Cancer Prevention Research Center

Seongnam, South Korea

Cancer Prevention Research Center

Seongnam, South Korea

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Lee S.H.,CHA Medical University | Park J.M.,Cancer Prevention Research Center | Han Y.M.,Cancer Prevention Research Center | Ko W.J.,CHA Medical University | Hahm K.B.,CHA Medical University
The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi | Year: 2015

As a commensal or a pathogen, Helicobacter pylori can change the balance of a complex interaction that exists among gastric epithelial cells, microbes, and their environment. Therefore, unraveling this complex relationship of these mixtures can be expected to help prevent cancer as well as troublesome unmet medical needs of H. pylori infection. Though gastric carcinogenesis is a multi-step process, precancerous lesion can be reversible in the early phase of mucosal damage before reaching the stage of no return. However, biomarkers to predict rejuvenation of precancerous atrophic gastritis have not been identified yet and gastric cancer prevention is still regarded as an impregnable fortress. However, when we take the journey from H. pylori-associated gastritis to gastric cancer, it provides us with the clue for prevention since there are two main preventive strategies: eradication and anti-inflammation. The evidence supporting the former strategy is now ongoing in Japan through a nation-wide effort to eradicate H. pylori in patients with chronic gastritis, but suboptimal apprehension to increasing H. pylori resistance to antibiotics and patient non-compliance still exists. The latter strategy has been continued in the author'sresearch center under siTRP (short-term intervention to revert premalignant lesion) strategy. By focusing on the role of inflammation in the development of H. pylori-associated gastric carcinogenesis, this review is intended to explain the connection between inflammation and gastric cancer. Strategies on H. pylori eradication, removal of inflammation, and reverting preneoplastic lesion will also be introduced. In the end, we expect to be able to prevent gastric cancer by take a detour from the unpleasant journey, i.e. from H. pylori-associated gastritis to gastric cancer.


Lee S.,Cancer Prevention Research Center | Park J.-M.,Cancer Prevention Research Center | Jeong M.,Cancer Prevention Research Center | Han Y.-M.,Cancer Prevention Research Center | And 5 more authors.
Pancreatology | Year: 2016

Aim: Effective therapy to treat acute pancreatitis (AP) or to prevent its recurrence/complication is still not available. Based on previous results that suggest that: i) hydrogen sulfide (H2S) levels were significantly increased in pancreatitis and gastritis and ii) Korean red ginseng (KRG) efficiently attenuated Helicobacter pylori-associated gastritis through the suppressive actions of H2S, we hypothesized that KRG can ameliorate experimental pancreatitis through suppression of H2S generation. Methods: C57BL/6 mice were pre-administered KRG and then subjected to cerulein injection or pancreatic duct ligation (PDL) to induce pancreatitis. Blood and pancreas tissues were collected and processed to measure serum levels of amylase, lipase and myeloperoxidase and the concentration of H2S and the levels of various inflammatory cytokine in pancreatic tissues of mice with induced AP. Results: KRG significantly inhibited NaHS-induced COX-2 and TNF-α mRNA in pancreatic cells, but dl-propargylglycine did not. KRG ameliorated cerulein-induced edematous pancreatitis accompanied with significant inactivation of NF-κB and JNK in pancreatic tissues of C57BL/6 mice (p < 0.001) and also significantly ameliorated PDL-induced necrotizing pancreatitis (p<0.01); in both conditions, the significant suppression of H2S resulting from KRG pretreatment afforded rescuing outcomes. Along with suppressed levels of H2S consequent to depressed expressions of CBS and CSE mRNA, KRG administration efficiently decreased the serum level of amylase, lipase, and myeloperoxidase and the expression of inflammatory cytokines in animal models of mild or severe AP. Conclusions: These results provide evidence for the preventive and therapeutic roles of KRG against AP mediated by H2S suppression. © 2016 IAP and EPC.


PubMed | CHA Medical University and Cancer Prevention Research Center
Type: Journal Article | Journal: The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi | Year: 2015

As a commensal or a pathogen, Helicobacter pylori can change the balance of a complex interaction that exists among gastric epithelial cells, microbes, and their environment. Therefore, unraveling this complex relationship of these mixtures can be expected to help prevent cancer as well as troublesome unmet medical needs of H. pylori infection. Though gastric carcinogenesis is a multi-step process, precancerous lesion can be reversible in the early phase of mucosal damage before reaching the stage of no return. However, biomarkers to predict rejuvenation of precancerous atrophic gastritis have not been identified yet and gastric cancer prevention is still regarded as an impregnable fortress. However, when we take the journey from H. pylori-associated gastritis to gastric cancer, it provides us with the clue for prevention since there are two main preventive strategies: eradication and anti-inflammation. The evidence supporting the former strategy is now ongoing in Japan through a nation-wide effort to eradicate H. pylori in patients with chronic gastritis, but suboptimal apprehension to increasing H. pylori resistance to antibiotics and patient non-compliance still exists. The latter strategy has been continued in the authorsresearch center under siTRP (short-term intervention to revert premalignant lesion) strategy. By focusing on the role of inflammation in the development of H. pylori-associated gastric carcinogenesis, this review is intended to explain the connection between inflammation and gastric cancer. Strategies on H. pylori eradication, removal of inflammation, and reverting preneoplastic lesion will also be introduced. In the end, we expect to be able to prevent gastric cancer by take a detour from the unpleasant journey, i.e. from H. pylori-associated gastritis to gastric cancer.


