• 제목/요약/키워드: tumor cells

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CD8-dependent Tumor Growth Inhibition by Tumor Cells Genetically Modified with 4-1BBL

  • Kim, Hong Sung
    • 대한의생명과학회지
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    • 제27권4호
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    • pp.329-333
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    • 2021
  • We previously identified that tumor cells genetically modified with a 4-1BBL co-stimulatory molecule had anticancer effects in a CT26 mouse colorectal tumor model. To identify the distinction between immune cells in a mouse tumor model treated with tumor cells genetically modified with 4-1BBL or β-gal, we examined the immune cells in CT26-WT, CT26-βgal, and CT26-4-1BBL tumor bearing mice 21 days after tumor cell administration. The CD8+ T cells population in mice treated with tumor cells genetically modified with 4-1BBL was significantly increased on day 21 compared to that of tumor cells genetically modified with β-gal in the spleen and tumor tissue. The CD4+ T cell population was not different between the two mice groups. The Foxp3+CD25high CD4 T cell population decreased on day 21 in tumor tissues, but the decrease was not significant. We also found that CD8 T cells had pivotal roles in inhibiting tumor growth by treating mice with ant-CD4 and CD8 antibodies. These results suggest that tumor cells genetically modified with 4-1BBL could inhibit tumor growth by affecting on CD8 T lymphocytes.

타액선 종양에 있어서 S-100 단백과 Lactoferrin에 관한 면역조직화학적 연구 (Immunohistochemical Studies on S-100 Protein and Lactoferrin in Salivary Gland Tumors)

  • 최대식;김상효
    • 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.

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Perspectives on immune checkpoint ligands: expression, regulation, and clinical implications

  • Moon, Jihyun;Oh, Yoo Min;Ha, Sang-Jun
    • BMB Reports
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    • 제54권8호
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    • pp.403-412
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    • 2021
  • In the tumor microenvironment, immune checkpoint ligands (ICLs) must be expressed in order to trigger the inhibitory signal via immune checkpoint receptors (ICRs). Although ICL expression frequently occurs in a manner intrinsic to tumor cells, extrinsic factors derived from the tumor microenvironment can fine-tune ICL expression by tumor cells or prompt non-tumor cells, including immune cells. Considering the extensive interaction between T cells and other immune cells within the tumor microenvironment, ICL expression on immune cells can be as significant as that of ICLs on tumor cells in promoting antitumor immune responses. Here, we introduce various regulators known to induce or suppress ICL expression in either tumor cells or immune cells, and concise mechanisms relevant to their induction. Finally, we focus on the clinical significance of understanding the mechanisms of ICLs for an optimized immunotherapy for individual cancer patients.

Licochalcone A, a Major Phenolic Constituent of Glycyrrhiza inflata, Suppresses Angiogenin Expression in Colon Cancer Cells

  • Kim, Jin-Kyung
    • 대한의생명과학회지
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    • 제17권1호
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    • pp.85-88
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    • 2011
  • Tumor angiogenesis, which is essential for tumor growth and tumor metastasis, depends on angiogenic factors produced by tumor cells and/or infiltrating cells such as endothelial cells and immune cells in tumor tissue. Previously, we reported that licochalcone A (LicA), an important bioactive compound of Glycyrrhiza inflate, suppresses angiogenesis, tumor growth and metastasis. In this study, we evaluated the effect of LicA on angiogenin production in colon cancer cells because angiogenin is an essential factor to regulate angiogenesis and tumor progression. When we examined the angiogenin levels in three human colon cancer cells, HT-29, SW480 and Caco-2, LicA treatment significantly reduced the amounts of angiogenin among three cancer cell lines. In an in vivo study in which mice were implanted with HT-29 cells, oral administration of LicA reduced angiogenin in tumor tissues when compared with vehicle-administered mice. These results suggest that reduced angiogenin in response to LicA treatment may play essential role to inhibit tumor growth, angiogenesis as well as metastasis.

과립세포종양의 압착도말 세포학적 소견 -1예 보고- (Imprint Cytology of Granular Cell Tumor -A Case Report-)

  • 성우정;최준혁
    • 대한세포병리학회지
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    • 제18권2호
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    • pp.170-174
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    • 2007
  • Granular cell tumor is a rare tumor of the soft tissue and this is characterized by proliferation of large cells with granular appearing eosinophilic cytoplasm. We report the imprint cytologic features of a case of granular cell tumor in the left calf of a 52-year-old woman. Microscopic examination showed moderate cellularity. The tumor cells were arranged both as single cells and in clusters. The cells were large polygonal-shaped and they had small round nuclei with finely granular chromatin and occasionally conspicuous nucleoli. The cytoplasm was abundant eosinophilic and granular. Naked nuclei and spindle-shaped tumor cells were occasionally noted. No mitosis and necrosis were present. The background showed cytoplasmic granular materials. The tumor cells showed positivity for S-100 protein. Ultrastructurally, abundant lysosomes were present in the cytoplasm of the tumor cells.

Comparison Analysis of Immune Cells between CT26 Tumor Bearing Mice and Normal Mice

  • Lee, Na Kyung;Kim, Hong Sung
    • 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.

