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제     목 : 한림대학교 생명공학연구소 제 8회 정기세미나
작 성 자 : 관리자 작성일 : 2010-10-22 14:34:29 조 회 : 6902 
인쇄
[교육과학기술부·한국연구재단 지정 한림대학교 생명공학연구소]

◎ 제8차 생명공학연구소 정기세미나 개최◎
▶ 일 시 : 2010. 10. 19(화) 오후 2시
▶ 장 소 : 산학협력단 세미나실(12102호)
▶ 연 자 : 김일진, 강효정 박사(University of California, San Francisco)
▶ 주 최 : 생명공학연구소

▶ 강의제목 : A systems genetics approach in human lung cancers (network analysis)【김일진 박사】


High throughput genomics approaches have been used in various types of human cancers. Expression microarray profiling is one of common genomics tools to analyze characteristics of gene expression of tumor or matched normal samples and identify unknown subtypes which were not found in histological
classification. Network analysis using gene expression correlation of different genes could be a new paradigm to identify unknown molecular characteristics of tumor or matched normal samples and find new diagnostic and therapeutic targets. Network analysis was performed by genome-wide gene expression analysis in around 100 matched lung adenocarcinomas and normal tissues. Mutation analysis of key lung cancer genes, EGFR, K-ras, and TP53 was also done to integrate somatic mutation information to network analysis. Several clear functional cliques were identified in tumor and matched normal tissues by network analysis. Oxidation phosphorylation was only found in normal samples and immune response clique was only identified in tumor tissues. Surfactant pulmonary proteins and clara cell specific markers which are important for controlling homeostatic function in lung were significantly down-regulated in tumor. One interesting gene, PEBP, was found to have strong correlations with other known type II pneumocyte markers, SFTPD, SFTPB, ABCA3, and LAMP3 by progression network, which suggested this could be a new type II pneumocyte marker. This was validated by immunohistochemistry.
Cell cycle network was significantly enriched in tumor samples than normal and even more significant in TP53 wild-type than TP53 mutant tumors. One of new mitotic cell cycle genes was VRK1 (vaccinia-related kinase 1) in lung tumor networks. Network of VRK1 gene showed a clear mitosis clique only in tumor, not normal. By searching available microarray databases, VRK1 network was found to be significant only in human or mice tumor or mildly immortalized normal cell lines. Down-regulation of VRK1 by shRNA caused a G1 arrest and increased sensitivity to Parp inhibitor (ABT-888) in lung cancer cell lines. VRK1 may be a good therapeutic target inhibiting mitosis mainly in lung tumor not in normal and minimizing a side-toxicity in normal tissues.

▶ 연사 학력 및 경력
1994-1999 College of Veterinary Medicine, Seoul National University B.S., D.V.M.
1999-2001 College of Medicine, Seoul National University M.S.
2001-2003 College of Medicine, Seoul National University Ph.D.
2004-2006 Seoul National University, Korea Postdoctoral Fellow
2007-현재 University of California, San Francisco Postdoctoral Fellow, Adjunct Assistant Professor



▶ 강의제목 : PTCH overexpression-driven skin carcinogenesis and developmental defects in
K14PTCHFVBmice【강효정 박사】


Skin squamous cell carcinoma (SCC) is one of the most common cutaneous cancers in the Western population. The risk factors for SCC development are sunlight exposure, immunosuppression, HPV infection, arsenic exposure, and other skin damaging factors. Previously, we showed that two mouse strains, FVB/N and C57BL/6 have different susceptibility to SCC development induced by Hras activation due to their different genetic polymorphism in the PTCH1 gene. PTCH1 is a critical signaling receptor for hedgehog ligands in the hedgehog signaling involved in the embryonic tissues development and processes for cell proliferation, differentiation, and tissue patterning. To further investigate the role of PTCH1 overexpression in the carcinoma development, we performed two-stage skin carcinogenesis (DMBA-TPA treatment) on the K14PTCHFVB transgenic and wild-type mice. By 20 weeks post-treatment, both K14PTCHFVB and wild-type mice developed papillomas, begin skin tumors, but the papilloma number was not significantly different between different genotypes. By 45 weeks post-treatment, 71-84% of K14PTCHFVB mice were observed for carcinoma development while only 35% of wild-type mice developed carcinomas. PTCH overexpression-driven skin carcinomas had no evidence of hedgehog signaling activation, suggesting that this carcinogenesis was promoted through non-canonical hedgehog signaling pathway. Notably, the presence of PTCH transgene expression was observed locally clustered as a single cell in the squamous and spinous area of the carcinomas. The cancer cells expressing PTCH transgene were less proliferative and more differentiated, indicating that these cells might be involved in the cancer development at the early stage. Developmental defects including small gross body size, abnormal limb development, and defective eye structures were also observed in PTCH transgenic mice with highly elevated PTCH expression

▶ 연사 학력 및 경력
1994-1999 College of Science, Sookmyung Women’s University B.S.
2001-2003 College of Medicine, Seoul National University Graduate School M.S.
2003-2005 College of Medicine, Seoul National University Graduate School Ph.D.
2005-2007 National Cancer Center, Korea
2007-현재 University of California, San Francisco Postdoctoral Fellow

※중점연구소 생명공학연구소에서는
연사분을 초청하여 제 8차 정기세미나를 개최하오니 많은 참석 부탁드리겠습니다.
 
 
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