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Search Results: 1 - 10 of 483720 matches for " Kyung-A Lee "
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Spectrum of EGFR Gene Copy Number Changes and KRAS Gene Mutation Status in Korean Triple Negative Breast Cancer Patients
Yoonjung Kim, Juwon Kim, Hy-De Lee, Joon Jeong, Woochang Lee, Kyung-A Lee
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0079014
Abstract: Anti-epidermal growth factor receptor (EGFR) therapy has been tried in triple negative breast cancer (TNBC) patients without evaluation of molecular and clinical predictors in several randomized clinical studies. Only fewer than 20% of metastatic TNBCs showed response to anti-EGFR therapy. In order to increase the overall response rate, first step would be to classify TNBC into good or poor responders according to oncogenic mutation profiles. This study provides the molecular characteristics of TNBCs including EGFR gene copy number changes and mutation status of EGFR and KRAS gene in Korean TNBC patients. Mutation analysis for EGFR, KRAS, BRAF and TP53 from a total of 105 TNBC tissue samples was performed by direct sequencing, peptide nucleic acid-mediated PCR clamping method and real-time PCR. Copy number changes of EGFR gene were evaluated using multiplex ligation-dependent probe amplification. Out of all 105 TNBCs, 15.2% (16/105) showed EGFR copy number changes. Among them, increased or decreased EGFR copy number was detected in 13 (5 single copy gain, 2 amplification and 4 high-copy number amplification) and 3 cases (3 hemizygous deletion), respectively. The mutation frequencies of KRAS, EGFR and TP53 gene were 1.9% (G12V and G12D), 1.0% (exon 19 del) and 31.4%, respectively. There was no BRAF V600E mutation found. Future studies are needed to evaluate the clinical outcomes of TNBC patients who undergo anti-EGFR therapy according to the genetic status of EGFR.
Cataloging Coding Sequence Variations in Human Genome Databases
Hong-Hee Won, Hee-Jin Kim, Kyung-A Lee, Jong-Won Kim
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0003575
Abstract: Background With the recent growth of information on sequence variations in the human genome, predictions regarding the functional effects and relevance to disease phenotypes of coding sequence variations are becoming increasingly important. The aims of this study were to catalog protein-coding sequence variations (CVs) occurring in genetic variation databases and to use bioinformatic programs to analyze CVs. In addition, we aim to provide insight into the functionality of the reference databases. Methodology and Findings To catalog CVs on a genome-wide scale with regard to protein function and disease, we investigated three representative databases; the Human Gene Mutation Database (HGMD), the Single Nucleotide Polymorphisms database (dbSNP), and the Haplotype Map (HapMap). Using these three databases, we analyzed CVs at the protein function level with bioinformatic programs. We proposed a combinatorial approach using the Support Vector Machine (SVM) to increase the performance of the prediction programs. By cataloging the coding sequence variations using these databases, we found that 4.36% of CVs from HGMD are concurrently registered in dbSNP (8.11% of CVs from dbSNP are concurrent in HGMD). The pattern of substitutions and functional consequences predicted by three bioinformatic programs was significantly different among concurrent CVs, and CVs occurring solely in HGMD or in dbSNP. The experimental results showed that the proposed SVM combination noticeably outperformed the individual prediction programs. Conclusions This is the first study to compare human sequence variations in HGMD, dbSNP and HapMap at the genome-wide level. We found that a significant proportion of CVs in HGMD and dbSNP overlap, and we emphasize the need to use caution when interpreting the phenotypic relevance of these concurrent CVs. Combining bioinformatic programs can be helpful in predicting the functional consequences of CVs because it improved the performance of functional predictions.
NF-κB-Targeted Anti-Inflammatory Activity of Prunella vulgaris var. lilacina in Macrophages RAW 264.7
Yu-Jin Hwang,Eun-Ju Lee,Haeng-Ran Kim,Kyung-A Hwang
International Journal of Molecular Sciences , 2013, DOI: 10.3390/ijms141121489
Abstract: Prunella vulgaris var. lilacina, a herbal medicine, has long been used in Korea for the treatment of sore throat, and to alleviate fever and accelerate wound healing. Although the therapeutic effect of P. vulgaris var. lilacina is likely associated with anti-inflammatory activity, the precise underlying mechanisms are largely unknown. Here, we sought to elucidate the possible mechanisms of the anti-inflammatory activity. We have investigated the anti-inflammatory activity of the various solvent fractions (hexane, butanol, chloroform and water) from the ethanol extract of P. vulgaris var. lilacina in activated macrophages. The hexane fraction exhibited higher anti-inflammatory activities, inducing inhibition of nitric oxide and prostaglandin E2 production as well as inducible nitric oxide synthase, cyclooxygenase-2, and tumor necrosis factor-α mRNA expression in response to lipopolysaccharide stimulation. Moreover, the hexane fraction from P. vulgaris var. lilacina significantly inhibited the activation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and the nuclear translocation of the NF-κB p50 and p65 subunits. These results indicate that P. vulgaris var. lilacina has an anti-inflammatory capacity in vitro, suggesting that it could be a potential source of natural anti-inflammatory agents.
