science in Dentistry
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• v.50 no.4
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• pp.359-363
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• 2020

Ameloblastic carcinoma is a rare odontogenic malignant tumor with the histologic features of both ameloblastoma and carcinoma. It occurs more frequently in the mandible than in the maxilla and it may appear de novo or develop from a preexisting ameloblastoma or odontogenic cyst. Rapidly progressing, painful swelling is the most common symptom, and radiographically, it shows significant bone resorption and cortical perforation. This report described a case of ameloblastic carcinoma in a 45-year-old man who presented with swelling in the left mandible. The lesion showed combined features of benign findings, such as an expansile cortex with a distinct border, and malignant findings, such as a large exophytic mass with frank bone resorption. Excisional biopsy was performed and a final diagnosis of ameloblastic carcinoma was made.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.12 no.2
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• pp.62-68
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• 1990

Intraosseous carcinoma of the jaw may arise as metastatic lesions most commonly from breast, lung, kindney and thyroid and also primarily occur from ameloblastoma or odontogenic cyst. Rarely primary intraosseous carcinoma could be originated from the epithelium involved in odontogenesis. According to WHO's classification, primary intraosseous carcinoma is defined as squamous cell carcinoma, occured in the Jaw without connection to the oral mucosa. However, Elzay defined primary intraosseous carcinoma as malignant epithelial tumor related to the odontogenic apparatus, including carcinoma ex-odontogenic cyst, carcinoma ex-ameloblastoma and carcinoma de novo. We experienced 2 cases of intraosseous carcinoma of the jaw. The first case, a 59-year-old man, showed a ill-defined mass on the left maxilla, measuring $8{\times}10cm$ in size. He received radical hemimaxillectomy and was diagnosed as ameloblastic carcinoma. The second case obtained from a 79-year-old woman showed a ill-defined $6{\times}8cm$ sized mass on the left mandibular body area. The mass was surgically removed by partial mandibulaectomy, which was diagnosed as the primary intraosseous carcinoma, probably odontogenic origin.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.36 no.3
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• pp.172-176
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• 2010

Postirradiation extraosseous osteogenic sarcomas are uncommon in the head and neck, despite the extensive use of high-dose radiation. It has been described as de novo radiation-induced neoplasm. We present a 73-year-old male who had been treated by radiotherapy for gingival cancer 7 years earlier and later developed extraosseous osteogenic sarcomas (EOSs) of the neck. Microscopically, the neck mass was composed with mesenchymal malignant cells with cartilaginous and osteogenic differentiation. Immunohistochemical stain demonstrated strong positivity of tumor cells for Snail, the one of major epithelial-mesenchymal transition (EMT) inducer. The E-cadherin expression was scarce, showing inverse relationship to Snail expression. Compared with previous squamous cell carcinoma (SCC) of the gingiva, the present EOS sample revealed the remained epithelial cells on cytokeratin immunohistochemistry, suggesting the tumor arise from the cells of epithelial origin. We have also reviewed the previous 6 cases of head and neck EOSs carefully. The clinicopathologic features of the unusual lesion suggest that it is an incomplete EMT of precedent epithelial malignancy rather than de novo pathology.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.3
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• pp.1051-1056
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• 2015

Aberrant expression of genes in de novo lipogenesis (DNL) pathway were associated with various cancers, including hepatocellular carcinoma (HCC). Single nucleotide polymorphisms (SNPs) of DNL genes have been reported to be associated with prognosis of some malignancies. However, the effects of SNPs in DNL genes on overall survival of HCC patients receiving transarterial chemoembolization (TACE) treatment are still unknown. In present study, nine SNPs in three genes (ACLY, ACACA and FASN) in DNL pathway were genotyped using the Sequenom iPLEX genotyping system in a hospital-based cohort with 419 HCC patients treated with TACE, and their associations with HCC overall survival were evaluated by Cox proportional hazard regression analysis under three genetic models (additive, dominant and recessive). Although we did not find any significant results in total analysis (all p>0.05), our stratified data showed that SNP rs9912300 in ACLY gene was significantly associated with overall survival of HCC patients with lower AFP level and SNP rs11871275 in ACACA gene was significantly associated with overall survival of HCC patients with higher AFP level. We further identified the significant interactions between AFP level and SNP rs9912300 or rs11871275 in the joint analysis. Conclusively, our data suggest that genetic variations in genes of DNL pathway may be a potential biomarker for predicting clinical outcome of HCC patients treated with TACE.

