1.Cancer Gene Therapy.
Journal of the Korean Medical Association 1998;41(8):836-840
No abstract available.
Genes, Neoplasm*
2.Cancer Gene Therapy: Limitations and Progress.
Cancer Research and Treatment 2003;35(3):175-176
No abstract available.
Genes, Neoplasm*
3.The rate of p53 gene carrier in the high risk group of exposure to dioxine
Journal of Medical Research 2005;38(5):15-16
Diseases caused by dioxine include mainly various types of cancers and p53 is one important gene in carcinogenesis-suppressing gene family. Objectives: This research's goal is detecting p53 gene's ratio in the high risk group of exposure to dioxine. Methods: In this study we detected p53 ratio in 50 cases in the group of high risk of exposure to dioxine and the control group of 30 cases. Gene p53 was detected by PCR technique. Results: The study showed that in the control group (no exposure to dioxine), p53 prevalence is 100% compared with 82% in high - risk group (p <0.05). Conclusions: p53 was not detected in 18% of the group of high risk exposure to dioxin, suggesting that there were serious damages in p53 gene (deletion...)
Genes, p53
4.Comparison of class switch recombination assays for immunoglobulin synthesis
Journal of Medical Research 2005;39(6):5-9
The second step of immunoglobulin gene alteration consists of somatic hypermutation and class switch recombination. 80th are regulated by activation-induced cytidine deaminase (AID). Methods: Study on possible application of class switch recombination assays for immunoglobulin gene alteration via AID. Cell based assays using AID B lymphocyte and NIH3T3 cell carrying switch substrate; gene transfer using retrovirus system; FACS analysis; PCR and ELISA. Results: DNA sequencing for S region and gamma1CT are the most sensitive and accurate assays. However, gamma1CT assay seemed to be more reliable and applicable. Others are accurate assays but less applicable. Conclusion: gamma1CT determination is the best class switch recombination assay for immunoglobulin gene alteration via AID.
Immunoglobulins, Genes
5.Diffuse Large B Cell Lymphoma Shows Distinct Methylation Profiles of the Tumor Suppressor Genes among the Non-Hodgkin's Lymphomas.
Sun Och YOON ; Young A KIM ; Yoon Kyung JEON ; Ji Eun KIM ; Gyeong Hoon KANG ; Chul Woo KIM
Korean Journal of Pathology 2008;42(1):16-20
BACKGROUND: Aberrant methylation of CpG islands in promoter regions is one of the major mechanisms for silencing of tumor suppressor genes in various types of human cancers including non-Hodgkin's lymphomas (NHL). In this study, we investigated the aberrant promoter methylation status of known or suspected tumor suppressor genes in NHLs and compared the methylation profiles between B-cell and T/NK-cell NHLs. METHODS: 54 cases of B-cell NHLs and 16 cases of T/NK-cell NHLs were examined for the methylation status of eight genes using methylation specific PCR. RESULTS: CpG islands methylation was variously found in eight genes as follows; DAPK (71%), MT1G (70%), p16 (53%), CDH1 (53%), THBS1 (56%), MGMT (27.1%), COX2 (13%), and RUNX3 (11.4%). In six cases (8 %), methylation was not observed in any of these genes. Overall methylation index of B-cell NHLs (0.48) was significantly higher than that of T/NK-cell NHLs (0.32). Of eight genes tested, THBS1 and CDH1 methylations were much more prominent in diffuse large B-cell lymphomas than in T/NK-cell NHLs or other B-cell NHLs. CONCLUSION: This study suggests that aberrant CpG island methylation is a frequent event in NHLs, and diffuse large B-cell lymphomas show overlapping but distinct methylation profiles.
Humans
;
Genes, Tumor Suppressor
6.The Study of p53 Expression and DNA Ploidy in Colorectal Carcinoma.
Ji Shin LEE ; Kwang Soo CHEON ; Chang Soo PARK
Korean Journal of Pathology 1996;30(9):775-783
Mutation of the p53 gene frequently results in overexpression of the p53 protein and loss of its tumor-suppressing properties. The overexpression of the p53 gene could be an indicator of rapid proliferation, poor differentiation, advanced stages, or poor prognosis. The prognostic value of the overexpression of the p53 gene in colorectal carcinoma is equivocal. The presence of DNA aneuploidy has been described as a powerful adverse prognostic indicator in relation to survival. To investigate the prognostic significance of p53 expression, and the relationship with DNA ploidy, 92 cases of colorectal carcinomas were analyzed. The overexpression of p53 gene product was present in 50(54.4%) of 92 cases. p53 expression only correlated with recurrence or metastasis during the follow-up periods (p=0.045). DNA aneuploidy was observed in 32(39.1%) of 82 cases. DNA ploidy was strongly associated with lymph node invasion(p=0.005), Dukes' stage(p=0.003), TNM classification (p=0.003), and recurrence or metastasis during the follow-up periods (p=0.045). The frequency of DNA aneuploidy was higher in the p53-positive colorectal carcinomas(58.3%) than in the p53-negative colorectal carcinomas (21.6%) (p=0.003). p53-positive colorectal carcinomas had a higher rate of cell proliferation than p53-negative cases(p<0.001). These results suggest that checking the p53 expression and DNA ploidy could be useful prognostic indicators of colorectal carcinoma.
Neoplasm Metastasis
;
Genes, p53
7.DNA Ploidy and Mutant p53 and Rb Gene Expression in the Ovarian Tumors.
Yong Wook KIM ; Pyong Sahm KU ; Inn Sun KIM
Korean Journal of Obstetrics and Gynecology 1997;40(12):2717-2727
No abstract available.
DNA*
;
Genes, Retinoblastoma*
;
Ploidies*
8.Are Mutations of the EGFR Gene Promising Predictive Markers for Anti-EGFR mAbs in Colorectal Carcinomas?.
Journal of the Korean Society of Coloproctology 2011;27(3):103-104
No abstract available.
Genes, erbB-1
9.A study about the involvement of H-ras oncogene in acromegalic patients.
Seung Kil LIM ; Yi Hyun KWON ; Yoon Suk CHUNG ; Kwang Jin AHN ; Eun Jik LEE ; Kyung Rae KIM ; Hyun Chul LEE ; Kab Bum HUH ; Tae Seung KIM
Korean Journal of Medicine 1993;45(3):353-360
No abstract available.
Genes, ras*
;
Humans
10.Detection of ras gene mutations in human cancer by PCR-SSCP.
Chul Min KIM ; Joo In PARK ; Chi Duk KANG ; Sun Hee KIM ; Young Hong PARK ; Soo Ja JUNG ; Byung Sun JUNG
Journal of the Korean Cancer Association 1993;25(3):429-444
No abstract available.
Genes, ras*
;
Humans*