• The Journal of the Korean bone and joint tumor society
• /
• v.13 no.2
• /
• pp.173-179
• /
• 2007

Brown tumor is tumor like lesion resulted from hyperparathyroidism, and it has been rarely reported recently. We evaluated a 29-year-old woman who had brown tumor on proximal humerus caused by primary hyperparathyroidism. She first had presented pain and swelling over the upper arm, and was suspected as giant cell tumor in biopsy combined with hyperparathyroidism. Wide marginal excision and tumor prosthesis were performed. However, it was confirmed as brown tumor resulted from parathyroid adenoma according to laboratory findings and radioactive isotopes image, and surgical excision of adenoma relieved clinical symptoms. We report this case with a review of literatures.

• Journal of Ginseng Research
• /
• v.10 no.1
• /
• pp.45-54
• /
• 1986

These studies were carried out to obtain the basic information about transformation of ginseng plant by potential vector system, utilization of opine compound by Agrobacterium sap. , and initiation of crown gall tumor callus. Crown gall tumors were induced from stem of Panax ginseng C.A. Meyer by infection of Agrobacterium tumefaciens. Therefore, it was clarified that transformation of ginseng by Ti plasmid was possible. The crown gall tumors induced by Agrobacterium tumefaciens isolated. from the soil were different in a shape, size, and growth rate. Especially, infection of ginseng by Agrobacterium tumefaciens Y104 led to the amorphic tumor, Tumor tissue derived from stem crown gall could not be continuously cultured on the medium which did not contain phytohormone, and did not form the callus even on the medium supplemented with 2,4-D. On the other hand, the root crown gall tumors formed the calli but the formation rate of callus was quite low. As for the utilization of octopine and nopaline, it was found that 3 strains of Agrobacterium app., Y104, Y110 and C58, utilized nopaline only, Y109 utilized octopine, and Y101 failed to utilize either compound.

• Journal of Gastric Cancer
• /
• v.12 no.3
• /
• pp.164-172
• /
• 2012

Purpose: The purpose of this study is to investigate the prognostic significance of tumor size for 5-year survival rate in patients with gastric cancer. Materials and Methods: A total of 1,697 patients with gastric cancer, who underwent potentially curative gastrectomy, were evaluated. Patients were divided into 4 groups as follows, according to the median size of early and advanced gastric cancer, respectively: small early gastric cancer (tumor size ${\leq}3$ cm), large early gastric cancer (tumor size >3 cm), small advanced gastric cancer (tumor size ${\leq}$ 6 cm), and large advanced gastric cancer (tumor size >6 cm). The prognostic value of tumor size for 5-year survival rate was investigated. Results: In a univariate analysis, tumor size is a significant prognostic factor in advanced gastric cancer, but not in early gastric cancer. Multivariate analysis showed that tumor size is an independent prognostic factor for 5-year survival rate in advanced gastric cancer (P=0.003, hazard ratio=1.372, 95% confidence interval=1.115~1.690). When advanced gastric cancer is subdivided into 2 groups, according to serosa invasion: Group 1; serosa negative (T2 and T3, 7th AJCC), and Group 2; serosa positive (T4a and T4b, 7th AJCC), tumor size is an independent prognostic factor in Group 1 (P=0.011, hazard ratio=1.810, 95% confidence interval=1.149~2.852) and in Group 2 (P=0.033, hazard ratio=1.288, 95% confidence interval=1.020~1.627), respectively. Conclusions: Tumor size is an independent prognostic factor in advanced gastric cancer irrespective of the serosa invasion, but not in early gastric cancer.

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

• Asian Pacific Journal of Cancer Prevention
• /
• v.16 no.15
• /
• pp.6215-6223
• /
• 2015

Tyrosine phosphorylation plays an important role in regulating human physiological and pathological processes. Functional stabilization of tyrosine phosphorylation largely contributes to the balanced, coordinated regulation of protein tyrosine kinases (PTKs) and protein tyrosine phosphatases (PTPs). Research has revealed PTPs play an important suppressive role in carcinogenesis and progression by reversing oncoprotein functions. Receptor-type protein tyrosine phosphatase O (PTPRO) as one member of the PTPs family has also been identified to have some roles in tumor development. Some reports have shown PTPRO over-expression in tumors can not only inhibit the frequency of tumor cell division and induce tumor cell death, but also suppress migration. However, the tumor-suppression mechanisms are very complex and understanding is incomplete, which in some degree blocks the further development of PTPRO. Hence, in order to resolve this problem, we here have summarized research findings to draw meaningful conclusions. We found tumor-suppression mechanisms of PTPRO to be diverse, such as controlling G0/G1 of the tumor cell proliferation cycle, inhibiting substrate phosphorylation, down-regulating transcription activators and other activities. In clinical anticancer efforts, expression level of PTPRO in tumors can not only serve as a biomarker to monitor the prognosis of patients, but act as an epigenetic biomarker for noninvasive diagnosis. In addition, the re-activation of PTPRO in tumor tissues, not only can induce tumor volume reduction, but also enhance the susceptibility to chemotherapy drugs. So, we can propose that these research findings of PTPRO will not only support new study ideas and directions for other tumor-suppressors, importantly, but also supply a theoretical basis for researching new molecular targeting agents in the future.