PubMed | CHA Medical University and Cancer Prevention Research Center
Type: Journal Article | Journal: Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] | Year: 2016

Effective therapy to treat acute pancreatitis (AP) or to prevent its recurrence/complication is still not available. Based on previous results that suggest that: i) hydrogen sulfide (H2S) levels were significantly increased in pancreatitis and gastritis and ii) Korean red ginseng (KRG) efficiently attenuated Helicobacter pylori-associated gastritis through the suppressive actions of H2S, we hypothesized that KRG can ameliorate experimental pancreatitis through suppression of H2S generation.C57BL/6 mice were pre-administered KRG and then subjected to cerulein injection or pancreatic duct ligation (PDL) to induce pancreatitis. Blood and pancreas tissues were collected and processed to measure serum levels of amylase, lipase and myeloperoxidase and the concentration of H2S and the levels of various inflammatory cytokine in pancreatic tissues of mice with induced AP.KRG significantly inhibited NaHS-induced COX-2 and TNF- mRNA in pancreatic cells, but dl-propargylglycine did not. KRG ameliorated cerulein-induced edematous pancreatitis accompanied with significant inactivation of NF-B and JNK in pancreatic tissues of C57BL/6 mice (p<0.001) and also significantly ameliorated PDL-induced necrotizing pancreatitis (p<0.01); in both conditions, the significant suppression of H2S resulting from KRG pretreatment afforded rescuing outcomes. Along with suppressed levels of H2S consequent to depressed expressions of CBS and CSE mRNA, KRG administration efficiently decreased the serum level of amylase, lipase, and myeloperoxidase and the expression of inflammatory cytokines in animal models of mild or severe AP.These results provide evidence for the preventive and therapeutic roles of KRG against AP mediated by H2S suppression.


Santiago-Rivas M.,University of Rhode Island | Velicer W.F.,Cancer Prevention Research Center | Redding C.A.,Cancer Prevention Research Center | Prochaska J.O.,Cancer Prevention Research Center | Paiva A.L.,University of Rhode Island
Psychology, Health and Medicine | Year: 2012

The aim of this study is to identify replicable cluster subtypes within the precontemplation stage of change for sun protection. Secondary data analysis of baseline data from a sample of participants in a home-based expert system intervention was performed. Three random samples were selected from participants in the precontemplation stage (N=570). Cluster analyses were performed using the scales of pros, cons, and self-efficacy. Interpretability of pattern, pseudo F-test, and dendograms were used to determine the number of clusters. A four-cluster solution replicated across subsamples. Significant differences between clusters on the nine processes of change and on behavioral measures were found. Cluster solutions were robust, interpretable and with good initial external validity. They replicated patterns found for other behaviors, demonstrating long-term predictability and providing basis for tailored interventions. © 2012 Copyright Taylor and Francis Group, LLC.


PubMed | Cancer Prevention Research Center, Gachon University and Harvard University
Type: | Journal: Scientific reports | Year: 2016

Non-steroidal anti-inflammatory drugs (NSAIDs) damage the gastrointestinal (GI) epithelial cell membranes by inducing several signals through lipid raft organization after membrane incorporation, whereas -3 polyunsaturated fatty acids (PUFAs) relieve inflammation, reduce oxidative stress, and provide cytoprotection, consequent to lipid raft disorganization. Therefore, we hypothesized that -3 PUFAs can protect the GI from NSAID-induced damages by initiating the gatekeeper action of cell membranes, subsequent to anti-inflammatory and anti-oxidative actions. Administration of indomethacin (IND) leads to the formation of lipid rafts and activation of caveolin-1; however, no such observations were made upon co-administration of eicosapentaenoic acid (EPA) and IND. In addition, the EPA-induced lipid raft disorganization, caveolin-1 inactivation, and cellular cytotoxicity were inhibited when target cells were knocked-out using G-protein coupled receptor 120 (GPR 120). EPA significantly attenuated IND-induced oxidative damage and apoptosis. IND administration induced significant ulceration, bleeding, and oedema in the stomach or small intestine of wild-type (WT) mice; however, such severe damages to the GI significantly decreased in fat-1 transgenic (TG) mice (P<0.001), which exhibited decreased cyclooxygenase-2 expression and apoptosis, decreased interleukin-1 and FAS concentrations, and increased heme oxygenase-1 concentration. Our study indicates that the gatekeeper function of -3 PUFAs improves GI safety when administered with NSAID.


