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- 저자 : OrloH (검색결과 2 건)
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갑상선암 세포주에서 Troglitazone에 의한 TRAIL-유도 세포소멸 감수성의 증가
박진우,OrloH.Clark<SUP>1<.SUP>.Jin-Woo Park and Orlo H. Clark<SUP>1<.SUP> 대한갑상선-내분비외과학회 2003 The Koreran journal of Endocrine Surgery Vol.3 No.2
Purpose: Tumor necrosis factor related apoptosis-inducing ligand (TRAIL) induces apoptosis in many human cancer cells but not in normal cells. Thyroid cancer cells, however, appear to be relatively resistant to TRAIL-induced apoptosis. We investigated the effect of troglitazone, a PPARγ agonist, on TRAIL-induced apoptosis in thyroid cancer cells. Methods: We used 6 thyroid cancer cell lines: TPC-1, FTC- 133, FTC-236, FTC-238, XTC-1, and ARO82-1. We used flow cytometry to detect apoptosis and used MTT assay to measure anti-proliferation effects. ANOVA was used for statistical analysis. Results: TPC-1 cells were the most sensitive to soluble TRAIL. FTC-133 and ARO82-1 were resistant to TRAIL and growth inhibition was less than 20% at concentration of 800 ng/ml of TRAIL. In both TPC-1 (TRAIL-sensitive) and FTC- 133 (TRAIL-resistant) thyroid cancer cell lines, pretreatment with troglitazone enhanced TRAIL-induced cell death significantly. Bcl-family proteins did not seem to be involved in sensitization of TRAIL-induced apoptosis by troglitazone. Conclusion: TRAIL in combination with troglitazone induces apoptosis in thyroid cancer cells at suboptimal concentrations that can not be achieved using TRAIL alone. (Korean J Endocrine Surg 2003;3:113-120)
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갑상선질환에서 Sonic Hedgehog 단백질 발현의 임상적 의의
유근수,이옥준<SUP>1<,SUP>,김원재<SUP>2<,SUP>,박성수,김동주,박진우,최재운,장이찬,OrloH,Clark<SUP>3<,SUP>,Kuhn-Soo Ryu,M,D,Ok-Jun Lee,M,D,<SUP>1<,SUP>,Wun-Jae Kim,M,D,<SUP>2<,SUP>,Sung Su Park,M,D,Dong-Ju Kim,M,D,Jin- Woo Park 대한갑상선-내분비외과학회 2011 The Koreran journal of Endocrine Surgery Vol.11 No.4
Purpose: The Hedgehog (Hh) signaling pathway is important in embryonic development including cell differentiation and proliferation. Recently, activation of this pathway has been implicated in several forms of solid cancers. We investigated sonic hedgehog (Shh) protein expression and its relation to differentiation and clinicopathologic characteristics in thyroid cancer cell lines and tissues. Methods: We used five thyroid cancer cell lines: TPC-1, FTC-133, FTC-236, FTC-238, and XTC-1. We made tissue microarray slides using 80 thyroid surgical specimen: 40 benign and 40 malignant lesions. Immunohistochemical staining was performed using anti-Shh antibody. mRNA expression of NIS, thyroglobulin, and CD97 were evaluated by RT-PCR. Cyclopamine was used as a Shh signal inhibitor. Results: Shh expression was more prominent in TPC-1, FTC-133, and XTC-1 cell lines than the others. Cyclopamine downregulated CD97 and upregulated thyroglobulin mRNA expression, but did not induce mRNA expression of NIS. Thyroid tissues showed varied expression of Shh in both benign and malignant diseases. Shh expression was detected in 38 of 50 (76%) normal, in 18 of 25 (72%) non-neoplastic benign, in nine of 15 (60%) benign tumors, and in 31 of 40 (77%) malignant tumors. Shh over-expression was significantly less frequent in papillary thyroid carcinomas than in normal or benign thyroid tissues. In addition, Shh protein expression did not relate to clinicopathologic characteristics in papillary thyroid carcinomas. Conclusion: Thyroid tissues and cell lines vary in expression of Shh. Cyclopamine can induce redifferentiation in thyroid cancer cell lines. Shh protein expression, however, is unrelated to clinicopathologic characteristics in papillary thyroid carcinomas. (Korean J Endocrine Surg 2011;11:234-241)
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