• THE JOURNAL OF KOREAN ORIENTAL ONCOLOGY
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• v.4 no.1
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• pp.37-53
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• 1998

The sprig of Jinryungtang Gagambang has been used for curing as a traditional medicine without any experimental evidence to support the rational basis for their clinical use. This experiment was carried out to evaluate the possible therapeutic or antitumoral effects of Jinryungtang Gagambang extract against cancer, and to study some mechanisms responsible for its effect. The cytotoxic and antitumor effects were evaluated on human cell liens (A549, hep3B, Caki-1, Sarcoma 180) after exposure to Jinryungtang Gagambang extract using in ILS, colony forming efficency and SRB assay which were regarded as a valuable method for cytotoxic and antitumor effects of unknown compound on tumor cell lines. The results obtained in this studies were as follows. 1. As a result of exposure to Jinryungtang Gagambang extract, the proliferation of A549, hep3B, Caki-1, good correlations were shown from the results of SRB assay and those of clogenetic assay. 2. The oral administration of Jinryungtang Gagambang extract showed significant effects of increase of MST(mean survival time) and ILS(increased life span) depending on the increasing concentration. 3. Against squamous cell carcinoma induced by MCA, Jinryungtang Gagambang decreased not only the frequency of tumor production but also the number and weight of tumors per tumor bearing mice(TBM). Jinryungtang Gagambang also significantly suppressed the development of 3LL cell-implanted tumors by frequency and their size, and some developed tumors were regressed by the continuous treatment of Jinryungtang Gagambang extract into TBM. 4. Jinryungtang Gagambang extract also increased NK cell activities. According to the above results, it could be suggested that Jinryungtang Gagambang extract has prominent antiutmor effect.

• Journal of Life Science
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• v.34 no.10
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• pp.744-754
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• 2024

Cancer cells exhibit a unique metabolic process for uncontrolled cell division, providing bioenergy and intermediates, which are significantly different from normal cells. Here an aerobic glycolysis converts most of the pyruvate produced from glucose into lactate and inefficiently produced ATP. Cancer cells counter their lack of energy through glutamine metabolism, together with glucose. Glutamine is the most abundant amino acid in the blood and is used for the synthesis of amino acids, nucleotides, and lipids, as well as bioenergy through glutaminolysis. Cancer cells rely on glutamine rather than normal cells, showing more than half of the tricarboxylic acid cycle metabolites derived from glutamine, called glutamine addiction. Oncogenes c-Myc also regulates the expression of various genes involved in glutamine metabolism and promotes the absorption of glutamine. Whether glutaminase (GLS) causes or inhibits tumors is controversial. However, GLS1 is a promising treatment target due to its higher carcinogenic incidence, whereas GLS2 is known to act as a tumor suppressor. The 4th-generation metabolic anti-cancer therapy, which has been actively investigated since the mid-2010s, is based on a complex and sophisticated network of cancer metabolites. These drugs directly regulate the energy metabolism of cancer cells to maximize anti-cancer effects without side effects. GLS is a crucial enzyme for cancer metabolism and tumor progression that catalyzes the first stage in the process of glutaminolysis. The development of anti-cancer drugs targeting GLS enzymes has emerged as a promising strategy.

• Proceedings of the Korean Information Science Society Conference
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• 2007.10d
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• pp.366-371
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• 2007

