• Restorative Dentistry and Endodontics
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• v.24 no.1
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• pp.187-199
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• 1999

Bone remodeling is characterized by the continuing processes of osteoblast-mediated bone formation and osteoclast-mediated bone resorption. Bone metabolism is tightly regulated at the local level by networks of hormones, cytokines, and other factors. In pathological conditions of bone remodeling, including osteoporosis and periodontal diseases, inflammatory cytokines and local mediators are responsible for enhancement of osteoclast resorption and inhibition of repair at the sites of bone resorption. TNF-${\alpha}$ is a pleiotropic hormone with actions on the differentiation, growth, and functional activities of normal and malignant cells from numerous tissues. TNF-${\alpha}$ has been proposed as a local mediator of the control of bone turnover in situations of chronic inflammation, and it has been assumed that the local source of TNF-${\alpha}$ is the monocyte in the adjacent bone marrow or the local circulation. TNF-${\alpha}$ is a potent inducer of bone resorption. TNF-${\alpha}$ is known to induce the activation of apoptotic signaling pathway, which leads to the apoptosis of bone cells. We demonstrated that treatment of murine osteoblastic MC3T3E1 cells with TNF-${\alpha}$ decreases proliferation as well as alkaline phosphatase (ALP) activity in a dose depenent manner. In addition, TNF-${\alpha}$ increases osteoclast-like cell formation in $1{\alpha}$, 25(OH)2D3 or PGE2-treated bone marrow cell culture. When cells were cultured in TNF-${\alpha}$ free ${\alpha}$-MEM, this inhibitory effect of ALP activity was reversible up to 10 ng/ml TNF-${\alpha}$, in contrast, at the 20 ng/ml TNF-${\alpha}$, irreversible. In this concentration, TNF-${\alpha}$ may induce apoptosis in MC3T3E1 cells. In this study, TNF-${\alpha}$ induces apoptosis resulting in chromosomal DNA fragmentation, preceded by JNK/SAPKs and caspase-3 activation. Our present results show that JNK/SAPKs and caspase-3 are activated by TNF-${\alpha}$, suggesting that the JNK/SAPKs and caspase-3 participate in the bone resorption, associated with apoptosis.

• BMB Reports
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• v.50 no.12
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• pp.621-627
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• 2017

We previously reported the involvement of zinc-finger protein 143 (ZNF143) on cancer cell motility in colon cancer cells. Here, ZNF143 was further characterized in breast cancer. Immunohistochemistry was used to determine the expression of ZNF143 in normal tissues and in tissues from metastatic breast cancer at various stages. Notably, ZNF143 was selectively expressed in duct and gland epithelium of normal breast tissues, which decreased when the tissue became malignant. To determine the molecular mechanism how ZNF143 affects breast cancer progression, it was knocked down by infecting benign breast cancer cells with short-hairpin (sh) RNA-lentiviral particles against ZNF143 (MCF7 sh-ZNF143). MCF7 sh-ZNF143 cells showed different cell-cell contacts and actin filament (F-actin) structures when compared with MCF7 sh-Control cells. In migration and invasion assays, ZNF143 knockdown induced increased cellular motility in breast carcinoma cells. This was reduced by the recovery of ZNF143 expression. Taken together, these results suggest that ZNF143 expression contributes to breast cancer progression.

• Environmental Mutagens and Carcinogens
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• v.22 no.4
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• pp.312-318
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• 2002

Dioxin represents a group of halogenated aromatic hydrocarbons of which 2,3,7,8-tetrachlorod-ibenzo-p-dioxin (TCDD) is well known for its extremely toxic properties as well as ubiquitous presence in our environment and ecosystems. In order to better assess the carcinogenic mechanism of dioxin, we should utilize the reliable biomarkers that can precisely and correctly reflect multi-stage carcinogenesis. When MCF10A cells were exposed to TCDD (10 nM), expression of both CYP1A1 and CYP1B1 was induced in a time-related manner. The expression as well as activity of ornithine decarboxylase was transiently induced by TCDD treatment. In contrast, the induction of COX-2 that is implicated in carcinogenesis as well as inflammation, was not induced by TCDD. In another study, gap-junctional intercellular communication (GJIC) was attenuated by TCDD treatment as revealed by the dye-transfer assay. Based on these findings, TCDD has both tumor initiating and promoting potential in human breast epithelial cells in culture. Also, treatment of MCF10A cells with the carcinogen 7,12-dimethylbenz[a]anthracene plus TCDD resulted in malignant cell transformation as revealed by increased anchorage-independent growth of exposed cells. Additional studies may be necessary to assess the effects of TCDD on multi-stage carcinogenesis in vivo.

