• Journal of Korean Academy of Nursing
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• v.49 no.6
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• pp.713-723
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• 2019

Purpose: The purpose of this study was to identify the impact of cigarette smoking and alcohol consumption on the incidence of colon cancer in adults with metabolic syndrome. Methods: This study employed a longitudinal study design and utilized secondary data drawn from the Korean Genome and Epidemiology Study (KoGES). The data of a sample of 2,327 adults with metabolic syndrome tracked every two years from 2001 to 2014 were used in this study. Statistical data analyses of the frequency, number of cases per 100,000 person-years, log-rank test, Kaplan-Meier curve, and Cox's proportional hazards regression were performed using IBM SPSS statistics version 24. Results: During the observation period, the number of colon cancer cases was 46, and the total person-years were 252,444. The incidence of colon cancer was higher in current, over 10 pack-year smokers when compared to non-smokers (hazard ratio=3.38, 95% confidence interval=1.09~8.42). Conclusion: Excessive and long-term smoking should be avoided to prevent colon cancer, especially in adults with metabolic syndrome, since it might exacerbate the risk factors of colon cancer. Particularly, health professionals need to provide individualized smoking cessation interventions to those at high risk of colon cancer.

• BMB Reports
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• v.48 no.10
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• pp.539-540
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• 2015

It has been proposed that the selective elimination of cancer stem cells (CSCs) using targeted therapy could greatly reduce tumor growth, recurrence, and metastasis. To develop effective therapeutic targets for CSC elimination, we aimed to define the properties of CSC mitochondria, and identify CSC-mitochondria-specific targets in colon cancer. We found that colon CSCs utilize mitochondrial oxidative phosphorylation (OXPHOS) to produce ATP. We also found that forkhead box protein 1 (FOXM1)-induced peroxiredoxin 3 (PRDX3) maintains the mitochondrial function, and the FOXM1/PRDX3 mitochondrial pathway maintains survival of colon CSCs. Furthermore, FOXM1 induces CD133 (PROM1/prominin 1) expression, which maintains the stemness of colon CSCs. Together, our findings indicate that FOXM1, PRDX3, and CD133 are potential therapeutic targets for the elimination of CSCs in colon cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.5
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• pp.2191-2194
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• 2014

Background: Fluorouracil-based regimens have been widely accepted and recommended in the guidelines for treating patients with early or advanced staged colon cancer, although results are controversial. Here we performed a systemic analysis to evaluate the impact of S-1 based regimens on response and survival of patients with colon cancer. Methods: Clinical studies evaluating the impact of S-1 based regimens on response and survival of patients with colon cancer were identified using a predefined search strategy. Summary response rates (RRs) to treatment were calculated. Results: Six clinical studies which including 227 patients with advanced colorectal cancer were considered eligible for inclusion. Two studies were conducted using combination of S-1 and Oxaliplatin, and four studies featured S-1 and irinotecan. Systemic analysis showed that, in all patients, pooled RRs was 43.17%. Major adverse effects were hematological toxicities, gastrointestinal disturbance, neurosensory toxicity. No treatment related death occurred. Conclusion: This systemic analysis suggests that S-1 based regimens, both with oxaliplatin or irinotean are associated with acceptable response and toxicity in patients with colon cancer.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.6
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• pp.617-625
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• 2018

Neddylation is a post-translational protein modification process. MLN4924 is a newly discovered pharmaceutical neddylation inhibitor that suppresses cancer growth with several cancer types. In our study, we first investigated the effect of MLN4924 on colon cancer cells (HCT116 and HT29). MLN4924 significantly inhibited the neddylation of cullin-1 and colon cancer cell growth in a time and dose-dependent manner. MLN4924 induced G2/M cell cycle arrest and apoptosis in HCT116 and HT29 cells. Moreover, MLN4924 also triggered autophagy in HCT116 and HT29 cells via suppressing the PI3K/AKT/mTOR pathway. Inhibiting autophagy by autophagy inhibitor 3-MA or ATG5 knockdown reversed the function of MLN4924 in suppressing colon cancer cell growth and cell death. Interestingly, MLN4924 suppresses colon cell growth in a xenograft model. Together, our finding revealed that blocking neddylation is an attractive colon cancer therapy strategy, and autophagy might act as a novel anti-cancer mechanism for the treatment of colon cancer by MLN4924.

