• Journal of Digestive Cancer Reports
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• v.8 no.2
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• pp.97-101
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• 2020

Metformin is a widely used first-line anti-diabetic drug worldwide. Epidemiologic studies using the large population-based cohort database have shown the association between metformin uses and reduced risk of various type cancers including gastric cancer. In the gastric cancer prevention, metformin use was associated with the significant reduction of gastric cancer risk, especially for long-term metformin users. However, there is no well-designed randomized controlled clinical trial investigating the effect of metformin as a chemopreventive drug for gastric cancer. Therefore, further well-designed clinical trials will be needed to implement metformin for chemoprevention of gastric cancer.

• 대한두경부종양학회:학술대회논문집
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• 1997.11a
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• pp.303-307
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• 1997

• 대한방사선치료학회:학술대회논문집
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• 2002.05a
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• pp.8-10
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• 2002

• BMB Reports
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• v.36 no.1
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• pp.78-81
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• 2003

The prevention of cancer is one of the most important public health and medical practices of the $21^{st}$ century. We have made much progress in this new emerging field, but so much remains to be accomplished before widespread use and practice become common place. Cancer chemoprevention encompasses the concepts of inhibition, reversal, and retardation of the cancer process. This process, called carcinogenesis, requires 20-40 years to reach the endpoint called invasive cancer. It typically follows multiple, diverse and complex pathways in a stochastic process of clonal evolution. These pathways appear amenable to inhibition, reversal or retardation at various points. We must therefore identify key pathways in the evolution of the cancer cell that can be exploited to prevent this carcinogenesis process. Basic research is identifying many genetic lesions and epigenetic processes associated with the progression of precancer to invasive disease. Many of these early precancerous lesions favor cell division over quiescence and protect cells against apoptosis when signals are present. Many oncogenes are active during early development and are reactivated in adulthood by aberrant gene promoting errors. Normal regulatory genes are mutated, making them insensitive to normal regulatory signals. Tumor suppressor genes are deleted or mutated rendering them inactive. Thus there is a wide range of defects in cellular machinery which can lead to evolution of the cancer phenotype. Mistakes may not have to appear in a certain order for cells to progress along the cancer pathway. To conquer this diverse disease, we must attack multiple key pathways at once for a predetermined period of time. Thus, agent combination prevention strategies are essential to decrease cancer morbidity. Furthermore, each cancer type may require custom combination of prevention strategies to be successful.

• Journal of Microbiology and Biotechnology
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• v.25 no.7
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• pp.1047-1055
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• 2015

For the search of a potent first-in-class compound to inactivate macrophages responsible for inflammatory responses, in the present study, we investigated the anti-nflammatory effects of YH-1118, a novel synthetic compound, in a lipopolysaccharide (LPS)-stimulated mouse macrophage cell line, Raw 264.7. YH-1118 inhibited LPS-induced nitric oxide (NO) production and inducible NO synthase (iNOS) expression at both the protein and mRNA levels. The suppression of LPS-induced iNOS expression by YH-1118 was mediated via nuclear factor kappa B (NF-κB), but not activator protein-1 (AP-1) transcription factor. This was supported by the finding that YH-1118 attenuated the phosphorylation of inhibitor of κBα (IκBα) and nuclear translocation and DNA binding activity of NF-κB. Through the mechanisms that YH-1118 inhibited the activation of IκB kinases (IKKs), upstream activators of NF-κB, or p38 MAPK, YH-1118 significantly suppressed LPS-induced production of pro-inflammatory cytokines, tumor necrosis factor-α, interleukin-1β (IL-1β), and IL-6 (p < 0.05). In conclusion, our results suggest that YH-1118 inhibits LPS-induced inflammatory responses by blocking IKK and NF-κB activation in macrophages, and may be a therapeutic candidate for the treatment of various inflammatory diseases.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.8
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• pp.3675-3686
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• 2016

Moringa oleifera Lam, family Moringaceae, is a perennial plant which is called various names, but is locally known in Malaysia as ''murungai'' or ''kelor''. Glucomoringin, a glucosinolate with from M. oleifera is a major secondary metabolite compound. The seeds and leaves of the plant are reported to have the highest amount of glucosinolates. M. oleifera is well known for its many uses health and benefits. It is claimed to have nutritional, medicinal and chemopreventive potentials. Chemopreventive effects of M. oleifera are expected due to the existence of glucosinolate which it is reported to have the ability to induce apoptosis in anticancer studies. Furthermore, chemopreventive value of M. oleifera has been demonstrated in studies utilizing its leaf extract to inhibit the growth of human cancer cell lines. This review highlights the advantages of M. oleifera targeting chemoprevention where glucosinolates could help to slow the process of carcinogenesis through several molecular targets. It is also includes inhibition of carcinogen activation and induction of carcinogen detoxification, anti-inflammatory, anti-tumor cell proliferation, induction of apoptosis and inhibition of tumor angiogenesis. Finally, for synergistic effects of M. oleifera with other drugs and safety, essential for chemoprevention, it is important that it safe to be consumed by human body and works well. Although there is promising evidence about M. oleifera in chemoprevention, extensive research need to be done due to the expected rise of cancer in coming years and to gain more information about the mechanisms involved in M. oleifera influence, which could be a good source to inhibit several major mechanisms involved in cancer development.

