• 한국방사선학회논문지
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• 제10권6호
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• pp.387-393
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• 2016

종양을 효율적으로 적출, 제거하기 위해서는 부수적으로 방사선 치료 및 항암화학요법을 이용하여 수술 전이나, 수술 후 종양의 크기를 줄이거나 작게 할 수는 있었으나, 종양을 적출하거나 제거하는 방법으로 외과적 절제수술요법이 가장 재래적인 수술 방법이다. 종양의 크기를 줄이거나 작게 하는 방법과, 종양을 사멸시킬 수 있는 항암화학요법은 방사성 감수성을 증가시키는 항암약제를 종양세포에 선택적으로 투여하여 방사선에 대한 감수성에 민감하게 반응 할 수 있도록 한 것이며, 다양한 생물학적인 세포증식억제 방법 중 TRAIL은 단백질을 변형 시킬 수 있으며 단백질 구조를 변형시켜 세포의 사멸에 일조를 하는 것으로 알려져 있다. 본 논문에서는 HCT-116세포를 암세포로 간주하여 TRAIL과 방사선과의 상호관계를 분석하였다. 실험결과 TRAIL과 방사선의 단독사용은 대조군과 비교해 본 결과 각각 세포증식과 세포자멸사에 유의적인 영향을 끼치지 않은 것으로 나타났다. 반대로 TRAIL로 처리하고, 방사선 조사를 병행해서 처리한 경우 HCT-116세포가 유의적으로 세포자멸사가 발생되었음을 알 수 있었고, G1대비 G0의 비율도 증가한 것으로 나타났다. 결론적으로 TRAIL은 방사선 방어적인 세포의 세포자멸사를 증가시켜 방사선 감수성을 증가시켰음을 알 수 있었으며, 또한 세포주기를 변화시켜 세포 증식 능력을 점진적으로 감소시킬 수 있었다. TRAIL은 세포자멸사를 증가시키고 세포증식 능력을 감소시켜 방사선 증감제로서 사용이 가능하다는 것으로 사료된다.

• IMMUNE NETWORK
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• 제23권4호
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• pp.35.1-35.16
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• 2023

Defining the molecular dynamics associated with T cell differentiation enhances our understanding of T cell biology and opens up new possibilities for clinical implications. In this study, we investigated the dynamics of CD5 expression in CD8⁺ T cell differentiation and explored its potential clinical uses. Using PBMCs from 29 healthy donors, we observed a stepwise decrease in CD5 expression as CD8⁺ T cells progressed through the differentiation stages. Interestingly, we found that CD5 expression was initially upregulated in response to T cell receptor stimulation, but diminished as the cells underwent proliferation, potentially explaining the differentiation-associated CD5 downregulation. Based on the proliferation-dependent downregulation of CD5, we hypothesized that relative CD5 expression could serve as a marker to distinguish the heterogeneous CD8⁺ T cell population based on their proliferation history. In support of this, we demonstrated that effector memory CD8⁺ T cells with higher CD5 expression exhibited phenotypic and functional characteristics resembling less differentiated cells compared to those with lower CD5 expression. Furthermore, in the retrospective analysis of PBMCs from 30 non-small cell lung cancer patients, we found that patients with higher CD5 expression in effector memory T cells displayed CD8⁺ T cells with a phenotype closer to the less differentiated cells, leading to favorable clinical outcomes in response to immune checkpoint inhibitor (ICI) therapy. These findings highlight the dynamics of CD5 expression as an indicator of CD8⁺ T cell differentiation status, and have implications for the development of predictive biomarker for ICI therapy.

• Journal of Nutrition and Health
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• 제33권6호
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• pp.632-638
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• 2000

This study was designed to observe the effect of green tea on colon tumor incidence and biomarkers of colon carcinogenesis in 1, 2-dimethlhydrazine-treated rats. Male Sprague Dawley rats at 7 weeks of age were divided into two groups: control and green tea(GT) groups. Control rats had distilled water as drinking water but GT group received green tea extracts(2.5%, w/v water) as drinking water throughout the experiment periods. All rats were fed the experimental diet containing 15% fat by weight for 20 weeks. and were i.m. injected with DMH for 6 weeks to give total dose of 180mg/kg body weight. Tumor incidence was reduced in GT group (39%) compared with control group (56%) Green tea significantly reduced cell proliferation (total cells per crypt, crypt length and proliferative zone) in colonic mucosa and also significantly reduced the levels of preformed prostalandin E2(PGE2) and thromboxance B2(TXB2) in colonic mucosa but the fatty acid profile of total lipid in colonic mucosa was not significantly influenced by green tea. However the relative percent of C20:4 and the levels f preformed PGE2 and TXB2. were significantly higher in tumor tissue compared with normal surrounding mucosa.Green tea increased the fecal excretion of total bile acid but not scondary bile acid which is known as one of promoters for colon cancer,. These results suggest that green tea could have preventive effect against colon cancer when consumed daily by influencing on antioxidant effect and the metabolism of arachidonic acid.

