• IMMUNE NETWORK
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• 제16권2호
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• pp.134-139
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• 2016

Programmed death-1 (PD-1) is a strong negative regulator of T lymphocytes in tumor-microenvironment. By engaging PD-1 ligand (PD-L1) on tumor cells, PD-1 on T cell surface inhibits anti-tumor reactivity of tumor-infiltrating T cells. Systemic blockade of PD-1 function using blocking antibodies has shown significant therapeutic efficacy in clinical trials. However, approximately 10 to 15% of treated patients exhibited serious autoimmune responses due to the activation of self-reactive lymphocytes. To achieve selective activation of tumor-specific T cells, we generated T cells expressing a dominant-negative deletion mutant of PD-1 (PD-1 decoy) via retroviral transduction. PD-1 decoy increased IFN-γ secretion of antigen-specific T cells in response to tumor cells expressing the cognate antigen. Adoptive transfer of PD-1 decoy-expressing T cells into tumor-bearing mice potentiated T cell-mediated tumor regression. Thus, T cell-specific blockade of PD-1 could be a useful strategy for enhancing both efficacy and safety of anti-tumor T cell therapy.

• 대한두경부종양학회지
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• 제9권1호
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• pp.74-87
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• 1993

Immunohistochemical studies on S-100 protein and lactoferrin were carried out to evaluate the existence and distribution pattern of S-100 protein and lactoferrin positive cells in salivary gland tumors. The specimens used were 25 cases of pleomorphic adenoma, 2 cases of monomorphic adenoma, 2 cases of mucoepidermoid tumor, 2 cases of acinic cell tumor, 3 cases of adenoid cystic carcinoma and 2 cases of adenocarcinoma occured in parotid and submandibular salivary gland. ABC kits(Dako corp. Copenhagen. Denmark) for S-100 protein and lactoferrin were used. The results obtained were summarized as follows: In the normal salivary gland. positive immunoreaction for S-100 protein was observed in myoepithelial cells of acini and intercalated ducts. Positive immunoreaction for lactoferrin was observed in serous acinic cells, epithelial cells of intercalated ducts, and excretory material in the ductal lumina. In the pleomorphic and monomorphic adenomas. most of tumor cells were positive for S-100 protein, while luminal tumor cells in gland-like or duct-like structures were rarely positive for lactoferrin. In mucoepidermoid tumor, most of squamous cells and a few of intermediate cells were positive for S-100 protein, but all of tumor cells were negative for lactoferrin. In acinic cell tumor, most of tumor cells were positive for lactoferrin, but all of tumor cells were negative for S-100 protein. In adenoid cystic carcinoma, basaloid tumor cells in trabecular structure were focally positive for S-100 protein. and in adenocarcinoma, many of tumor cells were posivive for both S-100 protein and lactoferrin. Thus, according to the embryonic stage of the development of the tumor cell origin, it was possible to classify the salivary gland tumor as followings: mucoepidermoid carcinoma which originated from the earliest stage, acinic cell tumor which originated from the end stage. Between these two extremes, there were pleomorphic adenoma, adenoid cystic carcinoma and adenocarcinoma which originated in the middle stage of the development of .the salivary glands. Based on the above results, it can be stated that S-100 protein is demonstrated in tumor cells orginated from myoepithelial cells and lactoferrin in glandular differentiated tumor cells.

• Nuclear Medicine and Molecular Imaging
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• 제42권sup1호
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• pp.137-139
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• 2008

Wilms Tumor is a great therapeutic success story within pediatric oncology. Therefore, accurate initial staging is needed to assess tumor spread and to assign patients appropriately to the different risk branches. However, it is recognized that FDG-PET can provide useful information about tumor and has better accuracy than CT and MRI for staging, but its role in Wilms tumor is unclear. According to clinical research data, FDG PET may be useful for the management of selected patients with Wilms tumors.

• Clinical and Experimental Pediatrics
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• 제48권1호
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• pp.112-115
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• 2005

저자들은 8세 남아에서 교통사고 후 우연히 발견된 혈흉과 복부 종물의 진단 과정에서 확진된 폐 및 골 전이를 동반한 후복강 내 신외 윌름 종양 1례를 경험하였기에 문헌 고찰과 함께 보고 하고자 한다.

• 한방안이비인후피부과학회지
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• 제23권1호
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• pp.158-168
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• 2010

Objective : Jeungson-Ojeok-Hwan Bijukbang(JOH) has been used to treat patients with tumor etc. In the theory of Korean medicine, JOH can treat Juk-Chui. JOH is known to have treat Juk-Chui. Juk-Chui is analogous to tumor. Methods : For these reasons, the present study was designed to investigate the effects of JOH on solid tumor in mice in terms of immune-potentiating and direct cytotoxic action of JOH in vitro and vivo study. The present author investigated thymocyte and splenocyte proliferation to confirm immune-potentiating activity of JOH and also investigated tumor/body weight ratio and survival rates in tumor bearing mice. Results : In this study, administration of JOH decreased tumor/body weight ratio significantly, and prolonged survival duration compared to non-treated control. In addition, treatment with JOH suppressed proliferation rate of Sarcoma 180 (S-180) cells significantly, and elevated proliferation rates of thymocytes isolated from normal mice. These results were co-related with in vivo study. Conclusion : these results suggest that JOH is useful to treat patient with solid tumor, because JOH has direct toxic action for tumor cell and immune-potentiating action for T cells. Further study will need to elucidate exact mechanisms related in anti-cancer action of JOH.