무선 센서 네트워크는 경제적, 환경적 목적으로 다양한 방면에서 활용되고 있다 이 때, 배치된 각 센서의 위치를 파악하는 것은 센서 네트워크에서 가장 기본적이며 가장 중요한 문제 중의 하나이다. 기존 논문에서 제안된 센서 위치 측정 방법은 특별한 장비를 장착하거나 특정한 환경의 지역에 한정시킨 방범으로 제한하고 있는 경우가 대부분이다. 하지만 어떠한 관심 지역의 환경은 언제라도 바뀔 수 있다. 또한, 센서가 위치할 환경의 기온, 풍속 등을 미리 안다는 것은 비현실적인 가정이다. 더구나 각각의 센서에 특별한 장비를 장착한다는 것은 비용 절감을 이유로 센서 네트워크를 운영하는 경우 오히려 그것을 이용하지 않는 경우보다 비용이 더 들 수도 있다. 이에 본 논문에서는 센서 노드의 기본적인 통신 기능은 이용하여, 환경에 순응적으로 센서의 위치를 측정할 수 있는 방법을 제안하고자 한다. 센서 노드에서 기본적으로 제공하는 통신 기능은 RF 전파를 보낼 때 전송 레벨을 달리하여 보낼 수 있다. 이러한 기본적인 기능을 이용하여 위치를 측정하게 되면 전체적인 센서 네트워크의 비용이 절감될 뿐만 아니라 환경에 순응적인 위치 측정이 가능하게 된다. 또한, 각 노드의 위치가 정해진 후 다른 노드와 통신할 때 전파의 세기를 조정함으로써 RF 통신에서 소모되는 전력량을 줄일 수 있다. 따라서 본 논문에서 제안하는 전송 레벨을 이용한 위치 측정 방법은 단순히 위치를 측정한다는 의미뿐 아니라 환경에 순응적으로 작동한다는 장점이 있다. 향후 네트워크 내에서 통신에 소비되는 전력을 줄일 수 있다는 점에서도 중요한 의미를 지닌다.를 집행하는 caspase의 활성 형태인 cleaved caspase-8, -9, -7, -3의 단백질 수준이 목향 헥산추출물의 처리에 의해 증가하였고 caspase-3의 표적 단백질 중 하나인 PARP의 불활성 형태인 cleaved PARP의 단백질 수준도 현저하게 증가하였다. 이 결과들은 목향 헥산 추출물이 LNCaP 세포의 apoptosis를 유도함으로써 전립선 암세포의 증식을 억제함을 보여주는 것이며 목향 헥산추출물에 의한 apoptosis 유도는 caspase 활성 증가와 Bak 및 t-Bid 단백질의 증가에 의한 것임을 제시한다. 따라서 앞으로 항암효과를 나타내는 성분의 동정 및 동물실험을 통하여 좀 더 면밀한 기전 연구가 수행된다면 목향 헥산추출물은 화학적 암예방 물질이나 치료제로 개발될 수 있을 것으로 사료된다.적 분해층과 마모질이가 가장 깊은 것으로 나타났으며 flowable type의 복합레진과 컴포머는 표면 경도와 마모도에서 양호한 결과를 보였다. 이상의 결과 복합레진과 컴포머의 평가요소로서 마모도와 함께 가수분해도 고려되어야 할 것으로 사료된다.증후군 환자에서 대조군에 비해 높은 비율을 보였다.er thinning은 3 군모두에서 관찰되었고 항암 3 일군이 가장 심하게 나타났다. 이상의 실험결과를 보면 술전 항암제투여가 초기에 시행한 경우에는 조직의 치유에 초기 5 일정도까지는 영향을 미치나 7 일이 지나면 정상범주로 회복함을 알수 있었고 실험결과 항암제 투여후 3 일째 피판 형성한 군에서 피판치유가 늦어진 것으로 관찰되어 인체에서 항암 투여후 수술시기는 인체면역계가 회복하는 시기를 3

• Proceedings of the Korean Society of Applied Pharmacology
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• 1993.04a
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• pp.37-37
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• 1993

1) 급성독성시험: 랫드와 마우스 공히 투여후 5~6일에 농도의존적의 강한 독성이 발현 되었으며 표적장기로는 소화기계, 임파계, 조혈기계 등으로 나타났다. 랫드에서의 반수 치사량은 암수 각각 771.9(505.6~1178.4)mg/kg과 479.8(302.7~760.4)mg/kg이었으며 마우스에서는 암수 각각 527.4(393.7~701.1)mg/kg과 463.0(308.8~694.2)mg/kg 이었다. 2) 유전독성: S. typhimurium을 이용한 복귀돌연변이시험, CHL세포를 이용한 염색체이상 시험, 마우스에서의 소핵시험결과 DA-125는 돌연변이 유발능을 갖는 것으로 나타났다. 3) 국소자극성: 혈관주위주사에 의한 피부자극성 시험결과 DA-125는 adriamycin의 3배 용량에서 궤양, 괴사등 유사한 병변이 유발되었으나, 병변회복은 adriamycin에 비해 빠른 것으로 나타났다. 또한 토끼에서의 안점막자극시험 결과에서 DA-125는 실제적으로 자극이 없는 것으로 나타났다.

