• Asian Pacific Journal of Cancer Prevention
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• v.14 no.2
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• pp.1155-1157
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• 2013

Cancer is a highly complex medical problem with ramifications for public health throughout the world. Most studies have mainly focused on change in the nuclei as being aetiologically responsible. Few have examined the relationship between the cytoplasm and cancer, despite the fact that research has indicated that the cytoplasmic environment is an important factor for cellular differentiation and that the genetic information provided by the nucleus is entirely dependent on this environment for its expression. Gene mutations may be the result, rather than the cause of carcinogenesis. We submit a new concept - "short base sequences" (50-500 bps, including DNA or RNA sequences) in the cytoplasm which could play an important role in carcinogenesis. This is a new theory to explain the origin of the cancer.

• Journal of Nutrition and Health
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• v.30 no.7
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• pp.803-812
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• 1997

The influences of dietary supplements of vitamin E on hepatocellular chemical carcinogenesis have been studied, Placental glutathione S-transferase(GST-P) positive foci area, antioxidant enzymes(superoxide dismutase(SOD), catalase, glutathione reductase, glutathione peroxidase, glutathione S-transferase(GST)), glucose 6-phosphatase(G6Pase) activities, and lipid peroxidation of mecrosomes(thiobarbituric acid reactive substances(TBARS) contents) were investigated. For is purpose , we used the murine chemical hepatocardinogenic procedure induced by modified Ito model, which consists of 200mg/kg body weight diethylinitrosamine (DEN) injection, 0.01% 2-acethlaminoflurene(2-AAF) feeding for 6 weeks, and partial hepatectomy on week 3. Weanling Sprague-Dawley male rats were fed pulverized Purina rat chow with 15, 000IU/kg diet vitamin E from initiation or promotion stages. We found that vitamin E supplement decreased the area of GST-P positive foci. Catalase, glutathione peroxidase, glutathione reductase. GST activities, and TBARS contents were decreased. On the other hand G6Pase activities were increased by vitamin E supplement. It seemed that vitamin E supplements helped endogenous defense systems against carcinogenesis by decreasing TBARS contents, $H_2O$$_2$ and organic peroxides. So, vitamin E seemed to protect cell from free radical damage in carcinogenesis. Anticarcinogenic effects of vitamin E were more effective at intiation that at promotion stage. These results suggest that vitamin E has suppressive effects on hepatocellular chemical carcinogenesis, probably through antioxidant effects against TBARS contents $H_2O$$_2$ and orgainc peroxides.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.27 no.2
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• pp.135-141
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• 2001

Recently, the consumption of soy products has been associated with low rates of hormone-dependent and hormone-independent cancers. Asians, who consume $20{\sim}50times$ more soy per capita than Americans, have lower incidence and death rates from breast and prostate cancer. Because soy contains the isoflavones genistein and daidzein (present as their glycosidic conjugates) at mg/g concentrations, it has been suggested that isoflavones might be acting as natural chemopreventive agents. During the 1980s several groups of investigators carried out experiments to test the effectiveness of soy in the diet in animal models of cancer. These studies reported a protective effect of soy; none showed that soy increased cancer risk. Genistein was shown to inhibit the growth of a wide variety of tumor cell types in culture. The purpose of this study was to evaluate the effects of genistein on the carcinogenesis induced by topical application of 0.5% 9, 10-dimethyl 1,2-benzanthracene (DMBA) on the hamster buccal pouch. 48 syrian hamsters were employed in this study, divided into experimental group and control. 24 animals (DMBA topical application group) had the right buccal pouch painted 3times weekly with 0.5% DMBA in mineral oil, 24 animals (genistein group) were supplied with 0.1mg genistein with DMBA topical application. 3 animals in the experimental group and control were sacrificed at serially each other week after experiments. Their buccal pouches were removed and routinely processed for microscopic examination. The results were as follows: 1. In DMBA topical application and genistein group, they showed carcinogenesis as time goes by experimental stage. 2. Genistein group was retarded in carcinogenesis related to the acanthosis, hyperkeratosis, epithelial dysplasia. 3. p53 immunohistochemical study showed that the p53 protein of genistein group was less expressed than that of the control group. Thus, it seems that genistein has chemopreventive effect on the carcinogenesis in the oral cavity, but further study is required to elucidate the anticancer mechanism of genistein.

