• Tuberculosis and Respiratory Diseases
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• v.49 no.3
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• pp.323-331
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• 2000

Purpose: Brain metastases are present in approximately 10-16% of small cell lung cancer patients at diagnosis. Brain metastasis is an important clinical problem associated with increasing the survival rate, with a cumulative incidence of up to 80% in patients surviving 2 years. Prophylactic cranial irradiation(PCI) reduces the incidence of brain matastasis and may prolong survival in patients with limited small-cell lung cancer who achieved complete remission. This study was performed to analyze the incidence of brain metastasis, survival and clinical aspects after PCI in patients with limited small-cell lung cancer who achieved complete remission. Methods : Between 1989 and 1999, forty-two patients with limited small-cell lung cancer who achived achieved complete remission after therapy were enrolled into this study retrospectively. All patients received etoposide and cisplatin(VPP) alternating with cytoxan, adriamycin, and vincristine(CAV) every 3 weeks for at least 6 cycles initially. All patients received thoracic radiotherapy: concurrent(38.1%) and sequential(61.9%). All patients received late PCI. Results : Most patients(88.1%) were men, and the median age was 58 years. The median follow-up duration was 18.1 months. During the follow-up period, 57.1% of the patients developed relapse. The most frequent site of relapse was chest(35.7%), followed by brain(14.3%), liver(11.9%), adrenal gland(44%), and bone(2.2%). With the Kaplan-Meier method, the average disease-free interval was 1,090 days(median 305 days). The average time to development of brain relapse after PCI and other sites relapse(except brain) were 2,548 days and 1,395 days(median 460 days), respectively. The average overall survival was 1,233 days(median 634 days, 21.1 months), and 2-year survival rates was 41.7%. The average overall survival in the relapse group was 642 days(median 489 days) and in the no relapse group was 2,622 days(p<0.001). The average overall survival in the brain relapse group was 928 days(median 822 days) and in the no brain relapse group was 1,308 days(median 634 days)(p=0.772). In most patients(85.7%), relapse(except brain) or systemic disease was the usual cause of death. Brain matastasis was the cause of death in 14.3% of the cases. Conclusions : We may conclude that PCI reduces and delays brain metastasis in patients with limited small cell lung cancer who achieved complete remission. We found decreased survival in relapse group but, no significant survival difference was noted according to brain matastasis. And relapse(except brain) or systemic disease was the usual cause of death. In order to increase survival, new treatment strategies for control methods for relapse and systemic disease are required.

• Tuberculosis and Respiratory Diseases
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• v.46 no.3
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• pp.350-362
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• 1999

Background: Acute Respiratory failure which is developed after extubation in the weaning process from mechanical ventilation is an important cause of weaning failure. Once it was developed, endotracheal reintubation has been done for respiratory support. Noninvasive Positive Pressure Ventilation (NIPPV) has been used in the management of acute or chronic respiratory failure, as an alternative to endotracheal intubation, using via nasal or facial mask. In this study, we evaluated the usefulness of NIPPV as an alternative method of reintubation in patients who developed acute respiratory failure after extubation. Method: We retrospectively analyzed thirty one patients(eighteen males and thirteen females, mean ages $63\pm13.2$ years) who were developed acute respiratory failure within forty eight hours after extubation, or were extubated unintentionally at medical intensive care unit(MICU) of Asan Medical Center. NIPPV was applied to the patients. Ventilatory mode of NIPPV, level of ventilatory support and inspiratory oxygen concentration were adjusted according to the patient condition and results of blood gas analysis by the attending doctors at MICU. NIPPV was completely weaned when the patients maintained stable clinical condition under 8 $cmH_2O$ of pressure support level. Weaning success was defined as maintenance of stable spontaneous breathing more than forty eight hours after discontinuation of NIPPV. Respiratory rate, heart rate, arterial blood gas analysis, level of pressure support, and level of PEEP were monitored just before extubation, at thirty minutes, six hours, twenty four hours after initiation of NIPPV. They were also measured at just before weaning from NIPPV in success group, and just before reintubation in failure group. Results: NIPPV was successfully applied to thirty-one patients of thirty-two trials and one patient could not tolerated NIPPV longer than thirty minutes. Endotracheal reintubation was successfully obviated in fourteen patients (45%) among them. There was no difference in age, sex, APACHE III score on admission at MICU, duration of intubation, interval from extubation to initiation of NIPPV, baseline heart rate, respiratory rate, arterial blood gas, and $PaO_2/FiO_2$ between the success and the failure group. Heart rate and respiration rate were significantly decreased with increase $SaO_2$ after thirty minutes of NIPPV in both groups(p<0.05). However, in the patients of failure group, heart rate and respiratory rate were increased again with decrease in $SaO_2$ leading to endotracheal reintubation. The success rate of NIPPV treatment was significantly higher in the patients with COPD compared to other diseases(62% vs 39%) (p=0.007). The causes of failure were deterioration of arterial blood gas without aggravation of underlying disease(n=9), aggravation of undelying disease(n=5), mask intolerance(n=2), and retained airway secretion(n=l). Conclusion: NIPPV would be a useful therapeutic alternative which can avoid reintubation in patient who developed acute respiratory failure after extubation.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1199-1213
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• 1998

