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Jung-Hye Choi,In-Soon Kim,Il-Young Choi,Myung-Ju Ahn,Seock-Ah Im,Bong-Seog Kim,Ho-Suk Oh,Heung Woo Lee,Yeung Chul Mun,Chu-Myung Seong,Soon Nam Lee,Young-Yeul Lee 대한암학회 2003 Cancer Research and Treatment Vol.35 No.3
Purpose: Gemcitabine and 5-fluorouracil (5-FU) are twocompounds with reproducible activity against advancedpancreatic carcinomas. To evaluate the activity and feasibilityof this combination chemotherapy, a multi-institutionalphase II study was performed.Materials and Methods: Twenty patients (maleခfemale15ခ5, median age: 60.5 years), with histologically verifiedlocally advanced or metastatic pancreatic carcinomas,were enrolled between April 2000 and March 2002.Gemcitabine was administered by intravenous injectionat the doses of 1,000 mg/m2 on days 1, 8 and 15, and5-FU 800 mg/m2/day, was given by continuous intravenousinfusion on days 1~5. The treatment was repeatedevery 4 weeks. The clinical benefit response (CBR) wasa composite of the pain, Karnofsky performance statusand body weight change measurement.Results: Nineteen of the twenty patients were assessablefor response. The median follow-up duration was 4.6months (0.4~15.2 months). Five patients achieved a partialresponse and eight a stable disease. The overall responserate was 25.0%. The CBR was assessable in 12 patients.The overall CBR was 41.7% (5/12). The median survivalof all the patients was 8.0 months. Grade 3~4 toxicitiesincluded neutropenia (9.3%) and thrombocytopenia (5.3%).Conclusion: This study suggested that gemcitabine,combined with infusional 5-FU, was well tolerated, andproduced modest antitumor activity and symptomaticrelief in advanced pancreatic cancer patients. (Cancer Res Treat. 2003;35:213-217)
Jung, Cho-Rok,Yoo, Jinsang,Jang, Ye Jin,Kim, Sangsoo,Chu, In-Sun,Yeom, Young Il,Choi, Jong Young,Im, Dong-Soo Wiley Subscription Services, Inc., A Wiley Company 2006 Hepatology Vol.43 No.5
<P>The pituitary tumor transforming (PTTG) gene family comprises PTTG1, 2, and 3. Forced expression of PTTG1 (securin) induces cellular transformation and promotes tumor development in animal models. PTTG1 is overexpressed in various human cancers. However, the expression and pathogenic implications of the PTTG gene family in hepatocellular carcinoma are largely unknown. Gene silencing using short interfering RNA (siRNA) has become an efficient means to study the functions of genes and has been increasingly used for cancer gene therapy approaches. We report that PTTG1, but not PTTG2 and 3, was highly and frequently expressed in liver cancer tissues from patients and highly in SH-J1, SK-Hep1, and Huh-7 hepatoma cell lines. Adenoviral vector encoding siRNA against PTTG1 (Ad.PTTG1-siRNA) depleted PTTG1 specifically and efficiently in SH-J1 hepatoma cells, which resulted in activation of p53 that led to increased p21 expression and induction of apoptosis. The depletion of PTTG1 in HCT116 colorectal cancer cells exhibited a cytotoxic effect in a p53-dependent manner. Ad.PTTG1-siRNA-mediated cytotoxic effect was dependent on expression levels of PTTG1 and p53 in hepatoma cell lines. Huh-7 hepatoma cells, once transduced with Ad.PTTG1-siRNA, displayed markedly attenuated growth potential in nude mice. Intra-tumor delivery of Ad.PTTG1-siRNA led to significant inhibition of tumor growth in SH-J1 tumor xenograft established in nude mice. In conclusion, PTTG1 overexpressed in hepatoma cell lines negatively regulates the ability of p53 to induce apoptosis. PTTG1 gene silencing using siRNA may be an effective modality to treat liver cancer, in which PTTG1 is abundantly expressed. (HEPATOLOGY 2006;43:1042–1052.)</P>
Hae Sun Jung,Gun-Woo Byun,Kyoung-Eun Lee,Yeung Chul Mun,Seung Hyun Nam,Jung Mi Kwon,Shi Nae Lee,Seock-Ah Im,Chu-Myong Seong,Soon Nam Lee 대한암학회 2005 Cancer Research and Treatment Vol.37 No.6
FA (Fanconi’s Anemia) is an autosomal recessive disorder that is characterized by pancytopenia with bone marrow hypoplasia, diverse congenital abnormalities and an increased predisposition towards malignancy. The mainstay of the treatment for these cancers has been surgery, because of the hypersensitive reactions of FA patients to DNA cross- linking agents or radiation. Therefore, there has been no effective therapy for advanced squa mous cell carcinoma. We report here on a patient suffering from advanced multiple squamous cell carcinoma and hepatocellular carcinoma along with an FA, and this patient was treated with gefitinib.
