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Mini-gel을 이용한 비방사성 SSCP의 위암 p53유전자 변이 검출
유경금(Kyung Kum Yoo),도재혁(Jae Hyuk Do),허철행(Cheol Heang Heo),문철(Cheol Moon),김형준(Hyung Jun Kim),이태진(Tae Jin Lee),유재형(Jae Hyeng Yoo),장진수(Jin Soo Chang),이상재(Sang Jea Lee),장세경(Sae Kyung Chang),박실무(Sill Moo Pa 대한소화기학회 1997 대한소화기학회지 Vol.29 No.5
N/A Background/Aims: p53 mutation was reported in many studies, but conventional PCR-SSCP protocol using radiolabeled PCR primers or nucleotides to generate a radioactive PCR products is cumbersome to handle. With the aim of a rapid and safe method for single-strand conformation polymorphism(SSCP) analysis of PCR products, we used Mini-SSCP method to detect the mutation of p53 gene of gastric cancer. Methods: In 27 pair of gastric cancer and normal tissues, PCR-SSCP was done with Mini-SSCP, and then Silver sequencing was done. Results: The p53 gene mutation of gastric cancer was found in 10 of 27(37%). Mutation of exon 4, 5 were 2, 5 cases and tnutation of exon 6, 7 mutation were 0, 3 cases respectively. Mutation rate was similar with other reports. P53 mutation was not correlated with stage, lymph node involvement and histological differentiation. Conclusions: Mini-SSCP method, modification of Cold-SSCP, greately increased our accessibility to detect polymorphisms with easiness and safeness. So, it is a useful method to detect genetic mutation. (Korean J Gastroenterol 1997;29:601-609)
궤양성 대장염에서 점소 당항원 sTn 과 Tn 의 발현에 관한 연구
장무선(Moo Sun Chang),도재혁(Jae Hyuk Do),김형준(Hyung Jun Kim),유경금(Kyung Kum Yoo),박수정(Soo Jeong Park),문철(Cheol Moon),허철행(Cheol Heang Heo),김재규(Jae Gyu Kim),장세경(Sae Kyung Chang),박실무(Sil Moo Park),김미경(Mi Kyung K 대한내과학회 1997 대한내과학회지 Vol.52 No.1
N/A Objectives: Long standing observation, which may relate either to the causes or the effects of UC, reveals that there is a pronounced alteration of mucin such as quantitative and qualitative abnormalities of mucin glycoprotein. But recently in situ hybridization technique showed no specific difference in the expression of apomucin mRNA in UC. Therefore we investigated whether abnormality of mucin was originated from defect in glycosylation. And we also tried to find differences in the expression of Tn and sTn antigens between Korean and Jewish patients with UC. Methods: We performed the immunohistochemical staining using the monoclonal antibody of mucin carbohydrate antigens Tn and sTn in 19 patients with UC. Results: Tn and sTn antigens were not expressed throughout the crypt and surface epithelium in normal colon but both of mucin carbohydrates antigens were well expressed in mild UC, Tn antigen was seen in the surface epithelium with perinuclear pattern and sTn antigen was shown not only in surface but also in crypt epithelium. In severe UC, Tn antigen was well expressed, but sTn antigen was not expressed. Tn antigen seemed to be ex-pressed more frequently than sTn antigen with severity of inflammation. These results were similar in Korean and Jewish patients with UC. Conclusion: These results suggest that inflammatory bowel disease has some deterioration in the step of glycosylation in the cytoplasm and there was no racial difference in the expression of Tn and sTn antigen in Korean and Jewish patients with UC.