• Korean Journal of Pharmacognosy
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• v.38 no.1
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• pp.62-66
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• 2007

Ethanol extract from Salvia miltiorrhiza (SME) was tested for breast cancer chemoprevention and metastasis by measuring the activites of cytochrome P45O 1A1, aromatase, ornithine decarboxylase (ODC), and matrix metalloproteinase (MMP)-9. SME significantly inhibited cytochrome P45O 1A1-mediated ethoxyresorufin O-deethylase (EROD) activity in a dose-dependent manner in a concentration range of 100${\sim}$l,200 ${\mu}g/ml$ (p<0.01). Microsomal aromatase (estrogen synthase) activity was suppressed 54.9%${\sim}$77.5% by the SME at concentration of 600${\sim}$l,200 ${\mu}g/ml$. ODC activity induced by 12-O-tet-radecanoylphorbol-13-acetate (TPA) was significantly reduced by the SME 900 and 1,200 ${\mu}g/ml$ (p<0.05) in MCF-7 breast cancer cells. In addition, SME (900 and 1,200 ${\mu}g/ml$) markedly inhibited MMP-9 activity, a key role in cancer metastasis. Therefore, SME is worth further investigation with respect to breast cancer chemoprevention or therapy.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.14
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• pp.5801-5805
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• 2015

As a cytosolic transcription factor, the aryl hydrocarbon (Ah) receptor is involved in several pathophysiological events leading to immunosuppression and cancer; hence antagonists of the Ah receptor may possess chemoprevention properties. It is known to modulate carcinogen-metabolising enzymes, for instance the CYP1 family of cytochromes P450 and quinone reductase, both important in the biotransformation of many chemical carcinogens via regulating phase I and phase II enzyme systems. Utilising chemically-activated luciferase expression (CALUX) assay it was revealed that intact glucosinolates, glucoraphanin and glucoerucin, isolated from Brassica oleracea L. var. acephala sabellica and Eruca sativa ripe seeds, respectively, are such antagonists. Both glucosinolates were poor ligands for the Ah receptor; however, they effectively antagonised activation of the receptor by the avid ligand benzo[a]pyrene. Indeed, intact glucosinolate glucoraphanin was a more potent antagonist to the receptor than glucoerucin. It can be concluded that both glucosinolates effectively act as antagonists for the Ah receptor, and this may contribute to their established chemoprevention potency.

• Journal of the Korean Society of Food Science and Nutrition
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• v.33 no.6
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• pp.946-950
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• 2004

Young radishes which were grown in the soil containing sulfur increased quinine reductase (QR) activity in Hepa 1clc cells and isothiocyanate-like compound analyzed by HPLC. QR inducing activity was maximum in young radishes grown with 1,818 g/㎥ sulfur and was decreased when the soil was neutralized with lime mortar in order to improve a recovery. These results have suggested that consumption of young radishes, especially grown in the presence of sulfur, would prevent from cancer incidence through inducing detoxification enzymes and could have therapeutic effects for chemoprevention.

• Journal of Digestive Cancer Research
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• v.11 no.1
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• pp.9-14
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• 2023

The prevalence of Barrett's esophagus is increasing in South Korea. Several strategies have been tried to prevent its progression to esophageal adenocarcinoma. It is questionable whether the strategies being tried in the West can be applied adequately in South Korea. However, despite the incidence of esophageal adenocarcinoma in the West, which is considerably higher than that in South Korea, the incidence of high-grade dysplasia/esophageal adenocarcinoma in population-based studies is as low as 0.23%/person-year. Therefore, in Korea, where the prevalence is lower than that, it is necessary to select high-risk groups more carefully for chemoprevention. The age of onset of gastroesophageal reflux disease-like symptoms at least once a week is related to the high-risk group rather than the presence or absence of chronic gastroesophageal reflux symptoms. The risk factors for esophageal adenocarcinoma include the patient's sex, age, smoking habit, and obesity. Proton pump inhibitors have a better preventive effect against esophageal adenocarcinoma compared to H2-receptor blockers, but their application to patients in Korea is limited due to the high number of individuals in need of treatment. Therefore, while considering the risk factors for the progression of esophageal adenocarcinoma, the administration of proton pump inhibitors should be considered for gastroesophageal reflux disease.