• Biomedical Science Letters
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• v.19 no.4
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• pp.303-309
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• 2013

Oncolytic vaccinia virus is an engineered vaccinia virus that selectively destroys cancer cells and induces tumor immune response. Oncolytic vaccinia expressing mouse GM-CSF showed cytotoxic activity against various kinds of cancer cells when oncolytic vaccinia virus expressing human GM-CSF and mouse GM-CSF is intravenously administered in the mouse CT26 colon tumor model. Cancer cells treated with isolated immunoglobulin G from the serum with complement showed these cytotoxic activity and complement observed dose-dependent cytotoxic effect. These results suggest that oncolytic vaccinia virus expressing mouse GM-CSF can increase oncolytic vaccinia virus by inducing anticancer antibody in a mouse tumor model. Further studies are needed on antitumor immunity of GM-CSF.

• Nutritional Sciences
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• v.9 no.3
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• pp.212-226
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• 2006

The involvement of arachidonic acid (AA) metabolizing enzyme, lipoxygenase (LOX), in the development of particular tumors in humans has gradually been acknowledged and LOX has emerged as a novel target to prevent or treat human cancers. In the mouse skin carcinogenesis model, which provides an excellent model to study multistage nature of human cancer development, many studies have shown that some of the LOXs are constitutively upregulated in their expression. Moreover, application of LOX inhibitors effectively reduced tumor burdens, which implicates the involvement of LOX in mouse skin tumor development as well. 8S-LOX is a recently cloned LOX, which is specifically expressed in mouse skin after 12-O-tetradecanoyl-phorbol-13-acetate (TPA) treatment but not in normal skin. Unlike other members of the LOX 'family' expressed in mouse skin, this TPA-induced expression of 8S-LOX is prominent only in the skin of the TPA tumor promotion-sensitive strains of mice (SENCAR, CD-1, and NMRI) but not in the promotion-resistant C57BL/6J mice. This is a very unique phenomenon among strains of mice. Constitutive upregulation of 8S-LOX was also found in early stage papillomas and the expression was gradually reduced as the tumors became malignant. Based on these observations, it has been thought that 8S-LOX is involved in TPA-induced tumor promotion as well as in tumor conversion from papillomas to carcinomas. In accordance with this hypothesis, several studies have suggested possible roles of 8S-hydroxyeicosatetraenoic acid (HETE), an AA metabolite of 8S-LOX, in mouse skin tumor development. A clastogenic activity of 8S-HETE was demonstrated in primary keratinocytes and a close correlation between the levels of etheno-DNA adducts and 8S-HETE during skin carcinogenesis was also reported. On the other hand, it has been reported that 8S-LOX protein expression is restricted to a differentiated keratinocyte compartment Moreover, reported findings on the ability of 8S-HETE to cause keratinocyte differentiation appear to be contrary to the procarcinogenic features of the 8S-LOX expression, presenting a question as to the role of 8S-LOX during mouse skin carcinogenesis. In this review, molecular and biological features of 8S-LOX as well as current views on the functional role of 8S-LOX/8S-HETE during mouse skin carcinogenesis are presented.

• The Korean Journal of Physiology
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• v.3 no.2
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• pp.17-23
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• 1969

Oxygen consumption rate $(QO_2)$ and protein content of liver and kidney of the Ehrlich ascites tumor-bearing mouse were measured from 6th till 14th day after the inoculation of $4{\times}10^6$ Ehrlich ascites tumor cells. The results thus obtained were compared with those of the groups in which; 1) Whole body x-irradiation with 400 r was done to mouse prior to the inoculation of $4{\times}10^6$ Ehrlich ascites tumor cells, 2) Same number of the irradiated tumor cells were inoculated after subjecting the tumor cells to x-irradiation with 400 r or 900 r in vitro, and 3) the normal, and the following results were obtained; 1. $QO_2$ of the liver and kidney of the tumor-bearing mouse were all lower than the normal and a gradual decrease of $QO_2$ in both liver and kidney was noted as the ascites tumor was progressively developing. 2. In the groups where whole body x-irradiation with 400 r was done, or x-irradiation of ascites tumor cells in vitro with either 400 r or 900 r, $QO_2$ of the liver and kidney were lower than the normal, and the pattern of the decrease was similar in the case of the tumor-bearing mouse. 3. Protein contents in all the groups showed lower values than the normal, and the decrease was gradual as the ascites tumor was developing. 4. $QO_2$ and protein levels in the liver were generally lower than those in the kidney. 5. A certain cancerous metabolism was, therefore, noted in the remote organs of Ehrlich ascites tumor-bearing animal.

