• Asian Pacific Journal of Cancer Prevention
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• 제17권12호
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• pp.5071-5074
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• 2016

Background: Azoxymethane (AOM) is a well-known colon cancer-inducing agent in experimental animals via mechanisms that include oxidative stress in rat colon and liver tissue. Few studies have investigated AOM-induced oxidative stress in rat liver tissue. Red seaweeds of the genera Hypnea Bryodies and Melanothamnus Somalensis are rich in polyphenolic compounds that may suppress cancer through antioxidant properties, yet limited research has been carried out to investigate their anti-carcinogenic and antioxidant influence against AOM-induced oxidative stress in rat liver. Objective: This study aims to determine protective effects of red seaweed (Hypnea Bryodies and Melanothamnus Somalensis) extracts against AOM-induced hepatotoxicity and oxidative stress. Materials and Methods: Sprague-Dawley rats received intraperitoneal injections of AOM, 15 mg/kg body weight, once a week for two consecutive weeks and then orally administered red seaweed (100 mg/kg body-weight) extracts for sixteen weeks. At the end of the experiment all animals were overnight fasted then sacrificed and blood and liver tissues were collected. Results: AOM treatment significantly decreased serum liver markers and induced hepatic oxidative stress as evidenced by increased liver tissue homogenate levels of nitric oxide and malondialdehyde, decreased total antioxidant capacity and glutathione, and inhibition of antioxidant enzymes (catalase, glutathione peroxidase, glutathione S-transferase, glutathione reductase and superoxide dismutase). Both red seaweed extracts abolished the AOM-associated oxidative stress and protected against liver injury as evidenced by increased serum levels of liver function markers. In addition, histological findings confirmed protective effects of the two red seaweed extracts against AOM-induced liver injury. Conclusion: Our findings indicate that red seaweed (Hypnea Bryodies and Melanothamnus Somalensis) extracts counteracted oxidative stress-induced hepatotoxicity in a rat model of colon cancer.

• Asian Pacific Journal of Cancer Prevention
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• 제15권7호
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• pp.3113-3121
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• 2014

Colorectal cancer remains one of the most common types of cancer and a leading cause of cancer death worldwide. In this study, we aimed to investigate effects of DuP-697, an irreversible selective inhibitor of COX-2 on colorectal cancer cells alone and in combination with a promising new multi-targeted kinase inhibitor E7080. The HT29 colorectal cancer cell line was used. Real time cell analysis (xCELLigence system) was conducted to determine effects on colorectal cell proliferation, angiogenesis was assessed with a chorioallantoic membrane model and apoptosis was determined with annexin V staining. We found that DuP-697 alone exerted antiproliferative, antiangiogenic and apoptotic effects on HT29 colorectal cancer cells. For the antiproliferative effect the half maximum inhibition concentration ($IC_{50}$) was $4.28{\times}10^{-8}mol/L$. Antiangiogenic scores were 1.2, 0.8 and 0.5 for 100, 10 and 1 nmol/L DuP-697 concentrations, respectively. We detected apoptosis in 52% of HT29 colorectal cancer cells after administration of 100 nmol/L DuP-697. Also in combination with the thyrosine kinase inhibitor E7080 strong antiproliferative, antiangiogenic and apoptotic effects on HT29 colorectal cancer cells were observed. This study indicates that DuP-697 may be a promising agent in the treatment of colorectal cancer. Additionally the increased effects observed in the combination with thyrosine kinase inhibitor give the possibility to use lower doses of DuP-697 and E7080 which can avoid and/or minimize side effects.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2001년도 International Symposium on Effects of Edible Phytochemicals and Their Synthetic Derivatives on Carcinogenesis and Mutagenesis
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• pp.15-15
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• 2001

In the present study, we examined the chemopreventive effects of indole-3-carbinol (I3C), a constituent of cruciferous vegetables (the Family of Cruciferae) such as cabbages, cauliflowers and broccoli on multiple intestinal neoplasia (Min) genetic mouse model and on mouse colon carcinogenesis induced by azoxymethane (AOM) as well as on rat mammary carcinogenesis induced by 7, 12-dimethybenz［$\alpha$］anthracene (DMBA).(omitted)

• 한국독성학회:학술대회논문집
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• 한국독성학회 2001년도 International Symposium on Dietary and Medicinal Antimutgens and Anticarcinogens
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• pp.58-58
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• 2001