Expression of GA733-Fc Fusion Protein as a Vaccine Candidate for Colorectal Cancer in Transgenic Plants
Zhe Lu,Kyung-Jin Lee,Yingxue Shao,Jeong-Hwan Lee,Yangkang So,Young-Kug Choo,Doo-Byoung Oh,Kyung-A Hwang,Seung Han Oh,Yeon Soo Han,Kisung Ko
Journal of Biomedicine and Biotechnology , 2012, DOI: 10.1155/2012/364240
Abstract: The tumor-associated antigen GA733 is a cell-surface glycoprotein highly expressed in colorectal carcinomas. In this study, 3 recombinant genes were constructed as follows: GA733 tagged to the ER retention sequence KDEL (GA733K), GA733 fused to the immunoglobulin Fc fragment (GA733-Fc), and GA733-Fc fused to the ER retention sequence (GA733-FcK). Agrobacterium-mediated transformation was used to generate transgenic plants expressing recombinant genes. The presence of transgenes was confirmed by genomic PCR. Western blot, confocal immunofluorescence, and sandwich ELISA showed the expression of recombinant proteins. The stability, flexibility, and bioactivity of recombinant proteins were analyzed and demonstrated through N-glycosylation analysis, animal trials, and sera ELISA. Our results suggest that the KDEL retained proteins in ER with oligomannose glycan structure and enhanced protein accumulation level. The sera of mice immunized with GA733-FcK purified from plants contained immunoglobulins which were at least as efficient as the mammalian-derived GA733-Fc at recognizing human colorectal cancer cell lines. Thus, a plant system can be used to express the KDEL fusion protein with oligomannose glycosylation, and this protein induces an immune response which is comparable to non-KDEL-tagged, mammalian-derived proteins.
A novel de novo mutation in the serine-threonine kinase STK11 gene in a Korean patient with Peutz-Jeghers syndrome
Jong-Ha Yoo, Jee-Hyoung Yoo, Yoon-Jung Choi, Jung-Gu Kang, Young-Kyu Sun, Chang-Seok Ki, Kyung-A Lee, Jong-Rak Choi
BMC Medical Genetics , 2008, DOI: 10.1186/1471-2350-9-44
Abstract: Using DNA samples obtained from the patient and his family members, we sequenced nine exons and flanking intron regions of the STK11 gene using polymerase chain reaction (PCR) and direct sequencing.Sequencing of the STK11 gene in the proband of the family revealed a novel 1-base pair deletion of guanine (G) in exon 6 (c.826delG; Gly276AlafsX11). This mutation resulted in a premature termination at codon 286, predicting a partial loss of the kinase domain and complete loss of the C-terminal domain. We did not observe this mutation in both parents of the PJS patient. Therefore, it is considered a novel de novo mutation.The results presented herein enlarge the spectrum of mutations of the STK11 gene by identifying a novel de novo mutation in a PJS patient and further support the hypothesis that STK11 mutations are disease-causing mutations for PJS with or without a positive family history.Peutz-Jeghers syndrome (PJS; OMIM 175200) is a rare, autosomal dominant disorder characterized by melanocytic macules of the lips, buccal mucosa, and digits, along with multiple gastrointestinal hamartomatous polyps, frequently in the small intestine [1,2]. Patients with PJS are at an increased risk of developing gastrointestinal cancer and extraintestinal neoplasms involving organs such as the ovaries, testes, breasts, pancreas, lungs, or uterine cervix [3].Currently, only mutations in the gene STK11 (also known as LKB1; OMIM 602216) at chromosome 19p13.3 have been identified as a cause of PJS [4,5]. The human STK11 gene encodes a 433 amino acid serine-threonine kinase. STK11 is known to be located both in the nucleus and the cytoplasm of all human tissues [6], and orthologs include mouse LKb1 [7], XEEK1 (Xenopus egg and embryo kinase 1) [8], Caenorhabditis elegans partitioning defective gene 4 (par-4) [9], and drosophila Lkb1 [10].Loss of the normal allele has been observed in polyps from patients with PJS, and loss of heterozygosity (LOH) has been noted to occur in some tumor tissu
Black rice (Oryza sativa L.) extract attenuates hepatic steatosis in C57BL/6 J mice fed a high-fat diet via fatty acid oxidation