• Journal of Digestive Cancer Research
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• v.3 no.1
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• pp.30-34
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• 2015

We report a case of a 55-year-old man who diagnosed with advanced gastric cancer (AGC), with A review of the literature. A 55-year old man was transferred to our hospital for further evaluation and treatment after being diagnosed with adenocarcinoma through endoscopic biopsy during a regular health examination. An abdominal computed tomography (CT) showed AGC, stage IIA (T3N3M0), while an endoscopic examination showed AGC, Borrmann type 2. The patient is currently under observation after undergoing radical subtotal gastrectomy with gastroduodenostomy and subsequent administration of oral chemotherapeutic agents. As an abdominal CT response assessment performed after surgery revealed new metastasis to the liver, the patient received palliative chemotherapy as progressive disease was suspected. After receiving chemotherapy in the order of FOLFOX (5-fluorouracil (5-FU)) + Leucovorin + Oxaliplatin), FOLFIRI (5-FU + Leucovorin + Irinotecan), EAP-II (Etoposide + Doxorubicin + Cisplatin), ELF (Etoposide + Leucovorin + 5-FU), TS-1 (Tegafur + Gimeracil) + Cisplatin, an abdominal CT response assessment showed progressive disease for which the regimen was altered to PFL (Paclitaxel + 5-FU + Leucovorin). The patient has currently completed his second cycle of chemotherapy and after an abdominal CT response assessment, further course of therapy will be decided.

• Journal of Life Science
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• v.15 no.3 s.70
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• pp.406-414
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• 2005

The genetic instability of cancer cells may be related to inappropriately activated DNA repair pathways. In present study, the modulated expression of DNA-dependent protein kinase (DNA-PK), a major DNA repair protein, in human cancer metastatic cells was tested. The expressions of Ku70/80, regulatory subunit of DNA-PK, and the Ku DNA-binding activity in various highly metastatic cell lines were higher than those in each parental cell line. Also, the expression of DNA-PKcs, catalytic subunit of DNA-PK, and the kinase activity of the whole DNA-PK complex in highly metastatic cells were significantly increased as compared to those of parental cells, suggesting that the enhanced DNA repair capacity of metastatic cells could be associated with aberrant use of DNA repair, which may mediate tumor progression and metastatic potential. Increased EGFR (epidermal growth factor receptor) signaling has been associated with tumor invasion and metastasis, and the linkage between EGFR-mediated signaling and DNA-PK has been suggested. This study showed that PKI166, the new EGFR tyrosine kinase inhibitor, modulated the expressions of Ku70/80 and DNA-PKcs and also revealed the chemosensitization effect of PKI166 against metastatic cells may be in part due to inhibition of Ku70/80. These results suggest that interference in EGFR signaling by EGFR inhibitor resulted in the impairment of DNA repair activity, and thus DNA-PK could be possible molecular targets for therapy against metastatic cancer cells.

• Tuberculosis and Respiratory Diseases
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• v.62 no.1
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• pp.33-42
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• 2007

Background: Heme oxygenase-1 (HO-1) is known to modulates the cellular functions, including cell proliferation and apoptosis. It is known that a high level of HO-1 expression is found in many tumors, and HO-1 plays an important role in rapid tumor growth on account of its antioxidant and antiapoptotic effects. Cisplatin is a widely used anti-cancer agent for the treatment of lung cancer. However, the development of resistance to cisplatin is a major obstacle to its use in clinical treatment. We previously demonstrated that inhibiting HO-1 expression through the transcriptional activation of Nrf2 induces apoptosis in A549 cells. The aim of this study was to determine of the inhibiting HO-1 enhance the chemosensitivity of A549 cells to cisplatin. Materials and Methods: The human lung cancer cell line, A549, was treated cisplatin, and the cell viability was measured by a MTT assay. The change in HO-1, Nrf2, and MAPK expression after the cisplatin treatment was examined by Western blotting. HO-1 inhibition was suppressed by ZnPP, which is a specific pharmacologic inhibitor of HO activity, and small interfering RNA (siRNA). Flow cytometry analysis and Western blot were performed in to determine the level of apoptosis. The level of hydrogen peroxide ($H_2O_2$) generation was monitored fluoimetrically using 2',7'-dichlorofluorescein diacetate. Results: The A549 cells showed more resistance to the cisplatin treatment than the other cell lines examined, whereas cisplatin increased the expression of HO-1 and Nrf2, as well as the phosphorylation of MAPK in a time-dependent fashion. Inhibitors of the MAPK pathway blocked the induction of HO-1 and Nrf2 by the cisplatin treatment in A549 cells. In addition, the cisplatin-treated A549 cells transfected with dither the HO-1 small interfering RNA (siRNA) or ZnPP, specific HO-1 inhibitor, showed in a more significantly decrease in viability than the cisplatin-only-treated group. The combination treatment of ZnPP and cisplatin caused in a marked increase in the ROS generation and a decrease in the HO-1 expression. Conclusion: Cisplatin increases the expression of HO-1, probably through the MAPK-Nrf2 pathway, and the inhibition of HO-1 enhances the chemosensitivity of A549 cells to cisplatin.