• Archives of Craniofacial Surgery
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• v.22 no.2
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• pp.126-130
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• 2021

Sebaceous neoplasms are rare adnexal tumors that can present a challenge to clinicians. Only four cases of sebaceous carcinoma with sebaceoma have been reported in the literature. Herein, we describe the case of a sebaceous carcinoma originating from a sebaceoma in a solitary nodule of the posterior neck. Immunohistochemically, the tumor cells were strongly positive for epithelial membrane antigen and p53. It is possible that adnexal carcinomas may arise from malignant transformation of their benign counterparts as well as de novo. Malignant transformation was likely in this case because the lesion was composed of distinct benign and malignant components, and the benign component showed the typical histopathological features of sebaceoma. This case underscores the fact that partial and superficial biopsies sometimes may not provide the correct diagnosis. If a surgeon suspects malignancy based on a clinical examination, then it is mandatory to perform a deep biopsy.

• Development and Reproduction
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• v.27 no.2
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• pp.77-89
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• 2023

Metformin is the most widely used anti-diabetic drug that helps maintain normal blood glucose levels primarily by suppressing hepatic gluconeogenesis in type II diabetic patients. We previously found that metformin induces apoptotic death in H4IIE rat hepatocellular carcinoma cells. Despite its anti-diabetic roles, the effect of metformin on hepatic de novo lipogenesis (DNL) remains unclear. We investigated the effect of metformin on hepatic DNL and apoptotic cell death in H4IIE cells. Metformin treatment stimulated glucose consumption, lactate production, intracellular fat accumulation, and the expressions of lipogenic proteins. It also stimulated apoptosis but reduced autophagic responses. These metformin-induced changes were clearly reversed by compound C, an inhibitor of AMP-activated protein kinase (AMPK). Interestingly, metformin massively increased the production of reactive oxygen species (ROS), which was completely blocked by compound C. Metformin also stimulated the phosphorylation of p38 mitogen-activated protein kinase (p38MAPK). Finally, inhibition of p38MAPK mimicked the effects of compound C, and suppressed the metformin-induced fat accumulation and apoptosis. Taken together, metformin stimulates dysregulated glucose metabolism, intracellular fat accumulation, and apoptosis. Our findings suggest that metformin induces excessive glucose-induced DNL, oxidative stress by ROS generation, activation of AMPK and p38MAPK, suppression of autophagy, and ultimately apoptosis.

• Nutrition Research and Practice
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• v.2 no.2
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• pp.80-84
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• 2008

Beneficial effects of dehydroepiandrosterone (DHEA) supplement on age-associated chronic diseases such as cancer, cardiovascular disease, insulin resistance and diabetes, have been reported. However, its mechanism of action in hepatocellular carcinoma in vivo has not been investigated in detail. We have previously shown that during hepatocellular carcinogenesis, DHEA treatment decreases formation of preneoplastic glutathione S-transferase placental form-positive foci in the liver and has antioxidant effects. Here we aimed to determine the mechanism of actions of DHEA, in comparison to vitamin E, in a chemically-induced hepatocellular carcinoma model in rats. Sprague-Dawley rats were administered with control diet without a carcinogen, diets with 1.5% vitamin E, 0.5% DHEA and both of the compounds with a carcinogen for 6 weeks. The doses were previously reported to have anti-cancer effects in animals without known toxicities. With DHEA treatment, cytosolic malate dehydrogenase activities were significantly increased by ${\sim}5$ fold and glucose 6-phosphate dehydrogenase activities were decreased by ${\sim}25%$ compared to carcinogen treated group. Activities of Se-glutathione peroxidase in the cytotol was decreased siguificantly with DHEA treatment, confirming its antioxidative effect. However, liver microsomal cytochrome P-450 content and NADPH-dependent cytochrome P-450 reductase activities were not altered with DHEA treatment. Vitamin E treatment decreased cytosolic Se-glutathione peroxidase activities in accordance with our previous reports. However, vitamin E did not alter glucose 6-phosphate dehydrogenase or malate dehydrogenase activities. Our results suggest that DHEA may have decreased tumor nodule formation and reduced lipid peroxidation as previously reported, possibly by increasing the production of NADPH, a reducing equivalent for NADPH-dependent antioxidant enzymes. DHEA treatment tended to reduce glucose 6-phosphate dehydrogenase activities, which may have resulted in limited supply for de novo synthesis of DNA via inhibiting the hexose monophophaste pathway. Although both DHEA and vitamin E effectively reduced preneoplastic foci in this model, they seemed to fimction in different mechanisms. In conclusion, DHEA may be used to reduce hepatocellular carcinoma growth by targeting NADPH synthesis, cell proliferation and anti-oxidant enzyme activities during tumor growth.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.31 no.6
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• pp.468-473
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• 2005

