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박원상,조장,이화성,송재휘,윤정환,박용규,남석우,이정용 대한병리학회 2010 Journal of Pathology and Translational Medicine Vol.44 No.4
Background : Osteoarthritis (OA) is a common disease characterized by degenerating joint cartilage in the knee, hip, and hand. A functional single nucleotide polymorphism (SNP) +104-T/C; rs143383 in the 5′untranslated region of the growth differentiation factor 5 (GDF5) gene was recently associated with susceptibility to OA in the Japanese and Chinese populations. Methods : To investigate whether this association is present in the Korean population, the frequency of the polymorphism was investigated in 276 patients with knee OA and 298 healthy subjects as controls. Polymorphism analysis was performed by amplifying the core promoter region of the GDF5 gene and digesting it with the BsiEI restriction enzyme. Results : The frequency of the TT, CT, and CC genotypes was 54.3% (150/276), 41.7% (115/276), and 4.0% (11/276), respectively, in patients with OA, and 53.4% (159/298), 37.9% (113/298), and 8.7% (26/298), respectively, in healthy controls. No significant differences in genotypic or allelic frequencies of the +104T/C SNP of the GDF5 gene were observed between patients with OA and controls. Also, no significant differences in allelic and genotypic frequencies were found when the individuals were stratified by age and gender. Conclusions : The results suggest that the +104T/C; rs143383 GDF5 core promoter polymorphism is not a risk factor for OA in the Korean population.
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Molecular Pathogenesis of Gastric Cancer
박원상 대한의사협회 2010 대한의사협회지 Vol.53 No.4
In this article, I will survey the major genetic susceptibility and somatic genetic alterations involved in gastric cancer and adenoma. These include germline and somatic genetic alterations in oncogenes, tumor suppressor genes, and apoptosis-related genes. A small proportion of gastric cancers arise as a consequence of hereditary predisposition caused by specific germline mutations in E-cadherin, mismatch repair genes, adenomatous polyposis coli,and STK11. Aberrant expression of activation induced cytidine deaminase, triggered by Helicobacter pylori infection, accumulates with genetic mutations of oncogenes and tumor suppressor genes, including p53 and CTNNB1. Inactivation of trefoil factor family 1, which is a gastric specific tumor suppressor, occurs in gastric adenomas and cancers. Ectopic expression of CDX2 leads to intestinal metaplasia and defective Cdx2 expression accelerates the transformation of metaplastic cells to gastric cancer. Genetic alterations of p53 and genes related to Wnt signaling pathway and microsatellite instability occur early in the development of gastric carcinoma, indicating that detection of certain genetic alterations in adenomas may be indicative of malignant transformation. In addition, inactivation of apoptosis-inducing gene caused by mutations may be an escaping mechanism against apoptotic cell death and contribute to the progression of gastric cancer. Although the results of many studies are contradictory with one another, genetic alterations in oncogenes and tumor suppressor genes are present even in gastric adenoma and increase in frequency during multistep gastric carcinogenesis. Genetic alterations described herein, and from as yet unidentified target genes in gastric cancer cells, will guide us towards more effective risk assessment, diagnosis, and treatment.
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Hypermethylation of the RUNX3 gene in hepatocellular carcinoma
박원상,조영구,김창재,송재휘,이연수,김수영,남석우,이석형,유남진,이종영 생화학분자생물학회 2005 Experimental and molecular medicine Vol.37 No.4
Methylation events play a critical role in various cellular processes including regulation of gene transcription and proliferation. Recently, RUNX3 β-Smads signaling transduction pathway genes, showed strong tumor-suppressor activity by regulation of epithelial proliferation and apoptosis. To elucidate the potential etiological role of the RUNX3 gene in the development of hepato-cellular carcinoma (HCC), we have analyzed the methylation status of 5' CpG island of the RUNX3 gene in a series of 73 HCC tissues and 1 liver cell lines. Expectedly, promoter methylation of RUNX3 gene was found in 2 (2.7%) of 73 corresponding normal liver, whereas 30 (41.1%) of 73 HCCs and 4 (40%) of 10 liver cancer cell lines showed hypermethylation of the gene, respectively. There was no significant difference between promoter hypermethylaion and clinicopathologic parameters of primary HCC sam-ples, including histologic grade, microvascular invasion, and clinical stage. Interestingly, demethy-lating agent 5-aza-2-deoxycytidine induced reacti-vation and more potent expression of RUNX3 gene in HCC cell lines. Our findings indicate that promoter hypermethylation of RUNX3 gene may occur as an early event in the development of HCC and that methylation may be a major mechanism for inactivation of RUNX3 gene in HCC.
