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Im, Seock-Ah,Mazano, Cankelaria Gomez,Fueyo, Juan,Liu, Ta-Jen,Ke, Li-Dao,Jeong Soo Kim,Lee, Ho-Young,Steck, Peter A.,Kyritsis, Athanassios P.,Yung, W.K. Alfred 가톨릭대학교 2000 Bulletin of The Catholic Research Institutes of Me Vol.28 No.-
Presently, there is no effective treatment for glioblastoma, the most malignant and common brain tumor. Angiogenic factors are potentially optimal targets for therapeutic strategies because they are essential for tumor growth and progression. In this study, we sought a strategy for efficiently delivering and antisinse cDNA molecule of the vascular endothelial growth factor(VEGF) to glioma cells. The recombinant adenoviral vector Ad5CMV-αVEGF carried the coding sequence of wild-type VEGF165 cDNA in an antisense orientation. Infection of U-87 MG malignant glioma cells with the Ad5CMV-αVEGF resulted in reduction of the level of the endogenous VEGF mRNA and drastically decreased the production of the targeted secretory form of the VEGF protein. Treatment of human glioma tumors established in nude mice with intralesional injection of Ad5CMV-αVEGF inhibited tumor growth. Taken together, these findings indicate that the efficient down-regulation of the VEGF produced by tumoral cells using antisense strategies has an antitumor effect in vivo, This is the first time that an adenoviral vector is used to transfer antisense VEGF sequence into glioma cells in an animal model, and our results suggest that this system may have a clinical and therapeutic utility. (Cancer Researcg 59:895-900, 1999)
본태성고혈압 환자에서의 Doppler 심초음파 소견에 대한 연구
임석아(Seock Ah Im),정혜경(Hye Kyung Jung),정성애(Sung Ae Jung),박정은(Jung En Park),신길자(Gil Ja Shin),이우형(Woo Hyung Lee) 대한내과학회 1995 대한내과학회지 Vol.48 No.1
Objectives: Systemic arterial hypertension causes structural and functional changes of myocardium and coronary circulation, increased tendency to ventricular arrhythmia, ischemic heart disease, and congestive heart failure. In recent years, the echocardiogram has been developed as noninvasive method for the evaluation of left ventricular performance. Estimation of systolic and diastolic function of left ventricle and measurement of left ventricular mass may predict outcome of hypertensive patients. Methods: We measured systolic and diastolic function of left ventricle and left ventricular mass with M-mode, two-dimensional, and Doppler echocardiography in 62 cases of hypertensives and 20 cases of healthy adults from November 1992 to August 1993. Results: 1) Hypertensive group was 62 cases (M:F=33:29), the mean age was 56±13 years. Normotensive group was 20 cases (M:F=8:12), the mean age was 53±10 years. There was no significant differences in age distribution, sex ratio, height, weight, and body mass index. 2) On M-mode echocardiographic measurements, interventricular septum thickness and LV posterior wall thickness were significantly increased in hypertensive group (14.4±2.9㎜, 13.9±2.9㎜) than normotensive group (10.7±1.1㎜, 10.3±1.6㎜) (p<0.01). 3) Ejection fraction was decreased in hypertensive group (55.8±12%) than normotensive group (63.0±6.7%) but within normal range. 4) There was no significant differences of cardiac output and cardiac index between hypertensive group (4.69±1.151/min., 3.20±2.641/min./㎡) and normotensive group (4.88±1.211/min., 3.02±0.791/min./㎡). 5) There was no significant differences of peak E velocity between hypertensive group (72.8±22.4㎝/sec) and normotensive group (77.1±16.3㎝/sec). Peak A velocity was significantly increased in hypertensive group (83.1±22.2㎝/sec) than normotensive group (62.6±15.0㎝/sec) (p<0.01). Peak E/A ratio was significantly decreased in hypertensive group (0.91±0.28) than normotensive group (1.22±0.25) (p<0.01). Mitral valve deceleration time was significantly prolonged in hypertensive group (240.0±48.4msec) than normotensive group (240.0±48.4msec) (p<0.01). Conclusion: Diastolic dysfunction and left ventricular hypertrophy were prominent in hypertensive group but systolic function was relatively saved.
임석아(Seock Ah Im),이순남(Soon Nam Lee),경난호(Nan Ho Kyung),박응범(Eung Bum Park),서정수(Jung Soo Seo),한운섭(Woon Sup Han) 대한내과학회 1996 대한내과학회지 Vol.50 No.3
Islet cell hyperlasia is a common cause of persistent hyperinsulinemic hypoglycemia in pediatric population, but is very rare in adults. We experienced 64-year-old woman with history of symptomatic hypoglycemia such as ligh-headedness and loss of consciousness. Her blood glucose level measured in the emergency room after this incident, was 33mg/dl and documented elevation of her fasting plasma insulin to glucose ratio(0.76). She responded to intravenous glucose administration. She was performed preoperative percutaneous transhepatic portal venous insulin sampling at 2cm intervals along the portal and splenic veins. Insulin levels at these sites were measured and localization of oversecretion of insulin preoperatively and the patient underwent a distal pancreatectomy, which revealed islet cell hyperplasia only without definite mass. She remains asymptomatic 4 years after surgery with normal blood glucose and insulin level.
