• Journal of the korean academy of Pediatric Dentistry
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• v.31 no.4
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• pp.680-684
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• 2004

The hemangioma, a benign proliferation of blood vessel, is the most common tumor of infancy and childhood. In many instances, the lesion probably represents a hamartoma or malformation rather than a true neoplasm. In the oral cavity, common sites are lips, followed by tongue, buccal mucosa and palate. Clinical characteristics appear as a flat or raised reddish-blue lesion and are generally solitary. They are classified on the basis of their histological appearance into capillary, mixed, cavernous or a sclerosing variety. A 6-year-old male of this case was referred to the Department of Pediatric Dentistry, Chonnam National University with a chief complaint of swelling lesion on gingiva. The strawberry appearance mass was detected by clinical examination on attached gingiva at the upper left primary lateral incisor and canine. Surgical excision and biopsy were carried out for histological examination and the lesion was diagnosed with a capillary hemangioma. The risk of recurrence after this therapy is rare, and there is no malignant transformation. Despite their benign origins and behaviour, hemangiomas in the region of oral cavity are always clinically important to the dental profession because of bleeding tendency.

• Journal of the korean academy of Pediatric Dentistry
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• v.37 no.1
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• pp.102-108
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• 2010

Impaction is the cessation of eruption process caused by physical obstacles on the eruption pathway, abnormal tooth position, or lack or space. It often occurs in association with supernumerary teeth, odontogenic tumor, or cystic lesions, and ameloblastic fibroma is one of the odontogenic tumors that can cause impaction of teeth. In many cases, ameloblastic fibroma occurs in association with one or more unerupted teeth. The proper management of ameloblastic fibroma is determined between conservative resection or more aggressive block resection, based size and morphologic features of the lesion and age of the patient. This is a case of a 8 year and 6 month old boy whose lower left permanent molar showed eruption disturbance. The impacted tooth was successfully repositioned favorably through surgical exposure and orthodontic traction using a modified halterman appliance. Long term follow-up, longer than 10 years, is planned considering relatively high recurrence rate and possibility of malignant transformation of ameloblastic fibroma, which cause impaction of the lower left permanent molar in this case.

• Journal of Digestive Cancer Reports
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• v.9 no.1
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• pp.1-7
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• 2021

The length, the frequency, and the methods of surveillance for intraductal papillary mucinous neoplasm (IPMN) of the pancreas are still debating. According to the recent guidelines, IPMN is stratified into "high-risk stigmata" or absolute indication and "worrisome features" or relative indication as a guide in managing these patients, either those with resection of the lesion or those under surveillance. The risk of malignant transformation was quite low for branch duct-IPMNs without worrisome features or high risk stigmata. However, because the incidence rate of pancreatic cancer in these patients increase linearly with time, continued long-term surveillance is therefore important for patients with low-risk, as well as higher-risk, IPMN. Considering the high prevalence of malignancy, main duct-IPMN should be treated by surgical resection. Among patients with these type IPMNs, segmental dilatation of the main pancreatic duct without any mural nodules and larger than 10 mm of main pancreatic duct might not be immediately resected and need very careful examination and observation. The risk related to a major pancreatic resection must balance the risk of surveillance in patients with IPMN of the pancreas who have co-morbidity and are elderly.

• Tuberculosis and Respiratory Diseases
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• v.63 no.3
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• pp.251-260
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• 2007

Purpose: An imbalance of cell proliferation and cell apoptosis is an important mechanism in carcinogenesis. Capase 3, survivin and p53 have been identified as important members of the apoptotic related proteins. This study evaluated the proliferating cell nuclear antigen(PCNA), apoptosis, apoptotic related protein such as capase 3, survivin and p53 using urethane-induced mouse lung carcinogenesis, which provides reproducible steps from hyperplasia to adenocarcinoma. Methods: Urethane was administered to the ICR mice through an intra-peritoneal injection, The mice were sacrificed at 5, 15, and 25 weeks after urethane intervention. The sequential morphological changes and immunohistochemical expression of PCNA, apoptosis, capase 3, survivin, and p53 were examined during mouse lung carcinogenesis. Results: During carcinogenesis, the sequential histological changes were observed from hyperplasia of type II pneumocytes, to anadenoma, and ultimately to an overt adenocarcinoma. The PCNA Labeling index (LI) was 9.6% in hyperplasia, 23.2% in adenoma, and 55.7% in adenocarcinoma, respectively. The apoptotic LI was 0.24% in hyperplasia, 1.25% in adenoma, and 5.27% in adenocarcinoma. A good correlation was observed between the PCNA LI and apoptotic LI. The expression of caspase 3 was remarkable- i.e., 46.7% in adenocarcinoma, in contrast to 15% in hyperplasia and 16% in adenoma. Survivin was detected weakly in the alveolar hyperplasia and showed an increasing expressional pattern in adenoma and adenocarcinoma. p53 expression was detected only in the adenocarcinoma lesions with an expression rate of 13.3%. The level of caspase 3 expression correlated with the increase in the apoptotic index. The positive expression of caspase 3 was associated with an increased apoptotic index. Conclusions: These results suggest that the PCNA LI and apoptotic LI might be useful markers for evaluating the risk of a malignant transformation. In addition, caspase, survivin and p53 might play a role in the early and late steges of urethane-induced mouse lung carcinogenesis.