• Biomedical Science Letters
• /
• v.21 no.4
• /
• pp.172-180
• /
• 2015

It is well reported that tumor cells can regulate host immune systems. To identify the detailed changes of immune cells between tumor bearing mice and normal mice, we evaluated the systemic immune cell phenotype of B16F10 tumor bearing mice in a time dependent manner. The lymphocytic population (CD4+ and CD8+ T cells) of tumor bearing mice significantly decreased compared to that of normal mice. We found that the Foxp3+CD25+ CD4 T cell decreased, but the Foxp3+$CD25^{high}$ CD4 T cell significantly increased. All subpopulations of CD8 T cells decreased, except the CD62L-CD44+ CD8 T cell subpopulation. The myeloid cell population (CD11b+ and Gr-1+ cells) of tumor bearing mice significantly increased. Specifically, Foxp3+$CD25^{high}$ CD4 T cell and CD11b+Gr-1+ cells significantly increased in early phase of tumor progression. These results are helpful to understand the change of the systemic immune cell subpopulation of tumor bearing mice in a time-dependent manner.

• The Journal of the Korean bone and joint tumor society
• /
• v.4 no.2
• /
• pp.103-106
• /
• 1998

Giant cell tumor was described by Sir Astley Cooper in 1818. This tumor is considered to be a benign tumor but has problems of recurrence and metastatic change after treatment. Methods of operative treatment of this tumor have included currettage, currettage and bone graft, excision, resection, excision and graft and amputation. We experienced a case of giant cell tumor which involved the distal part of right radius and treated by wide excision and fibular graft. The postoperative courses have been satisfactory because of no recurrence or malignant change. After 6 years and 1 month follow up, the patient was able to return to daily life without any problem.

• Proceedings of the KSME Conference
• /
• 2007.05b
• /
• pp.2951-2954
• /
• 2007

Tumor hemodynamics in vascular state is numerically simulated using pressure node solution. The tumor angiogenesis pattern in our previous study is used for the geometry of vessel networks. For tumor angiogenesis, the equation that governed angiogenesis comprises a tumor angiogenesis factor (TAF) conservation equation in time and space, which is solved numerically using the Galerkin finite element method. A stochastic process model is used to simulate vessel formation and vessel. In this study, we use a two-dimensional model with planar vessel structure. Hemodynamics in vessel is assumed as incompressible steady flow with Newtonian fluid properties. In parent vessel, arterial pressure is assigned as a boundary condition whereas a constant terminal pressure is specified in tumor inside. Kirchhoff's law is applied to each pressure node to simulate the pressure distribution in vessel networks. Transient pressure distribution along with angiogenesis pattern is presented to investigate the effect of tumor growth in tumor hemodynamics.

• Journal of Veterinary Clinics
• /
• v.19 no.4
• /
• pp.464-466
• /
• 2002

A case of spindle cell tumor was presented in a 16-month-old, female syrian hamster. In the left chest area, a 3cm firm elevated recurrent mass was found, surgically removed, and submitted to the Department of Veterinary Pathology, Seoul National University for diagnosis. The mass was soft to firm and tan on sectioning, and contained hemorrhagic area. Histologically, the tumor was composed of sheets of interlacing bundles of spindle-shaped cells with moderate amount of cytoplasm and oval to fusiform nuclei. They were plemorphic and contained 1 to 3 prominent nucleoli. Based on the gross and histological findings, the tumor was diagnosed as a subcutaneous spindle cell tumor. However, the exact origin of neoplastic cells remained undetermined.

• IMMUNE NETWORK
• /
• v.3 no.3
• /
• pp.188-200
• /
• 2003

Background: Immunization of dendritic cells (DCs) pulsed with tumor antigen can activate tumor-specific cytotoxic T lymphocytes (CTL) that are responsible for protection and regression. In this study, we examined whether the uptake of necrotic tumor cells could modulate DC phenotypes and whether the immunization of necrotic tumor cell-loaded DCs could elicit efficient tumor specific immune responses followed by a regression of established tumor burdens. Methods: We prepared necrotic tumor cell-pulsed DCs for the therapeutic vaccination and investigated their phenotypic characteristics, the immune responses induced by these DCs, and therapeutic vaccine efficacy against colon carcinoma in vivo. Several parameters including phagocytosis of tumor cells, surface antigen expression, chemokine receptor expression, IL-12 production, and NK as well as CTL activation were assessed to characterize the immune response. Results: DCs derived from mouse bone marrow efficiently phagocytosed necrotic tumor cells and after the uptake, they produced remarkably increased levels of IL-12. A decreased CCR1 and increased CCR7 expression on DCs was also observed after the tumor uptake, suggesting that antigen uptake could induce DC maturation. Furthermore, co-culturing of DCs with NK cells in vitro enhanced IL-12 production in DCs and IFN-${\gamma}$ production in NK cells, which was significantly dependent on IL-12 production and cell-to-cell contact. Immunization of necrotic tumor cell-loaded DCs induced cytotoxic T lymphocytes as well as NK activation, and protected mice against subsequent tumor challenge. In addition, intratumoral or contra-lateral immunization of these DCs not only inhibited the growth of established tumors, but also eradicated tumors in more than 60% of tumor-bearing mice. Conclusion: Our data indicate that production of IL-12, chemokine receptor expression and NK as well as CTL activation may serve as major parameters in assessing the effect of tumor cell-pulsed DC vaccine. Therefore, DCs loaded with necrotic tumor cells offer a rational strategy to treat tumors and eventually lead to prolonged survival.