Background : The number of immunocompromised hosts has been increasing steadily and a new pulmonary infiltrate in these patients is a potentially lethal condition which needs rapid diagnosis and treatment. In this study we sought to examine the clinical manifestations, radiologic findings, and therapeutic outcomes of pulmonary mycoses presenting as a new pulmonary infiltrate in immunocompromised hosts. Method : All cases presenting as a new pulmonary infiltrate in immunocompromised hosts and confirmed to be pulmonary mycoses by pathologic examination or by positive culture from a sterile site between October of 1996 and April of 1998 were included in the study and their chart and radiologic findings were retrospectively reviewed. Results : In all, 14 cases of pulmonary mycoses from 13 patients(male : female ratio = 8 : 5, median age 47 yr) were found. Twelve cases were diagnosed as aspergillosis while two were diagnosed as mucormycosis. Major risk factors for fungal infections were chemotherapy for hematologic malignancy(10 cases) and organ transplant recipients(4 cases). Three cases were receiving empirical amphotericin B at the time of appearance of new lung infiltrates. Cases in the hematologic malignancy group had more prominent symptoms : fever(9/10), cough(6/10), sputum(5/10), dyspnea(4/10), chest pain(5/10). Patients in the organ transplant group had minimal symptoms(p<0.05). On simple chest films, all of the cases presented as single or multiple nodules(6/14) or consolidations(8/14). High resolution computed tomograph showed peri-lesional ground glass opacities(14/14), pleural effusions(5/14), and cavitary changes(7/14). Definitive diagnostic methods were as follows : 10 cases underwent minithoracotomy, 2 underwent video-assisted thoracoscopic surgery, 1 underwent percutaneous needle aspiration and 1 case was diagnosed by culture of abscess fluid. All cases received treatment with amphotericin B with 1 case each being treated with liposomal amphotericin B and itraconazole due to renal toxicity. Lung lesion improved in 12 of 14 patient but 4 patients died before completing therapy. Conclusion : When a new lung infiltrate develops presenting either as a nodule or consolidation in a neutropenic patient with hematologic malignancy or in a transplant recipient, you should always consider pulmonary mycoses as one of the differential diagnosis. By performing aggressive work up and early treatment, we may improve prognosis of these patients.

• Tuberculosis and Respiratory Diseases
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• v.50 no.1
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• pp.52-66
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• 2001