• Biomedical Science Letters
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• v.26 no.4
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• pp.249-255
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• 2020

Radiation therapy is one of the primary options for the treatment of malignant tumors. Even though it is an effective anti-cancer treatment, it can cause serious complications owing to radiation-induced damage to the normal tissue around the tumor. It was recently reported that normal stem cell response to the genotoxic stress of ionizing radiation can boost the therapeutic effectiveness of radiation by repairing damaged cells. Therefore, we focused on annexin A-1 (ANXA1), one of the genes induced by low-dose irradiation, and assessed whether it can protect adipose-derived stem cells (ADSCs) against oxidative stress-induced damage caused by low-dose irradiation and improve effectively cell survival. After confirming ANXA1 expression in ADSCs transfected with an ANXA1 expression vector, exposure to hydrogen peroxide (H2O2) was used to mimic cellular damage induced by a chronic oxidative environment to assess cell survival under oxidative conditions. ANXA1-transfected ADSCs demonstrated that increased viability compared with un-transfected cells and exhibited enhanced anti-oxidative properties. Taken together, these results suggest that ANXA1 could be used as a potential therapeutic target to improve the survival of stem cells after low-dose radiation treatment.

• BMB Reports
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• v.57 no.6
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• pp.305-310
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• 2024

T-plastin (PLST), a member of the actin-bundling protein family, plays crucial roles in cytoskeletal structure, regulation, and motility. Studies have shown that the plastin family is associated with the malignant characteristics of cancer, such as circulating tumor cells and metastasis, by inducing epithelial-mesenchymal transition (EMT) in various cancer cells. However, the role of PLST in the EMT of human lung cancer cells remains unclear. In this study, we observed that PLST overexpression enhanced cell migratory and invasive abilities, whereas its downregulation resulted in their suppression. Moreover, PLST expression levels were associated with the expression patterns of EMT markers, including E-cadherin, vimentin, and Slug. Furthermore, the phosphorylation levels of focal adhesion kinase (FAK) and AKT serine/threonine kinase (AKT) were dependent on PLST expression levels. These findings indicate that PLST induces the migration and invasion of human lung cancer cells by promoting Slug-mediated EMT via the FAK/AKT signaling pathway.

• Korean Journal of Head & Neck Oncology
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• v.20 no.2
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• pp.128-134
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• 2004

Background and Objectives: Angiogenesis is the process of new blood vessel development from preexisting vessel. Angiogenenesis has been considered to be essential for the growth and expansion of a solid tumor. Vascular endothelial growth factor (VEGF), known as one of the most important vascular permeability factors, induces proliferation of endothelial cells, stiumulates angiogenesis, and increases vascular permeability. Several recents reports have documented that VEGF overexpression is associated with poor clinical outcomes in many maligmancies. The aims of this study were to determine whether microvessel density and VEGF expression are related to clinicopathologic factors such as age, sex, tumor size, tumor stage, and prognostic factors and to evaluate the relationship between VEGF expression and angiogenesis in benign and malignant thyroid tumors. Materials and Methods: The subjects were 65 patients (27 with papillary carcinoma, 27 with adenomatous hyperplasia, 11 with follicular adenoma) who underwent thyroidectomy from 1995 to 2001. Imuunohistochemistry was used to detect VEGF expression and microvessel density (MVD) in paraffin-embedded thryoid tumor specimens. Results: The intensity of the VEGF expression did not show stastically difference between benign and malignant thyroid tumors. There was no apparent correlation between VEGF expression and age, tumor size, T stage or scores of the AGES, AMES and MACIS systems. The neo-microvessel density was higher in the maligant tumor than the benign tumors. Also, higher neo-microvessel density was associated with metastases of the lymph nodes and scores of the AMES and AGES systems. Conclusion: Our results suggest that neo-microvessel vessel density may be a significant prognostic factor in the thyroid papillary carcinoma. But the VEGF expression does not appear to be an significant independent prognostic factor for thyroid papillary carcinoma.