Hwan-Hee Jang, Mi-Young Park, Heon-Woong Kim, Young-Min Lee, Kyung-A Hwang, Jae-Hak Park, Dong-Sik Park, Oran Kwon
Nutrition & Metabolism , 2012, DOI: 10.1186/1743-7075-9-27
Abstract: Twenty-four mice were randomly divided into three groups (n = 8 in each group): normal fat diet (ND), high fat diet (HF), and high fat diet supplemented with 1% (w/w) BRE (HF +1% BRE). The experimental diets were fed for seven weeks.A HF induced hepatic steatosis with significant increases in the serum levels of free fatty acids (FFAs), triglyceride (TG), total cholesterol (TC), and insulin. By contrast, supplementary BRE (10 g/kg of diet) included in the HF alleviated hepatic steatosis and significantly decreased serum TG and TC levels (p < 0.01 for both). Dietary BRE also increased expression of fatty acid metabolism-related genes, including carnitine palmitoyltransferase (CPT1A), acyl-CoA oxidase (ACO), cytochrome P450 (CYP4A10), and peroxisome proliferator activated receptor (PPAR)-α (p < 0.05 for all).Dietary BRE supplementation improved serum lipid profiles and significantly enhanced mRNA expression levels of fatty acid metabolism-related genes, primarily via β-oxidation and ω-oxidation in the liver. Taken together, these findings suggest that a BRE-supplemented diet could be useful in reducing the risks of hepatic steatosis and related disorders, including hyperlipidemia and hyperglycemia.The liver is the primary fat-metabolizing organ. Normal cellular fatty acid homeostasis is the product of a balance between fatty acid uptake, utilization, and export from the liver, which is controlled by a complex transcriptional network that is attuned to meeting the energy requirements of cells while preventing excessive accumulation of fatty acids [1]. However, excessive dietary fat can result in increased free fatty acids (FFAs) levels in the blood, thereby amplifying the delivery of FFAs to the liver [2]. Thus, excessive consumption of dietary fats induces lipid accumulation in the liver and can eventually cause obesity. However, in studies of rats subjected to short-term high-fat feeding, excess fat has been shown to accumulate in the liver before adipose tissue [3,4
Intracellular Reprogramming of Expression, Glycosylation, and Function of a Plant-Derived Antiviral Therapeutic Monoclonal Antibody
Jeong-Hwan Lee, Da-Young Park, Kyung-Jin Lee, Young-Kwan Kim, Yang-Kang So, Jae-Sung Ryu, Seung-Han Oh, Yeon-Soo Han, Kinarm Ko, Young-Kug Choo, Sung-Joo Park, Robert Brodzik, Kyoung-Ki Lee, Doo-Byoung Oh, Kyung-A Hwang, Hilary Koprowski, Yong Seong Lee, Kisung Ko
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0068772
Abstract: Plant genetic engineering, which has led to the production of plant-derived monoclonal antibodies (mAbPs), provides a safe and economically effective alternative to conventional antibody expression methods. In this study, the expression levels and biological properties of the anti-rabies virus mAbP SO57 with or without an endoplasmic reticulum (ER)-retention peptide signal (Lys-Asp-Glu-Leu; KDEL) in transgenic tobacco plants (Nicotiana tabacum) were analyzed. The expression levels of mAbP SO57 with KDEL (mAbPK) were significantly higher than those of mAbP SO57 without KDEL (mAbP) regardless of the transcription level. The Fc domains of both purified mAbP and mAbPK and hybridoma-derived mAb (mAbH) had similar levels of binding activity to the FcγRI receptor (CD64). The mAbPK had glycan profiles of both oligomannose (OM) type (91.7%) and Golgi type (8.3%), whereas the mAbP had mainly Golgi type glycans (96.8%) similar to those seen with mAbH. Confocal analysis showed that the mAbPK was co-localized to ER-tracker signal and cellular areas surrounding the nucleus indicating accumulation of the mAbP with KDEL in the ER. Both mAbP and mAbPK disappeared with similar trends to mAbH in BALB/c mice. In addition, mAbPK was as effective as mAbH at neutralizing the activity of the rabies virus CVS-11. These results suggest that the ER localization of the recombinant mAbP by KDEL reprograms OM glycosylation and enhances the production of the functional antivirus therapeutic antibody in the plant.