Han Y.-M.,Cancer Prevention Research Center | Park J.-M.,Cancer Prevention Research Center | Kangwan N.,Cancer Prevention Research Center | Jeong M.,Cancer Prevention Research Center | And 5 more authors.
Journal of Physiology and Pharmacology | Year: 2015

Gastrin is the main hormone stimulating gastric acid secretion, but it exerts proliferative and anti-apoptotic actions on various cancer cell types, in addition to its well-known trophic effect on enterochromaffin-like cells. As treatment with proton pump inhibitors (PPIs) increases the biosynthesis and secretion of gastrin, it has been postulated that treatment with PPIs could increase the risk of cancer, especially in Barrett’s esophagus, gastric carcinoids, and colorectal cancer (CRC). Some tumors produce gastrin of their own, which can act in an autocrine manner to promote tumor growth. In addition, gastrin is known to foster the tumor microenvironment. However, in spite of these potentially increased cancer risks due to PPI-induced hypergastrinemia, prospective, large-scale cohort studies did not show an increase in CRC prevalence. The question as to why the long-term use of PPIs was not associated with an increased cancer risk of CRC might be answered by the fact that the PPIs antagonized the trophic effects of hypergastrinemia. Furthermore, the blockade of proton pumps or potassium channels in cancer cells could limit the abnormal glycolytic energy metabolism of cancer cells. Apart from their suppressive effect on gastric acids, PPIs exert an anti-tumor effect through the selective induction of apoptosis as well as an anti-inflammatory effect, and they protect cells from developing chemo- or radiotherapeutic resistance. Moreover, the anti-carcinogenic actions of PPIs were augmented with PPI-induced hypergastrinemia. Together with their potential targeted killing of cancer stem cells, these effects demonstrate their potential anti-cancer actions. © 2015, Polish Physiological Society. All rights reserved.


PubMed | Cancer Prevention Research Center
Type: Journal Article | Journal: Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences | Year: 2013

Considering the limitations of current pathologic methods in distinguishing two subtypes of hydatidiform mole and non-molar pregnancy, the utility of immunohistochemical markers in this regards and the importance of differentiating of mentioned pathologic patterns, in this study the expression of P63 in patients with complete hydatidiform mole (CHM), partial hydatidiform mole (PHM) and non-molar pregnancy was determined.In this study, formalin-fixed and paraffin-embedded tissues of 61 patients with definitive pathologic diagnosis of CHM, PHM and non-molar pregnancy retrieved. Diagnoses were based on the study of hematoxylin and eosin stained slides. Sections from all samples were stained for P63 marker using immunohistochemistry method. The nuclear immune reactivity of P63 marker in the three pathologic groups was determined by two pathologists.P63 immune-staining was used to evaluate 20, 26 and 15 non-molar pregnancy, CHM and PHM cases, respectively. Mean SD of P63 nuclear immune-staining in molar pregnancy (CHM and PHM) and non-molar pregnancy were 32.4 17.4 and 18.9 17.2, respectively (P = 0.006). The means were significantly different between non-molar pregnancy and PHM (P < 0.000), CHM and PHM (P = 0.02) and non-molar pregnancy and CHM (P = 0.04).Considering the findings of the current study, though the nuclear immunoreactivity of P63 was higher in molar than non-molar pregnancy and in PHM than CHM, but using this marker alone is not suitable as a diagnostic test due to its low sensitivity and specificity. It could be used as adjuvant test in conflict cases. It is recommended to evaluate the role of other immunohistochemical markers like Ki-67 in this regard.


PubMed | Cancer Prevention Research Center
Type: Journal Article | Journal: Journal of physiology and pharmacology : an official journal of the Polish Physiological Society | Year: 2015

Gastrin is the main hormone stimulating gastric acid secretion, but it exerts proliferative and anti-apoptotic actions on various cancer cell types, in addition to its well-known trophic effect on enterochromaffin-like cells. As treatment with proton pump inhibitors (PPIs) increases the biosynthesis and secretion of gastrin, it has been postulated that treatment with PPIs could increase the risk of cancer, especially in Barretts esophagus, gastric carcinoids, and colorectal cancer (CRC). Some tumors produce gastrin of their own, which can act in an autocrine manner to promote tumor growth. In addition, gastrin is known to foster the tumor microenvironment. However, in spite of these potentially increased cancer risks due to PPI-induced hypergastrinemia, prospective, large-scale cohort studies did not show an increase in CRC prevalence. The question as to why the long-term use of PPIs was not associated with an increased cancer risk of CRC might be answered by the fact that the PPIs antagonized the trophic effects of hypergastrinemia. Furthermore, the blockade of proton pumps or potassium channels in cancer cells could limit the abnormal glycolytic energy metabolism of cancer cells. Apart from their suppressive effect on gastric acids, PPIs exert an anti-tumor effect through the selective induction of apoptosis as well as an anti-inflammatory effect, and they protect cells from developing chemo- or radiotherapeutic resistance. Moreover, the anti-carcinogenic actions of PPIs were augmented with PPI-induced hypergastrinemia. Together with their potential targeted killing of cancer stem cells, these effects demonstrate their potential anti-cancer actions.

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