Background : NF-${\kappa}B$ is the most important transcriptional factor in IL-8 gene expression. Triptolide is a new compound that recently has been shown to inhibit NF-${\kappa}B$ activation. The purpose of this study is to investigate how triptolide inhibits NF-${\kappa}B$-dependent IL-8 gene transcription in lung epithelial cells and to pilot the potential for the clinical application of triptolide in inflammatory lung diseases. Methods : A549 cells were used and triptolide was provided from Pharmagenesis Company (Palo Alto, CA). In order to examine NF-${\kappa}B$-dependent IL-8 transcriptional activity, we established stable A549 IL-8-NF-${\kappa}B$-luc. cells and performed luciferase assays. IL-8 gene expression was measured by RT-PCR and ELISA. A Western blot was done for the study of $I{\kappa}B{\alpha}$ degradation and an electromobility shift assay was done to analyze NF-${\kappa}B$ DNA binding. p65 specific transactivation was analyzed by a cotransfection study using a Gal4-p65 fusion protein expression system. To investigate the involvement of transcriptional coactivators, we perfomed a transfection study with CBP and SRC-1 expression vectors. Results : We observed that triptolide significantly suppresses NF-${\kappa}B$-dependent IL-8 transcriptional activity induced by IL-$1{\beta}$ and PMA. RT-PCR showed that triptolide represses both IL-$1{\beta}$ and PMA-induced IL-8 mRNA expression and ELISA confirmed this triptolide-mediated IL-8 suppression at the protein level. However, triptolide did not affect $I{\kappa}B{\alpha}$ degradation and NF-$_{\kappa}B$ DNA binding. In a p65-specific transactivation study, triptolide significantly suppressed Gal4-p65T Al and Gal4-p65T A2 activity suggesting that triptolide inhibits NF-${\kappa}B$ activation by inhibiting p65 transactivation. However, this triptolide-mediated inhibition of p65 transactivation was not rescued by the overexpression of CBP or SRC-1, thereby excluding the role of transcriptional coactivators. Conclusions : Triptolide is a new compound that inhibits NF-${\kappa}B$-dependent IL-8 transcriptional activation by inhibiting p65 transactivation, but not by an $I{\kappa}B{\alpha}$-dependent mechanism. This suggests that triptolide may have a therapeutic potential for inflammatory lung diseases.

• Nuclear Medicine and Molecular Imaging
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• v.42 no.4
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• pp.307-313
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• 2008

Purpose: Vascular endothelial growth factor (VEGF) and its receptor, fetal liver kinase 1 (Flk-1), play an important role in vascular permeability and tumor angiogenesis. The aim of this study is to evaluate the therapeutic efficacy of $^{131}I$ labeled anti-Flk-1 monoclonal antibody (DC101) on the growth of melanoma tumor, which is known to be very aggressive in vivo. Materials and Methods: Balb/c nude mice were injected subcutaneously with melanoma cells in the right flank. Tumors were allowed to grow up to $200-250\;mm^3$ in volume. Gamma camera imaging and biodistribution studies were performed to identify an uptake of $^{131}I$-DC101 in various organs. Mice with tumor were randomly divided into five groups (10 mice per group) and injected intravenously; control PBS (group 1), $^{131}I$-DC101 $50\;{\mu}g/mouse$ (group 2), non-labeled DC101 $50\;{\mu}g/mouse$ (group 3), $^{131}I$-DC101 $30\;{\mu}g/mouse$ (group 4) and $15\;{\mu}g/mouse$ (group 5) every 3 or 4 days for 20 days. Tumor volume was measured with caliper twice a week. Results: In gamma camera images, the uptake of $^{131}I$-DC101 into tumor and thyroid was increased with time. Biodistribution results showed that the radioactivity of blood and other major organ was gradually decreased with time whereas tumor uptake was increased up to 48 hr and then decreased. After 4th injection of $^{131}I$-DC101, tumor volume of group 2 and 4 was significantly smaller than that group 1. After 5th injection, the tumor volume of group 5 also significantly reduced. Conclusion: These results indicated that delivery of $^{131}I$ to tumor using FlK-1 antibody, DC101, effectively blocks tumor growth in aggressive melanoma xenograft model.