In the present study, we examined the chemopreventive effects of indole-3-carbinol (I3C), a constituent of cruciferous vegetables (the Family of Cruciferae) such as cabbages, cauliflowers and broccoli on multiple intestinal neoplasia (Min) genetic mouse model and on mouse colon carcinogenesis induced by azoxymethane (AOM) as well as on rat mammary carcinogenesis induced by 7, 12-dimethybenz［$\alpha$］anthracene (DMBA).(omitted)

• Asian Pacific Journal of Cancer Prevention
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• 제13권4호
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• pp.1115-1118
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• 2012

Diallyl sulfide (DAS), a flavoring compound derived from garlic, is considered to have cancer chemopreventive potential in experimental animals and humans. This study was designated to examine possible chemopreventive effects of DAS on colon carcinogenesis using genetically engineered transgenic $Apc^{Min/+}$ mice, a well-established animal model for familial adenomatous polyposis (FAP) and sporadic colorectal cancer. Male C57BL/6J-$Apc^{Min/+}$ mice were divided into three groups. Animals of group 1 were placed on the basal diet (AIN-76A) as non-treated controls. Animals of groups 2 and 3 were given DAS-containing diets (in doses of 100 and 300 ppm, respectively). All mice were sacrificed at the end of week 10 of the experiment. Histopathological investigation revealed that the incidence of colonic polyps was decreased dose-dependently by 19% (13/16) in group 2 and by 32% (13/20) in group 3 compared to the 100% incidence (10/10) in group 1. The multiplicity of colonic polyps per mouse was also slightly decreased by DAS treatment ($1.88{\pm}0.35$ in group 2 and $1.63{\pm}0.36$ in group 3) compared to $2.00{\pm}0.39$ in group 1. On the other hand, there were no significant differences in the numbers of total polyps per mouse in the small intestine between the groups. Taken together, we suggest that DAS may exert promising inhibitory effects on colon carcinogenesis in the transgenic $Apc^{Min/+}$ mice.

• Journal of Microbiology and Biotechnology
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• 제34권4호
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• pp.774-782
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• 2024

This study aimed to elucidate the anti-colon cancer mechanism of ginsenoside Rg1 in vitro and in vivo. Cell viability rate was detected using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) tetrazolium assay. The inhibitory effect of ginsenoside Rg1 against CT26 cell proliferation gradually increased with increasing concentration. The in vivo experiments also demonstrated an antitumor effect. The monodansylcadaverine (MDC), transmission electron microscopy (TEM), and expression of autophagy marker proteins confirmed that ginsenoside Rg1 induced autophagy in vitro. Ginsenoside Rg1 induced autophagy death of CT26 cells, but this effect could be diminished by autophagy inhibitor (3-methyladenine, 3-MA). Additionally, in a xenograft model, immunohistochemical analysis of tumor tissues showed that the LC3 and Beclin-1 proteins were highly expressed in the tumors from the ginsenoside Rg1-treated nude mice, confirming that ginsenoside Rg1 also induced autophagy in vivo. Furthermoer, both in vivo and in vitro, the protein expressions of p-Akt, p-mTOR, and p-p70S6K were inhibited by ginsenoside Rg1, which was verified by Akt inhibitors. These results indicated that the mechanism of ginsenoside Rg1 against colon cancer was associated with autophagy through inhibition of the Akt/mTOR/p70S6K signaling pathway.

• Journal of Preventive Medicine and Public Health
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• 제46권2호
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• pp.74-81
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• 2013

Objectives: The objective of this study was to evaluate the performance of risk-adjusted mortality models for colorectal cancer surgery. Methods: We investigated patients (n=652) who had undergone colorectal cancer surgery (colectomy, colectomy of the rectum and sigmoid colon, total colectomy, total proctectomy) at five teaching hospitals during 2008. Mortality was defined as 30-day or in-hospital surgical mortality. Risk-adjusted mortality models were constructed using claims data (basic model) with the addition of TNM staging (TNM model), physiological data (physiological model), surgical data (surgical model), or all clinical data (composite model). Multiple logistic regression analysis was performed to develop the risk-adjustment models. To compare the performance of the models, both c-statistics using Hanley-McNeil pair-wise testing and the ratio of the observed to the expected mortality within quartiles of mortality risk were evaluated to assess the abilities of discrimination and calibration. Results: The physiological model (c=0.92), surgical model (c=0.92), and composite model (c=0.93) displayed a similar improvement in discrimination, whereas the TNM model (c=0.87) displayed little improvement over the basic model (c=0.86). The discriminatory power of the models did not differ by the Hanley-McNeil test (p>0.05). Within each quartile of mortality, the composite and surgical models displayed an expected mortality ratio close to 1. Conclusions: The addition of clinical data to claims data efficiently enhances the performance of the risk-adjusted postoperative mortality models in colorectal cancer surgery. We recommended that the performance of models should be evaluated through both discrimination and calibration.