• Tuberculosis and Respiratory Diseases
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• v.46 no.2
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• pp.185-194
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• 1999

Background: NF-$\kappa$B is a characteristic transcriptional factor whose functional activity is determined by post-translational modification of protein and subsequent change of subcellular localization. The involvement of the NF-$\kappa$B family of the transcription factors in the control of such vital cellular functions as immune response, acute phase reaction, replication of certain viruses and development and differentiation of cells has been clearly documented in many previous studies. Several recent observations have suggested that the NF-$\kappa$B might also be involved in the carcinogenesis of some hematological and solid tumors. Investigating the possibility that members of the NF-$\kappa$B family participate in the molecular control of malignant cell transformation could provide invaluable information on both molecular pathogenesis and cancer-related gene therapy. Method: To determine the expression patterns and functional roles of NF-$\kappa$B family transcription factors in human lung cancer cell lines NCI-H792, NCI-H709, NCI-H226 and NCI-H157 were analysed by western blot, using their respective antibodies. The nuclear and the cytoplasmic fraction of protein extract of these cell lines were subsequently obtained and NF-$\kappa$B expression in each fraction was again determined by western blot analysis. The type of NF-$\kappa$B complex present in the cells was determined by immunoprecipitation. To detect the binding ability of cell-line nuclear extracts to the KB consensus oligonucleotide, electrophoretic mobility shift assay(EMSA) was performed. Results: In the cultured human lung cancer cell lines tested, transcription factors of the NF-$\kappa$B family, namely the p50 and p65 subunit were expressed and localized in the nuclear fraction of the cellular extract by western blot analysis and immunocytochemistry. Immunoprecipitation assay showed that in the cell, the p50 and p65 subunits made NF-$\kappa$B complex. Finally it was shown by Electrophoretic Mobility Shift Assay(EMSA) that nuclear extracts of lung cancer cell lines are able to bind to NF-$\kappa$B consensus DNA sequences. Conclusion: These data suggest that in human lung cancer cell lines the NF-$\kappa$B p50/p65 complex might be activated. and strengthen the hypothesis that NF-$\kappa$B family transcription factors might be involved in the carcinogenesis of human lung cancer.

• The Journal of the Korean bone and joint tumor society
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• v.13 no.1
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• pp.22-30
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• 2007

Purpose: We describe clinical, radiographic, MRI and pathologic findings as well as final outcome after simple curettage and bone graft of cystic fibrous dysplasia (FD) in the long bone, which has been rarely documented in the literature. Materials and Methods: Clinical records, radiographs, MRI and histologic slides of 11 patients with cystic FD in the long bone were retrospectively analyzed. Results: Six patients complained pain for several months, 4 patients presented pain after trivial injury event, and 1 patient suffered pathologic fracture. The mode of involvement was monostotic in 10 patients and polyostotic in l patient. The femur was affected in 7 patients, the humerus in 3, and the radius in 1. Radiography showed prominent, expansive lysis associated with ground-glass density of FD. MRI revealed 2 different signals of FD and cyst. Microscopic examination revealed classic findings of FD and non-specific cystic degeneration. The final outcome was satisfactory in every patient. Local recurrence was not observed. Conclusion: Cystic FD in the long bone seems not as rare as the scarcity of reported cases would indicate. MRI features provide a basis for differential diagnosis between benign cystic change and malignant transformation. Cystic FD would be an indication for surgery and simple curettage with allo-chip-bone graft is effective.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.6 no.2
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• pp.129-139
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• 2003