• 동의생리병리학회지
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• 제17권3호
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• pp.819-825
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• 2003

pharbitis nil and Taraxacum mongolicum are representative herbs that have been used for cancer treatment in Korean traditional medicine. To understand the molecular basis of the antitumor function, we analyzed the effect of these herbs on proliferation and apoptosis of tumor cells using a gastric cancer cell line AGS. Cell counting assay showed that pharbitis nil strongly inhibit cell proliferation Of AGS whereas Taraxacum mongolicum exhibit no detectable effect on cellular growth. [³H]thymidine uptake analysis also demonstrated that DNA replication of AGS is suppressed in a dose-dependent manner by treatment with pharbitis nil. Additionally, tryphan blue exclusion assay showed that Pharbitis nil induce apoptotic cell death of AGS in a dose-dependent. To explore whether anti antiproliferative and/or proapototic property of Pharbitis nil is associated with their effect on gene expression, we performed RT-PCR analysis of cell cycle- and apoptosis-related genes. Interestingly, mRNA expression levels of c-Jun, c-Fos, c-Myc, and Cyclin D1 were markedly reduced by Pharbitis nil. Taraxacum mongolicum also showed inhibitory action on expression of these growth-promoting protooncogene but there effects are less significant, as compared to Pharbitis nil. Furthermore, it was also found that Pharbitis nil activates expression of the p53 tumor suppressor and its downstream effector p21Waf1, which induce G1 cell cycle arrest and apoptosis. Collectively, our data demonstrate that Pharbitis nil induce growth inhibition and apoptosis of human gastric cancer cells and these effects are accompanied with down-and up-regulation of growth-regulating protooncogenes and tumor suppressor genes, respectively. This observation thus suggests that the anticancer effect of Pharbitis nil might be associated with its regulatory capability of tumor-related gene expression.

• The Korean Journal of Physiology and Pharmacology
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• 제27권4호
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• pp.333-344
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• 2023

Hepatocellular carcinoma (HCC) is a prevalent malignant tumor with high fatality. It has yet to be reported whether circ-SNX27 can affect the progression of HCC. This study attempted to analyze circ-SNX27's precise role and underlying mechanisms in HCC. HCC cell lines and tumor specimens from HCC patients were analyzed using quantitative real-time PCR and Western blotting to quantify the expressions of circ-SNX27, miR-375, and ribophorin I (RPN1). Cell invasion and cell counting kit 8 experiments were conducted for the evaluation of HCC cell invasion and proliferation. Caspase-3 Activity Assay Kit was utilized to gauge the caspase-3 activity. Luciferase reporter and RNA immunoprecipitation assays were executed to ascertain the relationships among miR-375, circ-SNX27, and RPN1. To determine how circ-SNX27 knockdown affects the growth of HCC xenografts in vivo, tumor-bearing mouse models were constructed. Elevated expressions of circ-SNX27 and RPN1 as well as a reduced miR-375 expression were observed among HCC cells and HCC patient tumor specimens. Knocking-down circ-SNX27 in HCC cells abated their proliferative and invasive abilities but raised their caspase-3 activity. Moreover, the poor levels of circ-SNX27 inhibited HCC tumor growth among the mice. Circ-SNX27 enhanced RPN1 by competitively binding with miR-375. Silencing miR-375 in HCC cells promoted their malignant phenotypes. Nonetheless, the promotive effect of miR375 silencing was reversible via the knockdown of circ-SNX27 or RPN1. This research demonstrated that circ-SNX27 accelerated the progression of HCC by modulating the miR-375/RPN1 axis. This is indicative of circ-SNX27's potential as a target for the treatment of HCC.

• 대한핵의학회지
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• 제36권1호
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• pp.8-18
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• 2002

Early and accurate diagnosis of tumors using positron omission tomography (PET) has been the focus of considerable interest due to its high metastasis and mortality rates at late detection. PET radiopharmaceuticals-which exhibit a high tumor-to-background uptake ratio, and appropriate metabolic characteristics, and pharmacokinetics-are attractive tools for tumor imaging. Tumor imaging by these radiopharmaceuticals are based on metabolic and receptor imaging. The former is based on accelerated metabolism in tumor tissue compared to normal tissue and the rate roughly corresponding to the rate of growth of tumors. Radiopharmaceuticals for this purpose include radiolabeled sugars, amino acids, and nucleosides which detect increased glucose utilization, protein synthesis, and DNA synthesis, respectively. Tumor receptor imaging is based on the proliferation of tumor cells regulated by many hormones and growth factors, which bind to the corresponding receptors and exhibit the biological responses Radiopharmaceuticals used to image the tumor receptor systems may be ligands for the specific receptors and antibodies for the growth factor receptors. Some antitumor agents have been labeled with radionuclides and used to study in vivo biodistribution and pharmacokinetics in humans. This overview describes typical PET radiopharmaceuticals used for tumor imaging based on their uptake mechanisms.