Decreased number and function of endothelial progenitor cells in patients with migraine
Lee, S. -T.,Chu, K.,Jung, K. -H.,Kim, D. -H.,Kim, E. -H.,Choe, V. N.,Kim, J. -H.,Im, W. -S.,Kang, L.,Park, J. -E.,Park, H. -J.,Park, H. -K.,Song, E. -C.,Lee, S. K.,Kim, M.,Roh, J. -K. Ovid Technologies (Wolters Kluwer) - American Acad 2008 Clinical Neurophysiology Vol.70 No.17
<P>OBJECTIVE: Migraine carries an increased risk for cardiovascular and cerebrovascular diseases that cannot be explained by traditional cardiovascular risk factors. The circulating endothelial progenitor cell (EPC) number is a surrogate biologic marker of vascular function, and diminished EPC counts are associated with higher cardiovascular risk. We investigated whether abnormalities in EPC levels and functions are present in migraine patients. METHODS: Consecutive headache patients (n =166) were enrolled, including those with tension type headache (TTH; n = 74), migraine without aura (MO; n = 67), and migraine with aura (MA; n = 25). EPC colony-forming units in peripheral blood samples and migratory capacity to chemoattractants (stromal cell-derived factor 1 and vascular endothelial growth factor) and cellular senescence levels were assayed in risk factor-matched subjects (n = 6 per group). RESULTS: The TTH group had more cardiovascular risk factors, more headache days, and higher Framingham risk scores than the other two groups. Mean numbers of EPC colony-forming units were 47.8 +/- 24.3 in TTH, 20.4 +/-22.2 in MO, and 8.6 +/- 10.1 in MA patients (p < 0.001 in TTH vs MO; p = 0.001 in MO vs MA). EPC colony counts of normal subjects (n = 37) were not significantly different from those with TTH. Multiple linear regression models identified only MO, MA, and the presence of migraine (MO + MA) as significant predictors of EPC levels. In addition, EPCs from migraine patients (MO and MA) showed reduced migratory capacity and increased cellular senescence compared with EPCs from TTH or normal subjects. CONCLUSION: Circulating endothelial progenitor cell (EPC) numbers and functions are reduced in migraine patients, suggesting that EPCs can be an underlying link between migraine and cardiovascular risk.</P>
Slowed progression in models of huntington disease by adipose stem cell transplantation
Lee, Soon-Tae,Chu, Kon,Jung, Keun-Hwa,Im, Woo-Seok,Park, Jeong-Eun,Lim, Hun-Chang,Won, Chong-Hyun,Shin, Seung-Hyun,Lee, Sang Kun,Kim, Manho,Roh, Jae-Kyu Wiley Subscription Services, Inc., A Wiley Company 2009 Annals of Neurology Vol.66 No.5
<B>Objective</B><P>Adipose-derived stem cells (ASCs) are readily accessible and secrete multiple growth factors. Here, we show that ASC transplantation rescues the striatal pathology of Huntington disease (HD) models.</P><B>Methods</B><P>ASCs were isolated from human subcutaneous adipose tissue. In a quinolinic acid (QA)-induced rat model of striatal degeneration, human ASCs (1 million cells) were transplanted into the ipsilateral striatal border immediately after the QA injection. In 60-day-old R6/2 mice transgenic for HD, ASCs (0.5 million cells) were transplanted into each bilateral striata. In in vitro experiments, we treated mutant huntingtin gene-transfected cerebral neurons with ASC-conditioned media.</P><B>Results</B><P>In the QA model, human ASCs reduced apomorphine-induced rotation behavior, lesion volume, and striatal apoptosis. In R6/2 transgenic mice, transplantation of ASCs improved Rota-Rod performance and limb clasping, increased survival, attenuated the loss of striatal neurons, and reduced the huntingtin aggregates. ASC-transplanted R6/2 mice expressed elevated levels of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and reactive oxygen defense enzymes and showed activation of the Akt/cAMP-response element-binding proteins. ASC-conditioned media decreased the level of N-terminal fragments of mutant huntingtin and associated apoptosis, and increased PGC-1α expression.</P><B>Interpretation</B><P>Collectively, ASC transplantation slowed striatal degeneration and behavioral deterioration of HD models, possibly via secreted factors. Ann Neurol 2009;66:671–681</P>