Purpose: The aim of the study was to evaluate the long-term outcome of glycogen storage disease (GSD) type 1 with particular reference to hepatic adenoma and hepatocellular carcinoma, and to analyze risk factors affecting the development of hepatic adenoma in GSD type 1. Methods: Forty-three GSD type 1 patients (31 males and 12 females, mean age $13.9{\pm}6.4$ years) were analyzed retrospectively. Hepatic adenoma was detected on abdominal USG and diagnosed on histologic examination. Clinical profiles were compared between patients with hepatic adenoma (n=16) and age-matched controls without hepatic adenoma (n=16). Results: 1) Of 43 GSD type 1 patients, 16 (37.2%) had hepatic adeoma. Hepatic adenoma was detected at the age of mean $14.2{\pm}4.1$ years (range: 7.9~25.7 years). Fourteen (87.5%) adenomas were multiple at detection. 2) Comparison of the clinical profiles between adenoma group and non-adenoma group revealed that age at first introduction of uncooked cornstarch treatment was significantly late in adenoma group compared with non-adenoma group ($9.1{\pm}5.2$ years vs. $3.0{\pm}1.8$ years, p=0.003). Portocaval shunt surgery was performed in 11 (68.8%) patients in adenoma group and 3 (18.8%) in non-adenoma group (p=0.004). Hepatic adenoma developed mean $5.8{\pm}4.2$ years after shunt operation. 3) One patient was diagnosed as hepatocellular carcinoma at the age of 25.7 years. Conclusion: Hepatic adenoma is an important late complication of GSD type 1 with the risk of malignant transformation. Early introduction of cornstarch therapy with strict metabolic control is needed to prevent the development of hepatic adenoma in GSD type 1.

• The Korean Journal of Nuclear Medicine
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• v.30 no.4
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• pp.476-483
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• 1996

Following radiation therapy for brain tumors, patients often have clinical deterioration due to either radiation necrosis or recurrent tumor progression in the treatment field. The distinction between these entities is important but difficult clinically or even with CT or MRI. T1-201 has been known to accumulate in various tumors and be useful to grade, predict prognosis or detect recurrence of glioma. The aim of this study was to evaluate the usefulness of T1-201 SPECT in the differentiation of recurrent tumor from radiation necrosis. Of 67 patients who did T1-201 brain SPECT imaging with clinically suspected recurrent tumor or radiation necrosis, 20 patients underwent histopathological examination and constituted the study population. T1-201 uptake indices on T1-201 brain SPECT imaging rrere calculated and correlated with histopathological diagnosis. Of 20 patients, 15 were histopathologically confirmed as recurrent original tumor or malignant transformation of benign tumor and 5 were diagnosed as radiation necrosis. On T1-201 SPECT, 18 of 20 had T1-201 index above 2.5 which was regarded as positive indicator for the presence of tumor. Seventeen cases showed concordance, which consisted of 15 true positive and 2 true negative. Discordant 3 cases were all false positive. There was no case of false negative. The sensitivity, specificity, positive and negative predictive value of T1-201 SPECT were 100%, 40%, 83% and 100%. In conclusion, T1-201 brain SPECT is a sensitive diagnostic test in the detection of recurrent tumor following radiation therapy and is useful in the differentiation of recurrent tumor from radiation necrosis. Relatively low specificity should be evaluated further in larger number of patients in consideration of sampling error and referral bias for pathologic examination.

• Tuberculosis and Respiratory Diseases
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• v.40 no.6
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• pp.653-658
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• 1993

Background: Recent advancement of molecular genetics has revealed that malignant transformation of a cell may be a complex multistep process and this process is grouped, in general, into two distinct categories, activation of protooncogenes and inactivation of tumor suppressor genes. This study was focused on the mutation of p53 tumor suppressor gene, because p53 gene mutation is now generally accepted to be one of the most frequent genetic changes in a variety of human cancers. Although lung cancer is one of the common cancers in Korea, the genetic change in the carcinogenesis process is not yet known clearly. To investigate the role of p53 gene mutation in lung cancer, we examined the mutations of exon 4-8 of the p53 gene in humna lung cancer cell lines, because most of the mutations of p53 gene have been reported to develop in exon 4-8. Method: Genomic DNA was obtained by the digestion of proteinase K and the extraction by phenol-chloroform-ethanol method from two human pulmonary adenocarcinoma cell lines, PC-9 and PC-14, and one human small cell lung cancer cell line, H69. To detect the mutations of exon 4-8 of the p53 gene, polymerase chain reaction single-strand conformation polymorphism(PCR-SSCP) analysis was performed with the DNA extracted from the cells. Results: The mutation of p53 gene was present in all three cell lines tested. In PC-9, PC-14 and H69, the altered mobility was detected in exon 7, 7 and 5, respectively. Conclusion: These results suggest that p53 gene mutation plays an important role in certain steps of the carcinogenesis of human non-small cell and small cell lung cancer.