• 대한의생명과학회지
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• 제20권3호
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• pp.147-155
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• 2014

It has well studied that immune cells are strongly related to tumor progression and tumor suppression. To identify the difference of immune cell between tumor bearing mice and normal mice, we examined systemically the immune cell of CT26 tumor bearing mice on 21 days after tumor cell administration. As previously reported, CD4+ and CD8+ T cells population of tumor bearing mice significantly decreased 38% and 30% on day 21 compared to that of normal mice, respectively. All subpopulation of CD4 and CD8+ T cell significantly decreased, except CD49b+ T cell subpopulation. But, myeloid cell population ($CD11b^{high}$ and all Gr-1+ subpopulation) of tumor bearing mice significantly increased on day 21. Especially, all subpopulation of CD11b+Gr-1+ cell of tumor bearing mice significantly increased on day 21. Also, Foxp3+$CD25^{high}$ CD4 T cell (regulatory T cells) population significantly increased on day 21. These results suggest that tumor can induce the decline of T lymphocyte and the expansion of myeloid cells and regulatory T cells, and provide the basic information for the study of tumor immunology.

• BMB Reports
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• 제56권7호
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• pp.365-373
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• 2023

Loss of skeletal muscle mass is a primary feature of sarcopenia and cancer cachexia. In cancer patients, tumor-derived inflammatory factors promote muscle atrophy via tumor-to-muscle effects, which is closely associated with poor prognosis. During the past decade, skeletal muscle has been considered to function as an autocrine, paracrine, and endocrine organ by releasing numerous myokines. The circulating myokines can modulate pathophysiology in the other organs, as well as in the tumor microenvironment, suggesting myokines function as muscle-to-tumor signaling molecules. Here, we highlight the roles of myokines in tumorigenesis, particularly in terms of crosstalk between skeletal muscle and tumor. Better understanding of tumor-to-muscle and muscle-to-tumor effects will shed light on novel strategies for the diagnosis and treatment of cancer.

• Journal of Korean Neurosurgical Society
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• 제60권1호
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• pp.102-107
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• 2017

A true collision tumor is a rare entity composed of two histologically distinct neoplasms coinciding in the same organ. This paper reports a unique case of cerebral collision tumor consisting of two benign components. On the first hand, meningioma which is usually a benign lesion arising from the meningothelial cell in the arachnoidal membrane. On the other, cerebral cavernoma which is a well-circumscribed, benign vascular hamartoma within the brain. To our knowledge, there is no previously documented case of cerebral collision tumor consisting of two benign components. A 56-year-old Caucasian male suffered in 2002 from an atypical meningioma WHO $II^{\circ}$ located in the left lateral ventricle. Three years after the tumor extirpation, the patient suffered from a hematoma in the fourth ventricle due to a recurrently haemorrhaged cavernoma. In 2008, a recurrence of the tumor in the left lateral ventricle was discovered. Additionally, another tumor located in the quadrigeminal lamina was detected. After surgical resection of the tumor in the left lateral ventricle, the pathological examination confirmed the diagnosis of a collision tumor consisting of components of a meningioma WHO $II^{\circ}$ and a cavernoma. Postoperatively, no adjuvant treatment was needed and no tumor recurrence is discovered up to the present. A possible explanation for the collision of those two different tumors may be migration of tumor cells mediated by the cerebrospinal fluid. After 5-years of follow-up, there is no sign of any tumor recurrence; therefore, surgical tumor removal without adjuvant therapy seems to be the treatment of choice.

• 한국산학기술학회:학술대회논문집
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• 한국산학기술학회 2011년도 춘계학술논문집 2부
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• pp.1068-1071
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• 2011

Cyclooxygenases (COX)-2 has been highly expressed in a variety of tumor cells and involved inflammatory process, tumor-associated angiogenesis, and vascular functions but the underlying mechanism is not clearly elucidated. We here investigated the molecular mechanism by which COX-2 regulates tumor-associated angiogenesis. In vivo, we injected B16-F1 cells overexpressed with COX-2 or mock in wild type or eNOS-deficient mice. Tumor cells overexpressed with COX-2 increase tumor-associated angiogenesis and tumor growth compared with control cells and that the effect of COX-2 was lower in eNOS-deficient mice than wild type mice. These results may contribute to further understanding of the regulation of angiogenesis by COX during tumor metastasis and inflammation.

• BMB Reports
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• 제45권12호
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• pp.677-685
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• 2012

In the process of tumorigenesis, normal cells are remodeled to cancer cells and protein expression patterns are changed to those of tumor cells. A newly formed tumor microenvironment elicits the immune system and, as a result, a humoral immune response takes place. Although the tumor antigens are undetectable in sera at the early stage of tumorigenesis, the nature of an antibody amplification response to antigens makes tumor-associated autoantibodies as promising early biomarkers in cancer diagnosis. Moreover, the recent development of proteomic techniques that make neo-epitopes of tumor-associated autoantigens discovered concomitantly has opened a new area of 'immuno-proteomics', which presents tumor-associated autoantibody signatures and confers information to redefine the process of tumorigenesis. In this article, the strategies recently used to identify and validate serum autoantibodies are outlined and tumor-associated antigens suggested until now as diagnostic/prognostic biomarkers in various tumor types are reviewed. Also, the meaning of autoantibody signatures and their clinical utility in personalized medicine are discussed.