• YAKHAK HOEJI
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• v.50 no.2
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• pp.84-92
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• 2006

The present study investigated an effect of arsenic trioxide on the urethane-induced lung carcinogenesis in mice. To understand its carcinogenesis, we examined proliferating cell nuclear antigen (PCNA), apoptotic index as well as cell cycle-related proteins (cyclin D1, p21, and p27). Urethane was injected intraperitoneally in ICR mice, and then they were sacrificed at 5, 15, or 25 weeks following treatment of arsenic trioxide. Arsenic trioxide was given with tap water at a concentration of 1 mg/l (low-dose) and 5mg/1 (high-dose) for 25 weeks. During the carcinogenesis, sequential histological changes from hyperplasia to adenomas, and ultimately to overt carcinomas were noted. The development of hyperplasias, adenomas, and carcinomas in the lung were slightly increased by the treatment of low-dose arsenic trioxide. However, there is no correlation between dose and tumor multiplicity. The administration of low-dose arsenic trioxide, significantly increased the tumor size. The proliferative index observed on 5 weeks after significantly increased. Cyclin D1 and p21 protein, cell cycle related proteins, were more significantly increased in hyperplasia and adenoma in low dose arsenic treated group than urethane alone group. The p27 protein expression did not show any significantly changes with arsenic treated or untreated group. Low dose exposure to arsenic trioxide resulted in increased expression of cyclin D1 and p21 protein. The present results indicate that low-dose treatment of arsenic trioxide, but not high dose of it, partly modulate the cellular proliferation, cyclin D1, and p21 protein expression, and that this effect may contribute to accelerated development of lung adenocarcinomas in urethane-induced mice.

• The Journal of Internal Korean Medicine
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• v.20 no.1
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• pp.133-142
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• 1999

To clarifiy the effects of Scolopendrae corpus(S-C) on turmor promotion in two-stage carcinogenesis in mice was investigated. In vivo system, S-C were seen to gave an inhibitory activity on TPA-induced mouse ear edema. In addition, the S-C were proved to have antitumor-promoting activity in two-stage mouse skin carcinogenesis induced by DMBA and two-stage mouse lung carcinogenesis induced by 4-NQO as a initiator plus TPA and glycerol as a promoter. Moreover, S-C significantly exhibited an cytolytic effect in $HepG_2$ cells and showed significant antitumor activity against Sarcoma-180 bearing mice by oral administration. These results suggest that S-C could be effective in adjuvant chemotherapy for human cancer.

• Korean Journal of Veterinary Pathology
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• v.2 no.2
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• pp.73-84
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• 1998

This study was carried out to investigate on the serum chemistry and the DNA ploidy changes in carcinogenesis of the rat liver and kidney. Sixty male Sprague-Dawley rats were divided into two groups. Group I was non-treated control. Group II was given initiators (2,2'-dihydroxy- di-N-propylnitrosamine, 0.1% in drinking water(d.w.) for 1 week and N-ethyl-N-hydroxy-ethylnitrosamine; 0.15% in d.w. for 1 week) and promoters (3'methyl-cholanthrene; 3'MC, l0mg/kg, intraperitoneally(i.p.) twice a week and DL-serine; 0.05% in d.w. for 5 weeks, from 3 to 8 weeks). All examinations were performed at 12 and 20 weeks RBC, HGBCp＜0.05) and PCVCp＜0.01) significantly decreased in Group II at 20 weeks. Activities of ALT, AST(p＜0.05) and GGT(p＜0.01) were significantly increased in Group II at 20 weeks. Flow cytometric analysis showed hepatocyte nuclei from normal livers were predominantly tetraploid(66~67%) and then diploid(28~30%). Most of hepatocyte nuclei from carcinogen-treated rats were diploid (52~68%) and less were tetraploid(28~42%). Neoplastic liver nodules and hepatocellular carcinoma contained almost exclusively diploid nuclei. Renal cell nuclei from normal kidney were predominantly diploid(88~93%), those from carcinogen-treated rats had an abnormal DNA-content peak(aneuploidy, 6-7%), near the tetraploidy area. These results suggest that diploidy may be an effective screening marker of the liver carcinogenesis. Aneuploidy may be an useful marker in assessment of the experimental renal carcinogenesis.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.28 no.2
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• pp.147-154
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• 2002