대장 선종 - 선암에서 bcl - 2 종양 단백 발현에 대한 연구
김정욱,김형준,도재혁,조준형,장세경,문철,허철행 대한소화기학회 1998 대한소화기학회지 Vol.31 No.2
Background/Aims: The bcl-2 gene is an oncogene that inhibits programmed cell death or apoptosis. Overexpression of bcl-2 probably plays a role in colorectal carcinogenesis. The aim of our study was to assess the possible role of bcl-2 in colorectal tumorigenesis and to evaluate its clinical significance. Methods: We investigated bcl-2 expression in adenomas and carcinomas of the large bowel by immunohistochemistry. The cases included 20 adenomas and 24 colorectal carcinomas. Results: In normal mucosa bcl-2 immunoreactivity was detected only in the proliferative cells of the colonic crypts. Conversely, bcl-2 immunoreactivity was noted in 60% of adenomas and the potency of immunoreactivity was noted to be one positive in 10 cases of adenomas and two positive in 2 cases of adenomas. In colorectal carcinomas, bcl-2 expression was noted in 70.8% of carcinomas and was undetectable in 29.2% and focal staining (less than 50% immunostained neoplastic cells) in 54.2% of carcinomas. The remaining 16.6% of the carcinomas displayed diffuse (more than 50% immunostained neoplastic cells) bcl-2 immunoreactivity. In colorectal adenornas bcl-2 expression was not correlated with the pathologic type of adenomas, but correlated with adenoma size. In colorectal carcinomas, bcl-2 expression was not correlated with relevant clinicopathologic parameters, including disease stage and tumor differen.iation. Conclusions: Our data suggest that the bcl-2 oncoprotein may play a role in colorectal tumorigenesis and be correlated with tumor size. In the case of carcinomas, the expression of the bcl-2 oncoprotein did not show statistical significance compared with adenomas. But, the potency of bcl-2 expression was more stronger in carcinomas than in adenomas and showed statistical significance.
대장선종 및 선암에서 비방사성 Single Strand Conformation Polymorphism을 이용한 p53 변이 검출
김정욱,김형준,도재혁,장세경,박실무,문철,유경금,허철행 대한소화기학회 1998 대한소화기학회지 Vol.31 No.1
Background/Aims: The p53 gene is a tumor suppressor gene that inhibits carcinogenesis. In colonic neoplasms, p53 mutation was reported in many studies, but conventional PCR-SSCP protocol using radioisotopic PCR primer or nucleotides to generate radioactive PCR products is cumbersome to handle. In a previous study, we reported a rapid and safe method for detecting p53 mutation using PCR products by modified cold SSCP (mini-SSCP) method to detect the p53 mutation in gastric cancers, In this study, we applied this method to detect p53 rnutation in colon polyps and cancers and to find the relationship between p53 mutation and clinicopathologic parameters. Methods: We investigated p53 mutation in adenomas and carcinomas of the large bowel by modified cold SSCP and silver sequencing. The cases studied included 28 adenomas and 40 colorectal carcinomas. Results: p53 mutation was noted in 25% of twenty-eight adenomas and in 58% of forty carcinomas. In colorectal adenomas p53 mutation was not related with pathologic type of adenomas but related with adenoma size. In colorectal carcinomas p53 mutation was not related with relevant clinicopathologic parameters, including disease stage and tumor differentiation. In using silver sequencing, the most frequent site of p53 mutation was exon 5 and the most frequent abnormality of DNA sequencing was insertion in colonic neoplasm. Conclusions: Our data suggest that p53 mutation may play an important role in late stage of adenoma-cancer sequence and is related with tumor size.
김정욱,김형준,도재혁,조준형,문철,유경금,장세경,허철행 대한소화기학회 1998 대한소화기학회지 Vol.31 No.6
Baekground/Aims: Tumor suppressor genes are characterized by inactivation of both alleles, that is, especially loss of heterozygosity (LOH). The LOH at 18q21 chromosome region has been reported to be frequent in pancreatic and colon cancer. The chromosome region 18q21 has been shown to be frequently deleted in colorectal cancer. Such frequent allelic loss indicates the presence of a tumor suppressor gene in colorectal cancer. The DPC4 gene, which is located at the 18q21, has been identified as a putative tumor suppressor gene he from the studies of pancreatic cancer. The aim of the present study was to determine whether it is also altered in colorectal cancer. Methods: For 30 colorectal cancer tissues, we performed PCR-single strand conformation polymarphism (SSCP) with modified 'cold SSCP' and silver sequencing. Results: The DPC4 gene mutation of coIorectal cancer was found in 9 out of the 30 specimens (30%). Among the 9 specimens, mutations of exon 1, 8, and 10 were observed in 2 of 9 (22%), in 6 of 9 (66%) and in 1 of 9 (11%), respectively. Silver sequence showed substitution in 4 cases (44%), insertion in 4 cases (44%), silent mutation in 1 case (12%) and deletion was not observed. Presence of DPC4 mutation was correlated with tumor differentiation (well or moderate vs. poorly differentiation; p$lt;0.05). Conclusions: The DPC4 gene may be related to tumor development in a fraction of colorectal cancers.