• The Korean Journal of Cytopathology
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• v.7 no.1
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• pp.103-106
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• 1996

Although exfoliative colonic cytology for the diagnosis of colorectal cancer has been largely abandoned due to the widespread use of colonoscopy, some authors still insiston the usefulness of colon lavage fluid. We tried evaluating the diagnostic feasibility of colon lavage fluid cytology using an orally administered balanced electrolyte solution. We collected colon lavage fluids in 106 patients prior to colonoscopy and reviewed the slides. Cytologic examination revealed neoplastic cells in 7 of 16(44%) cases of endoscopically proven adenocarcinoma patients. Therefore, we thin cytologic study of colon lavage fluid may be considered as one of the noninvasive diagnostic tools in colorectal cancer.

• Biomolecules & Therapeutics
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• v.24 no.2
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• pp.140-146
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• 2016

Naringenin (NAR) as one of the flavonoids observed in grapefruit has been reported to exhibit an anti-cancer activity. Activating transcription factor 3 (ATF3) is associated with apoptosis in human colon cancer cells. This study was performed to investigate the molecular mechanism by which NAR stimulates ATF3 expression and apoptosis in human colon cancer cells. NAR reduced the cell viability and induced an apoptosis in human colon cancer cells. ATF3 overexpression increased NAR-mediated cleaved PARP, while ATF3 knockdown attenuated the cleavage of PARP by NAR. NAR increased ATF3 expression in both protein and mRNA level, and increased the luciferase activity of ATF3 promoter in a dose-dependent manner. The responsible region for ATF3 transcriptional activation by NAR is located between -317 and -148 of ATF3 promoter. p38 inhibition blocked NAR-mediated ATF3 expression, its promoter activation and apoptosis. The results suggest that NAR induces apoptosis through p38-dependent ATF3 activation in human colon cancer cells.

• Genomics & Informatics
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• v.14 no.2
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• pp.46-52
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• 2016

Diverse somatic mutations have been reported to serve as cancer drivers. Recently, it has also been reported that epigenetic regulation is closely related to cancer development. However, the effect of epigenetic changes on cancer is still elusive. In this study, we analyzed DNA methylation data on colon cancer taken from The Caner Genome Atlas. We found that several promoters were significantly hypermethylated in colon cancer patients. Through clustering analysis of differentially methylated DNA regions, we were able to define subgroups of patients and observed clinical features associated with each subgroup. In addition, we analyzed the functional ontology of aberrantly methylated genes and identified the G-protein-coupled receptor signaling pathway as one of the major pathways affected epigenetically. In conclusion, our analysis shows the possibility of characterizing the clinical features of colon cancer subgroups based on DNA methylation patterns and provides lists of important genes and pathways possibly involved in colon cancer development.

• Journal of Digestive Cancer Research
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• v.3 no.2
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• pp.89-94
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• 2015

The role of adjuvant chemotherapy in patients with stage II colon cancer remains a controversial issue. Adjuvant chemotherapy aims to eliminate any micrometastatic disease that may have been missed, at the time of surgery. Although one prospective study showed a small but statistically significant benefit with respect to the overall survival for those who received adjuvant chemotherapy, multiple pooled data did not demonstrate any benefit of this therapy in patients with stage II colon cancer. Current national and international guidelines for the adjuvant treatment of stage II colon dose not advise routine implementation of adjuvant chemotherapy, but rather recommend selective use of this therapy for patients with high risk of recurrence. High risk features for recurrence include T4 disease, poorly differentiated histology, presence of lymphovascular invasion, presence of perineural invasion, inadequate retrieval of lymph nodes, bowel obstruction, localized perforation, or positive margins. More recently, prediction tools using gene expression cancer profiles are proposed to identify patients who are most likely to have recurrence and therefore may benefit from postoperative chemotherapy in stage II colon cancer. These novel methods together with conventional prognosticators, will allow us to implement more optimized personalizing adjuvant therapy in these patients.