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朴源常,李泰淑 충남대학교 의과대학 지역사회의학연구소 1980 충남의대잡지 Vol.7 No.1
To study for several malignancy-associated charges in the cervical tissues around squamous cell carcinoma of the female uterine cervix, which is most frequent malignancy in the Korean females, 180 cases of squamous cell carcinoma, collected from 1975 to 1979 at the Department of Pathology, Chungnam National University School of Medicine, were compared with cancer-associated changes between carcinoms in situ and invasive-carcinoma, and among types of invasive carcinoma. The results observed were as follows: 1. Dysplasia, which is thought of precursor of cervical carcinoma of the uterine cervix, was the most frequent and severe degree in poorly differentiated carcinoma and lowest frequency and mild degree in well differentiated carcinoma. 2. Squamous metaplasia was most frequent in carcinoma in situ, and the lowest in well differentiated type of invasive carcinoma. 3. The epithelial hyperplastic changes in the uterine cervix revealed the most frequent in carcinoma in situ, and the lowest in the poorly differentiated type of carcinoma. 4. Inflammatory lesions were the most frequent and severe in poorly differentiated type of carcinoma, and the lowest and mild in well differentiated type of carcinoma. 5. Retrogressive changes and erosion of the cervix revealed the most frequent and severe in poorly differentiated type of carcinoma, and the lowest and mild in well differentiated type of carcinoma.
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Chloramphenicol 前處置量이 多量의 四鹽化炭素에 依한 急性中毒性 肝病變에 미치는 影響에 關한 病利組織學的 硏究
朴源常,姜大榮 충남대학교 의과대학 지역사회의학연구소 1983 충남의대잡지 Vol.10 No.2
Carbon tetrachloride, a potent hepatotoxic agents, is metabolized mainly in the liver, and its hepatotoxic action is influenced by the administration of chloramphenicol which is thought of an antagonist of metabolism in the liver. Sprague-Dawley rats (male and female) were pretreated with 100 ㎎, 150 ㎎ and 200 ㎎ of 10% chloramphenicol saline solution per kilogram of body weight, and 30 minutes later were administered intraperitoneally, 5 ml of carbon tetrachloride(CCl_4) per kilogram of body weight after being anesthetized by ether. Food was withheld 12 hours before chloramphenicol or physiological saline administration. Controls received the equivalent amount of saline solution, and 30 minutes later 5ml/㎏ of the CCl_4. At 3, 6, 12, 24, 48, 72, 96 hours after CCl_4 administration, 6 animals of each group were sacrified, and the histopathogical changes in the liver of the control and experimental groups were noted as follows; 1. Vacuolar degeneration of the hepatic cells of chloramphenicol pretreated rats showed more marked in degree than the control group. 2. Fatty change of 100 ㎎ chloramphenicol pretreated rats was more mild than the control group, and that of 150 ㎎ or 200 ㎎ group was similar to the control. 3. The necrotic changes of the hepatic cells of chloramphenicol pretreated rats were more mild than the control, and the degree of mildness is in order of pretreated dosage of chloramphenicol. 4. Regeneration of hepatic cells and sinusoidal cells, and reconstruction of the hepatic lobules in the chloramphenicol pretreated rats were more active in degree than those of the control, and those wee proportionate to pretreated chloramphenicol dosage.
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