Study on the Immunomodulation Effect of Isodon japonicus Extract via Splenocyte Function and NK Anti-Tumor Activity
Yu-Jin Hwang,Jaehyun Kim,Dong-Sik Park,Kyung-A Hwang
International Journal of Molecular Sciences , 2012, DOI: 10.3390/ijms13044880
Abstract: Here we investigated the potential immune-enhancing activity of Isodon japonicus on murine splenocyte and natural-killer (NK) cells in vitro. The ethanol extract of I . japonicus significantly enhanced the proliferation of splenocyte and induced the significant enhancement of NK cells’ activity against tumor cells (YAC-1). In addition, I. japonicus increased the production of interferon (IFN)-γ and tumor necrosis factor (TNF)-α, suggesting that the increase in NK cell cytotoxicity could be due to the enhancement of the NK cell production of both cytokines. Taken together, I. japonicus extract inhibited the growth of human leukemia cells (K562) by 74%. Our observation indicated that the anti-tumor effects of I . japonicus may be attributed to its ability to serve as a stimulant of NK anti-tumor activity. In addition, our results support the development of functional food studies on I . japonicus.
Effects of Genetically Engineered Stem Cells Expressing Cytosine Deaminase and Interferon-Beta or Carboxyl Esterase on the Growth of LNCaP Prostate Cancer Cells
Bo-Rim Yi,Kyung-A. Hwang,Yun-Bae Kim,Seung U. Kim,Kyung-Chul Choi
International Journal of Molecular Sciences , 2012, DOI: 10.3390/ijms131012519
Abstract: The risk of prostate cancer has been increasing in men by degrees. To develop a new prostate cancer therapy, we used a stem cell-derived gene directed prodrug enzyme system using human neural stem cells (hNSCs) that have a tumor-tropic effect. These hNSCs were transduced with the therapeutic genes for bacterial cytosine deaminase (CD), alone or in combination with the one encoding human interferon-beta (IFN-β) or rabbit carboxyl esterase (CE) to generate HB1.F3.CD, HB1.F3.CD.IFN-β, and HB1.F3.CE cells, respectively. CD enzyme can convert the prodrug 5-fluorocytosine (5-FC) into the activated form 5-fluorouracil (5-FU). In addition, CE enzyme can convert the prodrug CPT-11 into a toxic agent, SN-38. In our study, the human stem cells were found to migrate toward LNCaP human prostate cancer cells rather than primary cells. This phenomenon may be due to interactions between chemoattractant ligands and receptors, such as VEGF/VEGFR2 and SCF/c-Kit, expressed as cancer and stem cells, respectively. The HB1.F3.CE, HB.F3.CD, or HB1.F3.CD.IFN-β cells significantly reduced the LNCaP cell viability in the presence of the prodrugs 5-FC or CPT-11. These results indicate that stem cells expressing therapeutic genes can be used to develop a new strategy for selectively treating human prostate cancer.
Jump exercise during hindlimb unloading protect against the deterioration of trabecular bone microarchitecture in growing young rats
Yong-In Ju, Teruki Sone, Kazuhiro Ohnaru, Hak-Jin Choi, Kyung-A Choi and Masao Fukunaga
SpringerPlus , 2013, DOI: 10.1186/2193-1801-2-35
Abstract: Three-dimensional femoral trabecular architecture was investigated in tail-suspended young growing rats and the effects of jump exercise during the period of tail-suspension were also examined. Eight-week-old male Wistar rats (n = 24) were randomly assigned to three body weight-matched groups: a tail suspended group (SUS, n = 8); a sedentary control group (CON, n = 8) and rats primed with jump exercise during the period of tail suspension (JUM, n = 8). The jump exercise protocol consisted of 30 jumps/day, five days/week with a 40 cm jump height. After 3 weeks of jump exercise, bone mineral density (BMD) of the entire right femur was measured using dual energy X-ray absorptiometry. Three-dimensional trabecular bone architecture at the distal femoral metaphysis was evaluated using microcomputed tomography (micro-CT). Tail suspension caused a decrease in femoral BMD ( 5%, p < 0.001) and trabecular bone architectural deterioration. Deterioration in the trabecular network during hindlimb unloading was mostly attributed to the reduction of trabecular number ( 32%, p < 0.001) in the distal femoral metaphysis. Jump exercise during the tail suspension period increased trabecular thickness (14%, p < 0.001) and the reduction of trabecular number was suppressed. The present data indicate that jump exercise applied during hindlimb unloading could be able to inhibit bone loss and trabecular bone architectural deterioration caused by tail suspension.
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