• Food Science and Biotechnology
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• 제15권6호
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• pp.931-936
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• 2006

This study sought to investigate any additive or interactive effects that soy isoflavones may have on the ecosystem of the gut, which is influenced by fructooligosaccharide (FOS) in colon-cancer model rats. Male Sprague-Dawley rats treated with 1,2-dimethylhydrazine were given experimental diets containing 0, 3, 6, or 9% FOS with or without 0.1% soy isoflavone for 12 weeks. In addition to the effects of FOS dosage on the gut ecosystem, dietary supplementation with soy isoflavone reduced the number of colonic aberrant crypts (ACs). The fecal weight, fecal pH, and gut transit time significantly decreased in a dose-dependent manner in rats fed FOS and the fecal concentration of bifidobacteria was higher in rats fed FOS than in control rats. The fecal output of total short-chain fatty acids, acetate, and propionate was significantly increased by the presence of FOS and was negatively correlated with the number of ACs, whereas the fecal output of butyrate showed no significant correlation with FOS dosage. The addition of soy isoflavone to the diet did not result in any significant differences in gut ecosystem parameters. Therefore, we conclude that the suppressive effect of soy isoflavone on ACs was not associated with the intestinal ecosystem, which was significantly altered by the dosage of FOS.

• 한국컴퓨터정보학회논문지
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• 제24권9호
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• pp.103-108
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• 2019

The purpose of this study is to identify the factors that may affect the 5-year survival of colon cancer through network model and to use it as a clinical decision supporting system for colorectal cancer patients. This study was conducted using data from 2,540 patients who underwent colorectal cancer surgery from 1996 to 2018. Eleven factors related to survival of colorectal cancer were selected by consulting medical experts and previous studies. Analysis was proceeded from the data sorted out into 1,839 patients excluding missing values and outliers. Logistic regression analysis showed that age, BMI, and heart disease were statistically significant in order to identify factors affecting 5-year survival of colorectal cancer. Additionally, a correlation analysis was carried out age, BMI, heart disease, diabetes, and other diseases were correlated with 5-year survival of colorectal cancer. Sex was related with BMI, lung disease, and liver disease. Age was associated with heart disease, heart disease, hypertension, diabetes, and other diseases, and BMI with hypertension, diabetes, and other diseases. Heart disease was associated with hypertension, diabetes, hypertension, diabetes, and other diseases. In addition, diabetes and kidney disease were associated. In the correlation analysis, the network model was constructed with the Network Correlation Coefficient less than p <0.001 as the weight. The network model showed that factors directly affecting survival were age, BMI levels, heart disease, and indirectly influencing factors were diabetes, high blood pressure, liver disease and other diseases. If the network model is used as an assistant indicator for the treatment of colorectal cancer, it could contribute to increasing the survival rate of patients.

• IMMUNE NETWORK
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• 제12권6호
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• pp.253-260
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• 2012

${\alpha}$-Mangostin is a xanthon derivative contained in the fruit hull of mangosteen (Garcinia mangostana L.), and the administration of ${\alpha}$-Mangostin inhibited the growth of transplanted colon cancer, Her/CT26 cells which expressed Her-2/neu as tumor antigen. Although ${\alpha}$-Mangostin was reported to have inhibitory activity against sarco/endoplasmic reticulum $Ca^{2+}$ ATPase like thapsigargin, it showed different activity for autophagy regulation. In the current study, we found that ${\alpha}$-Mangostin induced autophagy activation in mouse intestinal epithelial cells, as GFP-LC3 transgenic mice were orally administered with 20 mg/kg of ${\alpha}$-Mangostin daily for three days. However, the activation of autophagy by ${\alpha}$-Mangostin did not significantly increase OVA-specific T cell proliferation. As we assessed ER stress by using XBP-1 reporter system and phosphorylation of $eIF2{\alpha}$, thapsigargin-induced ER stress was significantly reduced by ${\alpha}$-Mangostin. However, coadministration of thapsigargin with ${\alpha}$-Mangostin completely blocked the antitumor activity of ${\alpha}$-Mangostin, suggesting ER stress with autophagy blockade accelerated tumor growth in mouse colon cancer model. Thus the antitumor activity of ${\alpha}$-Mangostin can be ascribable to the autophagy activation rather than ER stress induction.