• Asian Pacific Journal of Cancer Prevention
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• 제16권11호
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• pp.4549-4553
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• 2015

Background: Colorectal carcinoma (CRC) is one of the major causes of cancer death worldwide. Data from the literature indicate differences between the proliferation rate of endothelial cells relative to the morphology growth type, possibly due to origin of specimens (autopsy material, surgery fragments) or quantification methods. Vascular endothelial growth factor (VEGF) is a factor that stimulates the proliferation of endothelial cells. It is expressed in more than 90% of cases of metastatic CRC. Aim: The aim of this study was to evaluate the endothelial cell proliferation and VEGF expression in primary tumors and corresponding liver metastases. Materials and Methods: Our study included 24 recent biopsies of primary tumors and corresponding liver metastases of CRC cases. CD34/Ki67 double immunostaining and RNA scope assay for VEGF were performed. Results: In the primary tumors analysis of VEGFmRNA expression indicated no significant correlation with differentiation grade, proliferative and non-proliferative vessels in the intratumoral and peritumoral areas. In contrast, in the corresponding liver metastases, VEGFmRNA expression significantly correlated with the total number of non-proliferative vessels and total number of vessels. CD34/Ki67 double immunostaining in the cases with poorly differentiated carcinoma indicated a high number of proliferating endothelial cells in the peritumoral area and a low number in the intratumoral area for the primary tumor. Moderately differentiated carcinomas of colon showed no proliferating endothelial cells in the intratumoral area in half of the cases included in the study, for both, primary tumor and liver metastasis. In well differentiated CRCs, in primary tumors, a high proliferation rate of endothelial cells in the intratumoral area and a lower proliferation rate in the peritumoral area were found. A low value was found in corresponding liver metastasis. Conclusions: The absence of proliferative endothelial cells in half of the cases for the primary tumors and liver metastases in moderately differentiated carcinoma suggest a vascular mimicry phenomenon. The mismatch between the total number of vessels and endothelial proliferation in primary tumors indicate that a functional vascular network is already formed or the existence of some mechanisms influenced by other angiogenic factors.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2002년도 Current Trends in Toxicological Sciences
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• pp.105-105
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• 2002

A wide range of chemicals derived from plant and human-made xenobiotics are reported to have hormonal activity. The present studies were performed to examine the estrogenic effect of Kwao Keur, Pueraria mirifica (PM), that has been used a rejuvenating folk medicine from Thailand, using recombinant yeast, MCF-7 cell proliferation and HepG2 cell transient transfection assay.(omitted)

• Biomolecules & Therapeutics
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• 제31권5호
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• pp.473-483
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• 2023

Many cancers arise from sites of chronic inflammation, which creates an inflammatory microenvironment surrounding the tumor. Inflammatory substances secreted by cells in the inflammatory environment can induce the proliferation and survival of cancer cells, thereby promoting cancer metastasis and angiogenesis. Therefore, it is important to identify the role of inflammatory factors in cancer progression. This review summarizes the signaling pathways and roles of C-reactive protein (CRP) in various cancer types, including breast, liver, renal, and pancreatic cancer, and the tumor microenvironment. Mounting evidence suggests the role of CRP in breast cancer, particularly in triple-negative breast cancer (TNBC), which is typically associated with a worse prognosis. Increased CRP in the inflammatory environment contributes to enhanced invasiveness and tumor formation in TNBC cells. CRP promotes endothelial cell formation and angiogenesis and contributes to the initiation and progression of atherosclerosis. In pancreatic and kidney cancers, CRP contributes to tumor progression. In liver cancer, CRP regulates inflammatory responses and lipid metabolism. CRP modulates the activity of various signaling molecules in macrophages and monocytes present in the tumor microenvironment, contributing to tumor development, the immune response, and inflammation. In the present review, we overviewed the role of CRP signaling pathways and the association between inflammation and cancer in various types of cancer. Identifying the interactions between CRP signaling pathways and other inflammatory mediators in cancer progression is crucial for understanding the complex relationship between inflammation and cancer.

• 충청수학회지
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• 제28권1호
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• pp.161-172
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• 2015

In this paper, we consider the chemotaxis-haptotaxis model of tumor invasion with the proliferation and tissue re-establishment term in dimensions one and two. We show the global in time existence of a unique classical solution for the the model in two dimensional spatial domain without any restrictions on the coefficients.