Head and neck squamous cell carcinoma (HNSCC) is the sixth most common malignancy worldwide. The molecular mechanisms involved in the development and progression of these carcinomas are not well known. Abnormalities of genomic methylation patterns have been attributed a role in carcinogenesis and local de novo methylation at tumor suppressor loci was held to be involved in silencing of tumor suppressor genes. Using Ms APPCR, we previously isolated a hypermethylated fragment corresponded to the 5' end of TPEF gene from primary liver and lung cancer cells. To confirm the inactivation of TPEF gene by hypermethylation in HNSCC, we investigated correlation between methylation pattern and expression of TPEF in 10 HNSCC cell lines. In methylation analysis such as combined-bisulfite restriction analysis(COBRA) and bisulfite sequencing, only RPMI 2650 showed none methylated pattern and another 9 cell lines showed dense methylation. The TPEF gene expression level analysis using RT-PCR showed that these 9 cell lines had not or significantly low expression levels of TPEF as compared with RPMI 2650. In addition, the increase of TPEF reexpression by 5-AzaC as demethylating agent in 9 cell lines also indicated that TPEF expression was regulated by hypermethylation. These results of this study demonstrate that epigenetic silencing of TPEF gene by aberrant methylation could play an important role in HNSCC carcinogenesis.

• Journal of Yeungnam Medical Science
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• v.17 no.1
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• pp.39-48
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• 2000

Background: There arc two theories in the development of colon cancer. One is the adenoma-carcinoma sequence theory and the other is the de novo cancer theory. Western countries believe in the adenoma-carcinoma sequence theory, however there are many recent reports from, Japan about cancers developing from small adenomas. Methods: The present study analyzed 408 polyps from 508 cases that were taken by colonoscopic polypectomy at the Department of internal Medicine, Yeungnam University Hospital. Results: The percentage of patients who had a polyp was 41.3% (210 cases out of 526 cases), and the peak incidence was noted in patients in their 50s and 60s, There was no difference between the sexes, but we noted significant increase in the incidence of polyps in patients over the age of thirty. We found 395 polyps below 1cm and 13 polyps above 1cm. Among 408 polyps, 5 cases were cancerous polyps and 3 cases showed polyp size of less than 1cm each. The first case was a polyp of 0.4cm in size with elevated mucosa at the ascending colon. The second was 0.5cm in size with round elevation and hyperemic mucosa in the rectum. The third was 0.6cm in size with tubular elevation at the hepatic flexure. Conclusions: Colon polyp is a common disease in Koreans, Even small polyps can have cancer tissue, which should be removed if discovered during colonoscopy. We believe that not all colon cancer originates in the manner described by the adenoma-carcinoma sequence theory. However further studies with a larger sample population arc needed to determine the exact role of colon polyps in the development of colon cancer.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.36 no.6
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• pp.453-459
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• 2010

Introduction: Ameloblastic carcinoma is a rare malignant lesion, and may arise from either carcinoma ex-ameloblastoma or de novo carcinoma. Aberrant promoter hypermethylation of the tumor-associated genes leading to their inactivation is a common event in many cancer types. The p16/CDKN2/INK4A gene and p16 5 protein are involved directly in regulating the cell cycles. Cadherins are cell adhesion molecules that modulate the epithelial phenotype and regulate tumor invasion. The aim of this study was to evaluate the roles of p16 and E-cadherin methylation and loss of p16 and E-cadherin expression in the malignant transformation of an ameloblastoma. Materials and Methods: Eight cases of ameloblastoma, including 4 benign ameloblastomas without recurrence, 2 benign ameloblastomas with recurrence and 2 carcinoma ex-ameloblastomas, were examined. The promoter hypermethylation profile of the p16 and E-cadherin genes was studied using methylation-specific polymerase chain reaction (MSP) and immunohistochemical staining for p16 and E-cadherin expression. Results: 1) Aberrant CpG island methylation of the p16 gene was detected in 3 of the 4 benign ameloblastomas without recurrence and 1 of the 2 benign ameloblastomas with recurrence. 2) Aberrant CpG island methylation of the E-cadherin gene was found in 1 of the 4 benign ameloblastomas without recurrence. 3) A loss of p16 expression was noted in 1 of 4 benign ameloblastomas without recurrence and 1 of 2 carcinoma ex-ameloblastomas. 4) A loss of E-cadherin expression was noted in 2 of the 4 benign ameloblastomas without recurrence, 1 of the 2 benign ameloblastomas with recurrence and 2 of the 2 carcinoma ex-ameloblastomas. 5) A loss of p16 expression was observed in 1 of the 4 cases showing aberrant methylation of the p16 gene. 6) A loss of E-cadherin expression was observed in 3 benign ameloblastoma case showing aberrant methylation of the E-cadherin gene. Conclusion: These results suggest that loss of E-cadherin expression related to the other genetic pathway (not methylation) might be an adjuvant indicator predicting the malignant transformation of an ameloblastoma. However, the number of samples in this study was too small and the relationship between the treatment methods and clinical course were not defined. Therefore, further study will be needed.