Altered microRNA regulation in Huntington's disease models
Lee, S.T.,Chu, K.,Im, W.S.,Yoon, H.J.,Im, J.Y.,Park, J.E.,Park, K.H.,Jung, K.H.,Lee, S.K.,Kim, M.,Roh, J.K. Academic Press 2011 Experimental neurology Vol.227 No.1
Huntington's disease (HD) is a genetic neurodegenerative disease caused by abnormal CAG expansion. MicroRNAs (miRNAs) are short RNA molecules regulating gene expression, and are implicated in a variety of diseases including HD. However, the profiles and regulation of miRNAs in HD are not fully understood. Here, we analyzed the miRNA expression and miRNA regulators in two transgenic models of HD, YAC128 and R6/2 mice, and in a 3-nitropropionic acid (3NP)-induced striatal degeneration rat model. After characterizing the phenotypes by behavioral tests and histological analyses, we profiled striatal miRNAs using a miRNA microarray and we measured the key molecules involved in miRNA biogenesis and function. YAC128 mice showed upregulation-dominant miRNA expressions at 5months and downregulation-dominant expressions at 12months. Concomitantly, the expressions of Drosha-DGCR8, Exportin-5, and Dcp1 were increased at 5months, and the expression of Dicer was decreased at 12months. In 10-week-old R6/2 mice, downregulation was dominant in the miRNA expressions and the level of Drosha decreased concomitantly. Nine miRNAs (miR-22, miR-29c, miR-128, miR-132, miR-138, miR-218, miR-222, miR-344, and miR-674*) were commonly down-regulated in both the 12-month-old YAC128 and 10-week-old R6/2 mice. Meanwhile, 3NP rats showed dynamic changes in the miRNA profiles during disease development and a few miRNAs with altered expression. Our results show that transgenic HD mice have abnormal miRNA biogenesis. This information should aid in future studies on therapeutic application of miRNAs in HD.
Oh, Eui Geum,Chu, Sang Hui,Bang, So Youn,Lee, Mi Kyung,Kim, Soo Hyun,Hyun, Sa Saeng,Jeon, Justin Y,Jeon, Yong Kwan,Im, Jee Aee,Lee, Jung Eun Sage Publications, Inc 2011 Biological research for nursing Vol.13 No.2
<P>Although therapeutic lifestyle modification (TLM) effectively improves the values of diagnostic biomarkers of metabolic syndrome, less is known about its effects on inflammatory chemokines and insulin resistance (IR) in patients with this syndrome. Objectives. To examine the effects of a short-term TLM program on inflammatory chemokines (monocyte chemoattractant protein-1 [MCP-1], retinol binding protein-4 [RBP-4]) and IR in subjects with metabolic syndrome.</P>
Exosome-Based Delivery of miR-124 in a Huntington’s Disease Model
Lee, Soon-Tae,Im, Wooseok,Ban, Jae-Jun,Lee, Mijung,Jung, Keun-Hwa,Lee, Sang Kun,Chu, Kon,Kim, Manho The Korean Movement Disorder Society 2017 Journal of movement disorders: official journal of Vol.10 No.1
<P><B>Objective </B></P><P>Huntington’s disease (HD) is a genetic neurodegenerative disease that is caused by abnormal CAG expansion. Altered microRNA (miRNA) expression also causes abnormal gene regulation in this neurodegenerative disease. The delivery of abnormally downregulated miRNAs might restore normal gene regulation and have a therapeutic effect. </P><P><B>Methods </B></P><P>We developed an exosome-based delivery method to treat this neurodegenerative disease. miR-124, one of the key miRNAs that is repressed in HD, was stably overexpressed in a stable cell line. Exosomes were then harvested from these cells using an optimized protocol. The exosomes (Exo-124) exhibited a high level of miR-124 expression and were taken up by recipient cells. </P><P><B>Results </B></P><P>When Exo-124 was injected into the striatum of R6/2 transgenic HD mice, expression of the target gene, RE1-Silencing Transcription Factor, was reduced. However, Exo-124 treatment did not produce significant behavioral improvement. </P><P><B>Conclusion </B></P><P>This study serves as a proof of concept for exosome-based delivery of miRNA in neurodegenerative diseases.</P>