• Korean Journal of Head & Neck Oncology
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• v.22 no.2
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• pp.151-154
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• 2006

Epithelial-myoepithelial carcinoma is rare, low grade malignant tumor of the salivary glands that exhibits a dual composition of epithelial and myoepithelial cells. Most of these tumors arise in the parotid gland, and only few occur in the submandibular gland or minor salivary glands. We describe here a rare case of epithelialmyoepithelial carcinoma arising from a minor salivary gland in the nasopharynx, one of the most unusual locations. The clinical and biological behavior of this tumor is not yet known.

• Journal of Chest Surgery
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• v.30 no.6
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• pp.631-635
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• 1997

혈관에서 기원되는 종양은 혈관외피 세포로부터 발생되는 종양 혈관외피종과 glomus tumor)관 혈관내피 세포로부터 발생되는 종양(를상피 혈관내피종)의 두가지로 구분된다. 이들은 매우 드물게 발생되며 악성종양의 특성을 가지고 있는데, 폐에서 발생된 경우에는 무증상의 작은 종괴로부터 증상이 있는 커다란 종양 의 형태로 나타난다. 최근 저자들은 단일성의 유상피 혈관내피종과 혈관외피종 각각 1례를 치험하였기에 문헌고찰과 함께 보 고하는 바이다. a Tumors of vascular origin are subdivided into two groups: those composed of pericytes (hemangiopericytoma and glomus tumor), and those composed of endothelial cells(hemangioendothelioma). They are uncommon, potentially malignant tumors, and in the lung, the tumors may present as a small asymptomatic nodule or a large symptomatic lesion. Recently we experienced two cases of solitary pulmonary vascular tumors(epithelioid hemangioendothelioma and hemangiopericytoma), and reviewed them with references.

• Journal of Veterinary Clinics
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• v.36 no.2
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• pp.119-122
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• 2019

The prevailing discipline notes that primary pulmonary angiosarcoma is an extremely rare malignant tumor with almost grave prognosis when presented in a dog. No cases have been reported earlier as occurring in dogs. This is the first time we are reporting a case of primary lung angiosarcoma in a 12-year-old Yorkshire terrier breed dog, that will explore the clinical as well as histopathological features of the tumor as noted in a dog. In this case, radiography revealed a well-defined large soft tissue mass in the caudo-dorsal lung field across the left hemi-thorax. After necropsy, it is noted that the lung was found to have the blood-filled nodular lesions on its surface, as determined with no such lesions on other organs. Upon the histological examination, it showed the presence of an extensive necrotic hemorrhage with anastomosing vascular space. Later, the immunohistochemistry showed strongly positive CD31 cells confirming the endothelial origin of the tumor. This is the first report of canine primary lung angiosarcoma in the Republic of Korea.

• Nuclear Medicine and Molecular Imaging
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• v.42 no.sup1
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• pp.66-70
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• 2008

Reports about FDG PET in biliary tumor are limited and there are almost no reports regarding its efficacy. Biliary tumor is divided to intrahepatic and extrahepatic bile duct cancer, and intrahepatic bile duct cancer can be further divided to peripheral type which occurs at lobular duct and hilar type which occurs at hepatic hilum. Surgical resection is the only curative method for bile duct tumor, and accurate staging plays an important role in deciding treatment modality. Among intrahepatic bile duct tumors, peripheral type and hilar type have the same histological characteristics, but different clinical manifestations and tumor growth pattern. On PET image, FDG uptake is also different between peripheral type and hilar type. Most of the former shows high FDG uptake at primary and metastasis site so it is very useful for determining stage and changing treatment plans. However, the later is diversified among low uptake and very high uptake. The FDG uptake pattern of hilar type is similar to that of extrahepatic bile duct cancer, and mucinous component is an important factor, which affects FOG uptake. When tumor cells are scattered in desmoplatsic stroma, then FDG uptake is low as well. In contrast, when FDG uptake is high, it is likely to be tubular type which has high tumor density. Tumor growth pattern also affects FDG uptake. Nodular type mostly takes higher FDG compared to infiltrative type. There are many cases where benign inflammatory diseases take high FDG that PET alone can not distinguish malignant lesion from benign lesion. In conclusion, studies about PET using FDG are still limited. Thus, it is hard to make accurate conclusion about the roles of PET or PET/CT in biliary cancers, but peripheral type intrahepatic bile duct cancers and mass forming hilar and extrahepatic bile duct cancers appear to be good indications performing FDG PET or PET/CT.