Anti-tumor Immunity Induced by Tumor Cells Expressing a Membrane-bound Form of IL-2 and SDF-1

  • Choi, Jin-Wha;Lim, Ho-Yong;Chang, Mi-Ra;Cheon, Ji-Yeon;Kim, Young-Sang
    • Animal cells and systems
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    • 제12권4호
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    • pp.193-201
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    • 2008
  • The eventual goal of tumor immunotherapy is to develop a vaccine inducing a specific anti-tumor immunity. Cytokine gene therapy is an effective way at least in animal models, but limited efficacy and various side effects obstruct clinical applications. In this study, we developed a tumor vaccine expressing a membrane-bound form of IL-2(mbIL-2) and SDF-1 in B16F10 melanoma cells. The tumor clones expressing mbIL-2 showed reduced tumorigenicity, and additional expression of SDF-1 to mbIL-2 expressing tumor cells caused more severe reduction in tumorigenicity. However, expression of the SDF-1 alone did not affect on the tumorigenicity, probably because of limited production of SDF-1 in the SDF-1 transfected clones. When the mice once rejected mbIL-2/SDF-1 expressing tumor clone were re-challenged with wild type B16F10 tumor cells, all of the mice survived. This result suggests that mbIL-2/SDF-1 tumor clone is effective in inducing systemic anti-tumor immunity against wild type B16 melanoma. Furthermore, culture supernatant of tumor clones expressing SDF-1 induced lymphocyte migration in vitro. These results, all together, suggest that expression of mbIL-2 and SDF-1 in tumor cells enhances anti-tumor immune responses through different roles; the secreted SDF-1 may function as a chemoattractant to recruit immune cells to tumor vaccine injection site, and the mbIL-2 on tumor cells may provide costimulatory signal for CTL activation in physical contacts.

사기질모세포종에서 Cytokeratin 아형과 Vimentin의 발현 (EXPRESSION OF CYTOKERATIN SUBTYPES AND VIMENTIN IN AMELOBLASTOMA)

  • 강미선;윤혜경;김우형;최수임
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • 제31권4호
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    • pp.316-321
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    • 2005
  • Ameloblastoma is the most common odontogenic tumor of the jawbones, but the origin of this tumor has been remained to be unproven. Cytokeratins (CKs) are specific intermediate filament of epithelial cells, and vimentin is expressed in mesenchymal cells. The immunohistochemical detection of different CKs and vimentin has made it easier to know the origin of tumor. Paraffin-embedded tissue sections from 15 ameloblastomas and 1 ameloblastic carcinoma were used for immunohistochemical evaluation of CK 7, 8, 13, 14, 19 and vimentin. Their expression is evaluated in different tumor cells, which are observed in different type of tumors. In the follicular and reticular subtype, central stellate cells of tumor nests expressed CK 8, 14, 19 and peripheral columnar cells expressed CK 14. CK 7, and 13 were not expressed. Vimentin was detected in fibrous stroma around tumor nest, not in tumor cells. The tumor cells of ameloblastic carcinoma expressed CK 7, 14 and 19, but CK 8 was more weakly stained than that in ameloblastoma. Central stellate cells and peripheral columnar cells of acanthomatous subtype showed same expression pattern with others. Meta plastic squamous cells expressed CK 8, 14, 19 and keratinizing squamous cells expressed CK 13, 19. CK 7 and vimentin were not detected in tumor cells and vimentin was expressed in fibrous stroma. Most of the tumor cells of ameloblastoma showed CK 14 and CK 19 and did not express CK 7 and vimentin. These findings were similar to the immunophenotype of dental lamina. And these results will be beneficial to differential diagnosis of odontogenic tumors and other kind of tumors arising at the oral cavity.

Regulation of Tumor Immune Surveillance and Tumor Immune Subversion by TGF-$\beta$

  • Park, Hae-Young;Wakefield, Lalage M;Mamura, Mizuko
    • IMMUNE NETWORK
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    • 제9권4호
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    • pp.122-126
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    • 2009
  • Transforming growth factor-$\beta$ (TGF-$\beta$) is a highly pleiotropic cytokine playing pivotal roles in immune regulation. TGF-$\beta$ facilitates tumor cell survival and metastasis by targeting multiple cellular components. Focusing on its immunosuppressive functions, TGF-$\beta$ antagonists have been employed for cancer treatment to enhance tumor immunity. TGF-$\beta$ antagonists exert anti-tumor effects through #1 activating effector cells such as NK cells and cytotoxic $CD8^+$ Tcells (CTLs), #2 inhibiting regulatory/suppressor cell populations, #3 making tumor cells visible to immune cells, #4 inhibiting the production of tumor growth factors. This review focuses on the effect of TGF-$\beta$ on T cells, which are differentiated into effector T cells or newly identified tumor-supporting T cells.

Tumor Induces the Expansion of Foxp3+CD25high and CD11b+Gr-1+ Cell Population in the Early Phase of Tumor Progression

  • Lee, Na Kyung;Kim, Hong Sung
    • 대한의생명과학회지
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    • 제21권4호
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    • pp.172-180
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    • 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.