• The Korean Journal of Nuclear Medicine
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• v.18 no.1
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• pp.1-8
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• 1984

To evaluate the clinical significance of serum tissue polypeptide antigen (TPA) levels in patients with malignancy, serum TP A levels were measured by radioimmunoassay in 49 normal controls, 9 patients of postoperative colon cancer without recurrence and 68 patients with various untreated malignancy, who visited Seoul National University Hospital from February, 1983 to September, 1983. The results were as follows; 1) Serum TPA levels in 49 normal controls were in the range of 22-135 U/L $(74{\pm}28U/L,\;mean{\pm}S.D.)$. There was no sex or age difference. Normal upper limit of serum TPA was defined as 130 U/L (mean+2S.D.). 2) Serum TPA levels in 68 patients with various untreated malignancy (stomach cancer 33 cases, colon cancer 11 cases, lung cancer 10 cases, primary liver cancer 9 cases and metastatic cancer of unknown primary site 5 cases) were in the range of 10-800 U/L $(189{\pm}170U/L,\;mean{\pm}S.D.)$ and significantly elevated, compared with those of normal controls (p<0.005). 3) The sensitivities of serum TPA in various untreated malignancy were 39% in stomach cancer, 55% in colon cancer, 50% in lung cancer, 67% in primary liver cancer and 80% in metastatic cancer of unknown primary site respectively. 4) The sensitivities of serum TPA related to resectability in stomach and colon cancer were 32% in resectable stomach cancer, 50% in unresectable stomach cancer, 29% in resectable colon cancer and 100% in unresectable colon cancer respectively. 5) The mean value of serum TPA levels in 9 patients of postoperative colon cancer without recurrence was $70{\pm}39U/L$ and significantly decreased, compared with that of untreated colon cancer, $180{\pm}150U/L$ U/L (p<0.05). 6) In patients with stomach or colon cancer, there was no significant correlation between serum TP A and serum CEA levels, but simultaneous measurement of serum TPA and serum CEA levels increased sensitivities. From above results, we concluded that serum TPA level is a useful indicator reflecting tumor activity and responses to anticancer treatment in patients with malignancy.

• The Korea Journal of Herbology
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• v.28 no.4
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• pp.33-40
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• 2013

Objectives : To study the apoptosis effects of fermented Undaria pinnatifida extracts(FUP) against HCT-15 colon cancer cells. Method : By measuring cell proliferation, DNA fragmentation, cell cycle, morphology, and western blot from FUP, the study investigated the effects of the extractions had upon the HCT-15 colon cancer cells, and concluded that the inhibiting effects upon cells were induced by apoptosis. Result : FUP effectively inhibited the growth of HCT-15 colon cancer cells. After analyzing the DNA fragmentation, the study observed a DNA ladder, while examining the cells, and found an increase of sub-G1 hypodiploid cells. On the changes regarding the nucleus of the cells, a condensation of cells and chromatin, as well as an apoptotic body was clearly observed. By observing through western blot from FUP, the study found a decreased level of Bcl-2 from HCT-15 colon cancer cells, but the increased level of Bax and cleaved caspase-3, which as a result induced apoptosis, inhibiting the growth of HCT-15 colon cancer cells. FUP increased the natural death of HCT-15 colon cancer cells by the induction of apoptosis. FUP seemed to have no suppressing effect upon HL-60/MX2 cells. However, compared to the fucoidan, the study was able to clearly observe morphological changes of HCT-15 cells apoptosis, in a 1/2 concentration. Conclusion : FUP had antiproliferative effects on different kinds of cancer cells, while proving especially efficacious against colon cancer cells.