염색체 이상과 동반된 원발성 알도스테론증 환자의 8년 후 추적 관찰 1예 보고
임석아,남은미,박시훈,신길자,이우형,심봉석 梨花女子大學校 醫科大學 醫科學硏究所 1996 EMJ (Ewha medical journal) Vol.19 No.1
8년전 양측성 부신증식에 의한 원발성 알토스테론증으로 진단받고 spironolactone 및 칼슘차단제를 투여하여 혈압이 조절되던 환제에서 최근 혈압이 조절되지 않아 전산화 단층 촬영을 제디행한 결과 부신선종이 동반된 것을 발견하고 부신 적출술 후 소량의 항고혈압제로 혈압이 조절되었던 1예를 보고하는 바이다. We describe an unusual 30-year-old female patient with a history of refractory hypertension and hypokalemia. She was diagnosed as primary aldosteronoism with bilateral adrenal hyperplasia 8 years age and blood pressure has been controlled with spironolactone 200mg/day, nifedipine 40mg/day, Cardura 4mg/day and oral potassium supplement till these days. Recently refractory high blood pressure was developed and about 5*4*4.5cm sized left a-drenal mass was observed by abdominal CT. The hypertension and hypokalemia was controlled by left adrenalectomy.
Src as a Therapeutic Target in Biliary Tract Cancer
Nam, Ah-Rong,Kim, Ji-Won,Park, Ji Eun,Bang, Ju-Hee,Jin, Mei Hua,Lee, Kyung-Hun,Kim, Tae-Yong,Han, Sae-Won,Im, Seock-Ah,Kim, Tae-You,Oh, Do-Youn,Bang, Yung-Jue American Association for Cancer Research 2016 Molecular Cancer Therapeutics Vol.15 No.7
<P>Src, a nonreceptor tyrosine kinase, is involved in a number of cancer-related signaling pathways and aberrantly activated in biliary tract cancer (BTC). This study aimed to elucidate the potential role of Src as a therapeutic target in BTC. We tested bosutinib, an orally active c-Src/Abl kinase inhibitor, alone or in combination with cytotoxic agents using 9 human BTC cell lines: SNU-245, SNU-308, SNU-478, SNU-869, SNU-1079, SNU-1196, HuCCT1, TFK-1, and EGI-1. Of these, SNU-308 and SNU-478 were relatively sensitive to bosutinib. Bosutinib abrogated phosphorylation of Src and its downstream molecules, and significantly increased G(1) cell-cycle arrest and apoptosis. Bosutinib significantly inhibited cell migration and invasion and decreased epithelial-mesenchymal transition markers. Bosutinib combined with gemcitabine or cisplatin showed synergistic antiproliferative and antimigratory effects. In addition, this combination further inhibited phosphorylation of Src and its downstream molecules and decreased epithelial-mesenchymal transition marker expression compared with bosutinib alone. We established a SNU-478 xenograft model for in vivo experiments, because SNU-478 was more tumorigenic than SNU-308. Bosutinib combined with gemcitabine or cisplatin showed significantly more potent antitumor effects than bosutinib alone. Bosutinib combined with gemcitabine further decreased Ki-67 expression and Src phosphorylation, and further increased TUNEL expression. Our data suggest that Src might be a potential therapeutic target in BTC. Bosutinib demonstrated promising antitumor activity alone or in combination with gemcitabine or cisplatin in BTC cells, which supports further clinical development in patients with advanced BTC. (C) 2016 AACR.</P>
Min, Ahrum,Im, Seock-Ah,Jang, Hyemin,Kim, Seongyeong,Lee, Miso,Kim, Debora Keunyoung,Yang, Yaewon,Kim, Hee-Jun,Lee, Kyung-Hun,Kim, Jin Won,Kim, Tae-Yong,Oh, Do-Youn,Brown, Jeff,Lau, Alan,O'Connor, Mar American Association for Cancer Research 2017 Molecular Cancer Therapeutics Vol.16 No.4
<P>These findings suggest synthetic lethality between ATR inhibition and ATM deficiency in gastric cancer cells. Further clinical studies on the interaction between AZD 6738 and ATM deficiency are warranted to develop novel treatment strategies for gastric cancer. (C)2017 AACR.</P>
Min, Ahrum,Im, Seock-Ah,Kim, Debora Keunyoung,Song, Sang-Hyun,Kim, Hee-Jun,Lee, Kyung-Hun,Kim, Tae-Yong,Han, Sae-Won,Oh, Do-Youn,Kim, Tae-You,O’Connor, Mark J,Bang, Yung-Jue BioMed Central 2015 Breast cancer research Vol.17 No.-