• The Journal of Korean Society for Radiation Therapy
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• v.31 no.1
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• pp.75-81
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• 2019

Purpose: Helmet type bolus for 3D printer is being manufactured because of the disadvantages of Bolus materials when photon beam is used for the treatment of scalp malignancy. However, PLA, which is a used material, has a higher density than a tissue equivalent material and inconveniences occur when the patient wears PLA. In this study, we try to treat malignant scalp tumors by using M3 wax helmet with 3D printer. Methods and materials: For the modeling of the helmet type M3 wax, the head phantom was photographed by CT, which was acquired with a DICOM file. The part for helmet on the scalp was made with Helmet contour. The M3 Wax helmet was made by dissolving paraffin wax, mixing magnesium oxide and calcium carbonate, solidifying it in a PLA 3D helmet, and then eliminated PLA 3D Helmet of the surface. The treatment plan was based on Intensity-Modulated Radiation Therapy (IMRT) of 10 Portals, and the therapeutic dose was 200 cGy, using Analytical Anisotropic Algorithm (AAA) of Eclipse. Then, the dose was verified by using EBT3 film and Mosfet (Metal Oxide Semiconductor Field Effect Transistor: USA), and the IMRT plan was measured 3 times in 3 parts by reproducing the phantom of the head human model under the same condition with the CT simulation room. Results: The Hounsfield unit (HU) of the bolus measured by CT was $52{\pm}37.1$. The dose of TPS was 186.6 cGy, 193.2 cGy and 190.6 cGy at the M3 Wax bolus measurement points of A, B and C, and the dose measured three times at Mostet was $179.66{\pm}2.62cGy$, $184.33{\pm}1.24cGy$ and $195.33{\pm}1.69cGy$. And the error rates were -3.71 %, -4.59 %, and 2.48 %. The dose measured with EBT3 film was $182.00{\pm}1.63cGy$, $193.66{\pm}2.05cGy$ and $196{\pm}2.16cGy$. The error rates were -2.46 %, 0.23 % and 2.83 %. Conclusions: The thickness of the M3 wax bolus was 2 cm, which could help the treatment plan to be established by easily lowering the dose of the brain part. The maximum error rate of the scalp surface dose was measured within 5 % and generally within 3 %, even in the A, B, C measurements of dosimeters of EBT3 film and Mosfet in the treatment dose verification. The making period of M3 wax bolus is shorter, cheaper than that of 3D printer, can be reused and is very useful for the treatment of scalp malignancies as human tissue equivalent material. Therefore, we think that the use of casting type M3 wax bolus, which will complement the making period and cost of high capacity Bolus and Compensator in 3D printer, will increase later.

• The Korean Journal of Nuclear Medicine Technology
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• v.26 no.2
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• pp.20-31
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• 2022

Purpose Broad Quantification Calibration(B.Q.C) is the procedure for Quantitative Analysis to measure Standard Uptake Value(SUV) in SPECT/CT scanner. B.Q.C was performed with Tc-99m, I-123, I-131, Lu-177 respectively and then we acquired the phantom images whether the SUVs were measured accurately. Because there is no standard for SUV test in SPECT, we used ACR Esser PET phantom alternatively. The purpose of this study was to lay the groundwork for Quantitative Analysis with various isotopes in SPECT/CT scanner. Materials and Methods Siemens SPECT/CT Symbia Intevo 16 and Intevo Bold were used for this study. The procedure of B.Q.C has two steps; first is point source Sensitivity Cal. and second is Volume Sensitivity Cal. to calculate Volume Sensitivity Factor(VSF) using cylinder phantom. To verify SUV, we acquired the images with ACR Esser PET phantom and then we measured SUV_mean on background and SUV_max on hot vials(25, 16, 12, 8 mm). SPSS was used to analyze the difference in the SUV between Intevo 16 and Intevo Bold by Mann-Whitney test. Results The results of Sensitivity(CPS/MBq) and VSF were in Detector 1, 2 of four isotopes (Intevo 16 D1 sensitivity/D2 sensitivity/VSF and Intevo Bold) 87.7/88.6/1.08, 91.9/91.2/1.07 on Tc-99m, 79.9/81.9/0.98, 89.4/89.4/0.98 on I-123, 124.8/128.9/0.69, 130.9, 126.8/0.71, on I-131, 8.7/8.9/1.02, 9.1/8.9/1.00 on Lu-177 respectively. The results of SUV test with ACR Esser PET phantom were (Intevo 16 BKG SUV_mean/25mm SUV_max/16mm/12mm/8mm and Intevo Bold) 1.03/2.95/2.41/1.96/1.84, 1.03/2.91/2.38/1.87/1.82 on Tc-99m, 0.97/2.91/2.33/1.68/1.45, 1.00/2.80/2.23/1.57/1.32 on I-123, 0.96/1.61/1.13/1.02/0.69, 0.94/1.54/1.08/0.98/ 0.66 on I-131, 1.00/6.34/4.67/2.96/2.28, 1.01/6.21/4.49/2.86/2.21 on Lu-177. And there was no statistically significant difference of SUV between Intevo 16 and Intevo Bold(p>0.05). Conclusion Only Qualitative Analysis was possible with gamma camera in the past. On the other hand, it's possible to acquire not only anatomic localization, 3D tomography but also Quantitative Analysis with SUV measurements in SPECT/CT scanner. We could lay the groundwork for Quantitative Analysis with various isotopes; Tc-99m, I-123, I-131, Lu-177 by carrying out B.Q.C and could verify the SUV measurement with ACR phantom. It needs periodic calibration to maintain for precision of Quantitative evaluation. As a result, we can provide Quantitative Analysis on follow up scan with the SPECT/CT exams and evaluate the therapeutic response in theranosis.