• Journal of Life Science
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• v.28 no.4
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• pp.488-495
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• 2018

The p53 gene plays a critical role in the transcriptional regulation of cellular response to stress, DNA damage, hypoxia, and tumor development. Keeping in mind the recently discovered manifold physiological functions of p53, its involvement in the regulation of cancer is not surprising. In about 50% of all human cancers, inactivation of p53's protein function occurs either through mutations in the gene itself or defects in the mechanisms that activate it. This disorder plays a crucial role in tumor evolution by allowing the evasion of a p53-dependent response. Many recent studies have focused on directly targeting p53 mutants by identifying selective, small molecular compounds to deplete them or to restore their tumor-suppressive function. These small molecules should effectively regulate various interactions while maintaining good drug-like properties. Among them, the discovery of the key p53-negative regulator, MDM2, has led to the design of new small molecule inhibitors that block the interaction between p53 and MDM2. Some of these small molecule compounds have now moved from proof-of-concept studies into clinical trials, with prospects for further, more personalized anti-carcinogenic medicines. Here, we review the structural and functional consequences of wild type and mutant p53 as well as the development of therapeutic agents that directly target this gene, and compounds that inhibit the interaction between it and MDM2.

• Korean Journal of Microbiology
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• v.47 no.1
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• pp.1-6
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• 2011

Inefficiency of in vivo gene transfer using currently available vectors reflects a major hurdle in cancer gene therapy. Both viral and non-viral approaches have been described to improve gene transfer efficiency but suffer from a number of limitations. Here we tested an adenovirus carrying the small peptide ligand derived from heregulin${\beta}$ EGF-like domain onto fiber, the adenoviral capsid protein, to deliver transgene to ovarian cancer cells which overexpress ErbB, the cognate receptors for heregulin. The attachement of 53 amino acids to fiber didn't affect on the fiber's trimer structure that is critical for the viral entry to cells. The fiber-modified adenovirus can mediate entry and expression of a ${\beta}$-galactosidase into cancer cells in an increased efficiency compared the unmodified adenovirus. Particularly, the gene transfer efficiency was improved up to 5 times in OVCAR3 cells, an ovarian cancer cell line. Such transduction systems hold promise for delivering genes to ErbB receptor overexpressing cancer cells, and could be used for future cancer gene therapy.

• Journal of Life Science
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• v.18 no.1
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• pp.75-83
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• 2008

This studies were designed to elucidate whether inhibitors of topoisomerase regulate function and activity of topoisomerase, and gene expression in HL-60 human leukemia cells. HL-60 cells were treated with 10-hydroxycamptothecin or doxorubicin, total RNA was isolated, and expressed genes were investigated with human oligonucleotide microarray containing 10K gene, respectively. Expression profiles of the human leukemia HL-60 cells treated with 10-hydroxycamptothecin (10-CIT) or doxorubicin associated with signal transduction,. cell adhesion, cell cycle, cell growth, cell proliferation, cell differentiation, transcription and immune response, especially genes related with transcription and cell growth. In HL-60 cells treated with 10-CPT, the expression of topoisomerase III${\alpha}$, III${\beta}$ and I gene from oligo chip microarray analysis were increased over, but the expression of topoisomerase II${\alpha}$ and II${\beta}$ gene were decreased over. In contrast, the expression of topoisomerase II${\alpha}$ and II${\beta}$ gene were increased over in HL-60 cells treated with doxorubicin, whereas the expression of topoisomerase III${\alpha}$ and III${\beta}$ mRNA remained no significant change. These results suggest that these data may be useful for novel therapeutic markers.