• Clinical and Experimental Reproductive Medicine
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• v.43 no.1
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• pp.1-8
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• 2016

Granulosa cell tumors (GCTs) are rare sex cord-stromal tumors that have been studied for decades. However, their infrequency has delayed efforts to research their etiology. Recently, mutations in human GCTs have been discovered, which has led to further research aimed at determining the molecular mechanisms underlying the disease. Mouse models have been important tools for studying GCTs, and have provided means to develop and improve diagnostics and therapeutics. Thus far, several genetically modified mouse models, along with one spontaneous mouse model, have been reported. This review summarizes the phenotypes of these mouse models and their applicability in elucidating the mechanisms of granulosa cell tumor development.

• Proceedings of the KSAR Conference
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• 2003.06a
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• pp.44-44
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• 2003

In previous reports, pVPSV.IGR2.1 transgenic mouse were described that brain tumor and lymphoma by reason of Vasopressin-SV40 T antigen. In this study, we produced pVPSV.IGR3.6 transgenic mouse that used pVPSV.IGR3.6 vector. Expression of transgene was vary different in transgenic mouse. We obtained 6 transgenic mouse line, moreover they had died at the age of 2~6 weeks without transmitting the transgene to their offspring, and had tumorigenesis on same location with pVPSV.IGR2.1 transgenic mouse. Only a founder mouse was investigated for expression of fusion gene. Here we extended this transgenic approach to the study of tumor progression. From the mouse, we confirmed brain tumor cell, after then cultured for investigate characterization. In this report, we demonstrate that reduction of survival rate in transgenic mouse fused vasopressin gene length, acquisition of brain tumor cell, composition with astrocyte cells and neuronal cells. Finally, cells had no change with increase of passage.

• Journal of Environmental Health Sciences
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• v.19 no.3
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• pp.64-73
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• 1993

The study was conducted to investigate the mechanism of tumor promotion as the time courses and the doses of promoter, and the effect of plant fiavonoids on the TPA-induced ODC responses. The results are summarized as follows: 1. A single, toppical application of 17 nmole of the potent tumor promoter, 12-O-tetradecanoyl phorbol-13-acetate, resulted in an induction of mouse epidermal Ornithine Decarboxylase with a peak at 5 hours after treatment and maximized 5.1 times as large as ODC activities of control. 2. Dose-response curve indicated that the tumor promotion increases proportionally between 1.7 and 170 nmole of TPA. This dose dependency relationship indicated that the ability of TPA to stimulate ODC is linked its ability to promote tumors. 3. Naturally occurring plant fiavonoids with anticarcinogenic and antipromotional activities were tested for their abilities to inhibit ODC response induced by skin tumor promoter TPA. Intra peritoneal administration of fiavonoids compounds (rutin, naphthofiavone, baicalein, quercitrin) and herbal drugs (sophorae rios, crataegi fructus, armeniacae semen) inhibited 17 nmole TPA-induced ODC activities in mouse epidermis in vivo.

• Journal of Korean Physical Therapy Science
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• v.11 no.3
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• pp.5-13
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• 2004

The use of therapeutic ultrasound(US) in humans with malignant neoplasms has been contra-indicated in physical therapy practice. Some studies have shown the results after application of US inhibited of tumor growth but some studies have shown the results facilitated of tumor growth in mouse. The purpose of this study were to determine the effects of US on rectal sarcoma(CT-26) in mouse and to determine the histological change of tumor. Thirty-five female BALB/C mouse, age 6 to 8 weeks received subcutaneous injection of 0.1 105 tumor cells. When tumors grew to 5 mm in diameters, the mouse were randomly assigned to control group(n=7) and high powered continuous US group(n=7) and low powered continuous US group(n=7) and high powered pulsed US group(n=7) and low powered pulsed US group(n=7). The experimental group (four groups) received 10 treatments over a 10-day period of 3 MHz ultrasound. Tumor dimension were measured on days 1(start of treatment), 5(midtreatment), and 10(end of treatment, preexcision and postexcision). Tumors were weighed after excision and the mouse were observated histological change of tumor. All tumors grew larger over time. Mean tumor weights(in grams) and volumes(in cubic millimeters) were 2.063 g and $2729.313\;mm^3$ for the high powered continuous US group 1.881 g and $2428.002\;mm^3$ for the low powered continuous US group 1.730 g and $2381.002\;mm^3$ for the high powered pulsed US 1.673 g and $2289.562\;mm^3$ for the low powered pulsed US group 1.670 g and $2297.333\;mm^3$ for the control group. Ultrasound increased the weight and volume of subcutaneous tumor in mouse. We urge caution in the use of ultrasound in the areas of tumors.