• Tuberculosis and Respiratory Diseases
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• v.49 no.6
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• pp.691-702
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• 2000

Background : Acute lung injury (ALI) is a commonly encountered respiratory disease and its prognosis is poor when the treatment is not provided promptly and properly. However no specific pharmacologic treatment is currently available for ALI, although recently several supportive drugs have been under scrutiny. We studied anti-inflammatory effects of pentoxifylline (PF), a methylated xanthine, and ONO-5046, a synthetic neutrophil elastase inhibitor on lipopolysaccharide (LPS)-induced ALI in vitro. Methods : To establish an in vitro model of LPS-induced ALI, primary rat alveolar macrophages and peripheral neutrophils in various ratios (1:0, 5:1, 1:1, 1:5, 0:1) were co-cultured with transformed rat alveolar epithelial cells (L2 cell line) or vascular endothelial cells (IP2-E4 cell line) under LPS stimulation. Each experiment was divided into five groups-control, LPS, LPS+PF, LPS+ONO, and LPS+PF+ONO. We compared LPS-induced superoxide anion productions from primary rat alveolar macrophages and peripheral neutrophils in various ratios, and the resultant cytotoxicity on L2 cells or IP2-E4 cells between groups. In addition we also compared the productions of tumor necrosis factor (TNF)-$\alpha$ interleukin (IL)-$1{\beta}$, monocyte chemotactic protein(MCP)-1, IL-6, and IL-10 as well as mRNA expressions of TNF-$\alpha$ inducible nitric oxide synthetase(iNOS), and MCP-1 from LPS-stimulated primary rat alveolar macrophages between groups. Results : (1) PF and ONO-5046 in each or both showed a trend to suppress LPS-induced superoxide anion productions from primary rat alveolar macrophages and peripheral neutrophils regardless of their ratio, except for the LPS+PF+ONO group with the 1:5 ratio, although statistical significance was limited to a few selected experimental conditions. (2) PF and ONO-5046 in each or both showed a trend to prevent IP2-E4 cells from LPS-induced cytotoxicity by primary rat alveolar macrophages and peripheral neutrophils regardless their ratio, although statistical significance was limited to a few selected experimental conditions. the effects of PF and/or ONO-5046 on LPS-induced L2 cell cytotoxicity varied according to experimental conditions. (3) PF showed a trend to inhibit LPS-induced productions of INF-$\alpha$ MCP-1, and IL-10 from primary rat alveolar macrophages. ONO-5046 alone didnot affect the LPS-induced productions of proinflammatory cytokines from primary rat alveolar macrophages but the combination of PF and ONO-5046 showed a trend to suppress LPS-induced productions of INF-$\alpha$ and IL-10 PF and ONO-5046 in each or both showed a trend to increase LPS-induced IL-$\beta$ and IL-6 productions from primary rat alveolar macrophages. (4) PF and ONO-5046 in each or both showed a trend to attenuate LPS-induced mRNA expressions of TNF-$\alpha$ and MCP-1 from primary rat alveolar macrophages but at the same time showed a trend increase iNOS mRNA expression. Conclusion : These results suggest that PF and ONO-5046 may play a role in attenuating inflammation in LPS-induced ALI and that further study is needed to use these drugs as a new supportive therapeutic strategy for ALI.