<P><B>Introduction</B></P><P>Olaparib, a poly (ADP-ribose) polymerase (PARP) inhibitor, has been found to have therapeutic potential for treating cancers associated with impaired DNA repair capabilities, particularly those with deficiencies in the homologous recombination repair (HRR) pathway. Histone deacetylases (HDACs) are important for enabling functional HRR of DNA by regulating the expression of HRR-related genes and promoting the accurate assembly of HRR-directed sub-nuclear foci. Thus, HDAC inhibitors have recently emerged as a therapeutic agent for treating cancer by inhibiting DNA repair. Based on this, HDAC inhibition could be predicted to enhance the anti-tumor effect of PARP inhibitors in cancer cells by blocking the HRR pathway.</P><P><B>Methods</B></P><P>We determined whether suberoylanilide hydroxamic acid (SAHA), a HDAC inhibitor, could enhance the anti-tumor effects of olaparib on breast cancer cell lines using a cytotoxic assay, cell cycle analysis, and Western blotting. We evaluated how exposure to SAHA affects the expression of HRR-associated genes. The accumulation of DNA double strand breaks (DSBs) induced by combination treatment was assessed. Induction of autophagy was monitored by imaging green fluorescent protein-tagged microtubule-associated protein 1A/1B-light chain 3 (LC3) expression following co-treatment with olaparib and SAHA. These <I>in vitro</I> data were validated <I>in vivo</I> using a human breast cancer xenograft model.</P><P><B>Results</B></P><P>Triple-negative breast cancer cell (TNBC) lines showed heterogeneous responses to the PARP and HDAC inhibitors. Co-administration of olaparib and SAHA synergistically inhibited the growth of TNBC cells that expressed functional Phosphatase and tensin homolog (PTEN). This effect was associated with down-regulation of the proliferative signaling pathway, increased apoptotic and autophagic cell death, and accumulation of DNA damage. The combined anti-tumor effect of olaparib and SAHA was also observed in a xenograft model. These data suggest that PTEN expression in TNBC cells can sensitize the cell response to simultaneous inhibition of PARP and HDAC both <I>in vitro</I> and <I>in vivo</I>.</P><P><B>Conclusion</B></P><P>Our findings suggest that expression of functional PTEN may serve as a biomarker for selecting TNBC patients that would favorably respond to a combination of olaparib with SAHA. This provides a strong rationale for treating TNBC patients with PTEN expression with a combination therapy consisting of olaparib and SAHA.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (doi:10.1186/s13058-015-0534-y) contains supplementary material, which is available to authorized users.</P>
RAD51C-Deficient Cancer Cells Are Highly Sensitive to the PARP Inhibitor Olaparib
Min, Ahrum,Im, Seock-Ah,Yoon, Young-Kwang,Song, Sang-Hyun,Nam, Hyun-Jin,Hur, Hyung-Seok,Kim, Hwang-Phill,Lee, Kyung-Hun,Han, Sae-Won,Oh, Do-Youn,Kim, Tae-You,O'Connor, Mark J.,Kim, Woo-Ho,Bang, Yung-J American Association for Cancer Research 2013 Molecular cancer therapeutics Vol.12 No.6
<P>A PARP inhibitor is a rationally designed targeted therapy for cancers with impaired DNA repair abilities. RAD51C is a paralog of RAD51 that has an important role in the DNA damage response. We found that cell lines sensitive to a novel oral PARP inhibitor, olaparib, had low levels of RAD51C expression using microarray analysis, and we therefore hypothesized that low expression of RAD51C may hamper the DNA repair process, resulting in increased sensitivity to olaparib. Compared with the cells with normal RAD51C expression levels, RAD51C-deficient cancer cells were more sensitive to olaparib, and a higher proportion underwent cell death by inducing G<SUB>2</SUB>–M cell-cycle arrest and apoptosis. The restoration of RAD51C in a sensitive cell line caused attenuation of olaparib sensitivity. In contrast, silencing of RAD51C in a resistant cell line enhanced the sensitivity to olaparib, and the number of RAD51 foci decreased with ablated RAD51C expression. We also found the expression of RAD51C was downregulated in cancer cells due to epigenetic changes and RAD51C expression was low in some gastric cancer tissues. Furthermore, olaparib significantly suppressed RAD51C-deficient tumor growth in a xenograft model. In summary, RAD51C-deficient cancer cells are highly sensitive to olaparib and offer preclinical proof-of-principle that RAD51C deficiency may be considered a biomarker for predicting the antitumor effects of olaparib. <I>Mol Cancer Ther; 12(6); 865–77. ©2013 AACR</I>.</P>