• Proceedings of the Korean Society of Developmental Biology Conference
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• 2003.10a
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• pp.105-105
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• 2003

In previous reports, pVPSV.IGR2.1 transgenic mouse were described that brain tumor and lymphoma by reason of Vasopressin-SV40 T antigen. In this study, we produced pVPSV.IGR3.6 transgenic mouse that used pVPSV.IGR3.6 vector. Expression of transgene was vary different in transgenic mouse. We obtained 6 transgenic mouse line, moreover they had died at the age of 2-6 weeks without transmitting the transgene to their offspring, and had tumorigenesis on same location with pVPSV.IGR2.1 transgenic mouse. Only a founder mouse was investigated for expression of fusion gene. Here we extended this transgenic approach to the study of tumor progression. From the mouse, we confirmed brain tumor cell, after then cultured for investigate characterization. In this report, we demonstrate that reduction of survival rate in transgenic mouse fused vasopressin gene length, acquisition of brain tumor cell, composition with astrocyte cells and neuronal cells. Finally, cells had no change with increase of passage.

• Journal of Korean Neurosurgical Society
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• v.55 no.3
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• pp.131-135
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• 2014

Objective : With the growing interests of bacteria as a targeting vector for cancer treatment, diverse genetically engineered Salmonella has been reported to be capable of targeting primary or metastatic tumor regions after intravenous injection into mouse tumor models. The purpose of this study was to investigate the capability of the genetically engineered Salmonella typhimurium (S. typhimurium) to access the glioma xenograft, which was monitored in mouse brain tumor models using optical bioluminescence imaging technique. Methods : U87 malignant glioma cells (U87-MG) stably transfected with firefly luciferase (Fluc) were implanted into BALB/cAnN nude mice by stereotactic injection into the striatum. After tumor formation, attenuated S. typhimurium expressing bacterial luciferase (Lux) was injected into the tail vein. Bioluminescence signals from transfected cells or bacteria were monitored using a cooled charge-coupled device camera to identify the tumor location or to trace the bacterial migration. Immunofluorescence staining was also performed in frozen sections of mouse glioma xenograft. Results : The injected S. typhimurium exclusively localized in the glioma xenograft region of U87-MG-bearing mouse. Immunofluorescence staining also demonstrated the accumulation of S. typhimurium in the brain tumors. Conclusion : The present study demonstrated that S. typhimurium can target glioma xenograft, and may provide a potentially therapeutic probe for glioma.

• YAKHAK HOEJI
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• v.47 no.3
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• pp.159-166
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• 2003

In order to study the clinical usefulness of crude polysaccharides fractionated from Eleutherococcus senticosus, EN-3, in eliminating tumors, we have investigated the effect of combination therapy on the murine tumor metastasis and growth models. In experimental metastasis of colon26-M3.1 cells, prophylactic intravenous (i.v.) administration of EN-3 (0.5, 5, and 50 $\mu\textrm{g}$/mouse) inhibited tumor metastasis compared with tumor control group in 33.6, 66.8, and 81.8％ respectively. The administration of EN-3 (50 $\mu\textrm{g}$/mouse) also exhibited a 66.1％ therapeutic effect on lung tumor metastasis. Although EN-3 induced no toxic effect on both tumor cell and normal splenocyte in the concentration below 100 $\mu\textrm{g}$/mι in in vitro, it induced significant proliferating activity on normal splenocyte in the concentration-dependent manner. In an analysis of NK-cell activity, i.v. administration of EN-3 (4∼100 $\mu\textrm{g}$/mouse) significantly augmented NK cytotoxicity to YAC-1 tumor cells. The combination treatments of cisplatin (10 $\mu\textrm{g}$) and EN-3 (5 $\mu\textrm{g}$) induced synergistic effect on the inhibition of tumor metastasis in experimental tumor metastasis model produced by colon26-M3.1 cells. In addition, the combination treatments also exhibited prolongation of lifespan in S∼180 tumor bearing mouse for over the 60 days. Even though cisplatin (2.5 $\mu\textrm{g}$/mι) exhibited cytotoxicity to tumor cells and inhibited tumor growth over 95％ in in vitro, combination treatment with EN-3 (20 $\mu\textrm{g}$/mι) was induced splenocyte proliferation and produced cytokines, such as TNF-$\alpha$, IL-1 and IL-12, from the macrophages. These results suggested that EN-3 stimulate immune system non-specifically and apply to the biological response modifiers (BRM) in chemo-immunotherapy for tumor prevention.