• Tuberculosis and Respiratory Diseases
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• v.44 no.4
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• pp.822-835
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• 1997

Background : There have been many in vitro evidences that interleukin-4(IL-4) might be the most important cytokine inducing IgE synthesis from B-cells, and interferon-gamma(IFN-$\gamma$) might be a main cytokine antagonizing IL-4-mediated IgE synthesis. Recently some reports demonstrated that IFN-$\gamma$ might be used as a new therapeutic modality in some allergic diseases with high serum IgE level, such as atopic dermatitis or bronchial asthma. To evaluate the in vivo effect of IFN-$\gamma$ in bronchial asthma we tried a clinical study. Methods : Fifty bronchial asthmatics(serum IgE level over 200 IU/ml) who did not respond to inhaled or systemic corticosteroid treatment, and 17 healthy nonsmoking volunteers were included in this study. The CD 23 expressions of peripheral B-cells, the IL-4 activities of peripheral T-cells, the serum soluble CD23(sCD23) levels, and the superoxide anion(${O_2}^-$) generations by peripheral PMN were compared between bronchial asthmatics and normal subjects. The IL-4 activities of peripheral T-cells were analyzed by T-cell supernatant (T-sup)-induced CD23 expression from tonsil B-cells. In bronchial asthmatics the serum IgE levels and histamine $PC_{20}$ in addition to the above parameters were also compared before and after IFN-$\gamma$ treatment. IFN-$\gamma$ was administered subcutaneously with a weekly dose of 30,000 IU per kilogram of body weight for 4 weeks. Results : The ${O_2}^-$ generations by peripheral PMNs in bronchial asthmatics were higher than normal subjects($8.23{\pm}0.94$ vs $5.00{\pm}0.68\;nmol/1{\times}10^6$ cells, P<0.05), and significantly decreased after IFN-$\gamma$ treatment compared to initial values($3.69{\pm}0.88$ vs $8.61{\pm}1.53\;nmol/1{\times}10^6$ cells, P<0.05). CD23 expression of peripheral B-cells in bronchial asthmatics was higher than normal subjects($47.47{\pm}2.96%$, vs $31.62{\pm}1.92%$, P<0.05), but showed no significant change after IFN-$\gamma$ treatment. The serum sCD23 levels in bronchial asthmatics were slightly higher than normal subjects($191.04{\pm}23.3\;U/ml$ vs $162.85{\pm}4.85\;U/ml$), and 11(64.7%) of 17 patients showed a decreasing pattern in their serum sCD23 levels after IFN-$\gamma$ treatment. However the means of serum sCD23 levels were not different before and after IFN-$\gamma$ treatment. The IL-4 activities of peripheral T-cells in bronchial asthmatics were slightly higher than normal subjects($22.48{\pm}6.81%$ vs $18.90{\pm}2.43%$), and slightly increased after IFN-$\gamma$ treatment($27.90{\pm}2.56%$). Nine(60%) of 15 patients showed a decreasing pattern in their serum IgE levels after IFN-$\gamma$ treatment. And the levels of serum IgE were significantly decreased after IFN-$\gamma$ treatment compared to initial values ($658.67{\pm}120.84\;IU/ml$ vs $1394.32{\pm}314.42\;IU/ml$, P<0.05). Ten(83.3%) of 12 patients showed an improving pattern in bronchial hyperresponsiveness after IFN-$\gamma$ treatment, and the means of histamine $PC_{20}$ were significantly increased after IFN-$\gamma$ treatment compared to initial values ($1.22{\pm}0.29mg/ml$ vs $0.69{\pm}0.17mg/ml$, P<0.05). Conclusion : Our results suggest that IFN-$\gamma$ may be useful as well as safety in the treatment of bronchial asthmatics with high serum IgE level and that in vivo effects of IFN-$\gamma$ may be different from its in vitro effects on the regulations of IgE synthesis or the respiratory burst of PMN.

• 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.