Genistein that is a component of soy has been reported to have a protective effect on the carcinogenesis of various tumors and to inhibit the growth of a wide variety of tumor cell in vitro. Angiogenesis is an essential process for the carcinogenesis, growth, invasion and metastasis of cancer and genistein has been suggested to act as natural anti-angiogenic agent. The purpose of this study was to evaluate the effects of genistein on the vascular endothelial growth factor (VEGF) expression in hamster buccal pouch oral carcinogenesis model induced by 9, 10-dimethyl 1,2-benzanthracene (DMBA). Experimental group that were supplied with 0.1mg/day genistein were sacrificed by time schedules and routinely processed for immunohistochemical examination of VEGF. In genistein treated group, carcinogenesis was retarded with respect to the acanthosis, hyperkeratosis, and epithelial dysplasia. Immunohistochemical study showed that the VEGF protein of genistein group was less expressed than that of the control group. (p<0.05) Thus, it is postulated that genistein has chemopreventive effect on the oral carcinogenesis, and this chemopreventive effect, at least partly, is originated from the anti-angiogenic effect of genistein

• Journal of Life Science
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• v.17 no.7 s.87
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• pp.1002-1018
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• 2007

Ever since the World Health Organization classified Helicobacter pylori as a class I carcinogen, a variety of discussions over the actual role of H. pylori infection in gastric carcinogenesis has existed. Although a majority of researches support the positive correlation between H. pylori infection and the development of gastric cancer, many aspects of this association are yet uncertain, and some data even suggest that there may be no correlation between H. pylori infection and gastric carcinogenesis. However, there are proofs indicating these reports underestimated the prevalence of H. pylori infection and therefore, the association of the infection and gastric adenocarcinoma. In this report, I reviewed the epidemiology of H. pylori and gastric cancer, evidence supporting and against the positive correlation of the infection and the disease, and the possible pathological role H. pylori infection may have in gastric carcinogenesis referring particular to published literature. As a conclusion, despite a few reports of a possible negative or no relationship between gastric cancer and H. pylori infection, I was able to find that H. pylori infection did have a pathological role in the development of gastric cancer.

• Environmental Mutagens and Carcinogens
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• v.25 no.1
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• pp.40-46
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• 2005

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) displays high toxicity in animals and has been implicated in human carcinogenesis. Although the mechanism of carcinogenesis by TCDD is unclear, it is considered to be a non-genotoxic compound and tumor promoter. In our experiment, we investigated the effects of TCDD on gene expression in mouse skin carcinogenesis. We used cDNA microarray to detect the differential gene expression in tumors induced in hairless mouse skin by MNNG plus TCDD protocol. We found that erb-2, c-ets2 and p27$^{kip1}$ were significantly up-regulated, but TNFR2, AKT-l, integrin $\beta$l, maspin, IGF-l, c-raf-l, Rb were significantly down-regulated, in tumor region, respectively. We also found that the expression of 53 genes involved in cen cycle, signal transduction, apoptosis, adhesion molecule, angiogenesis, and invasion, were changed two fold more, in tumor surrounding region. These data suggest that TCDD alters the expression of a large array of genes involved in apoptosis, cytokine production and angiogenesis in mouse skin carcinogenesis.

• Intestinal research
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• v.15 no.1
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• pp.75-82
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• 2017

Background/Aims: Cyclooxygenase-2 (COX-2), 15-hydroxyprostaglandin dehydrogenase (15-PGDH), and microsomal prostaglandin E synthase-1 (mPGEs-1) regulate prostaglandin $E_2$ ($PGE_2$) expression and are involved in colon carcinogenesis. We investigated the expression of $PGE_2$ and its regulating genes in sporadic human colon tumors and matched normal tissues. Methods: Twenty colonic adenomas and 27 colonic adenocarcinomas were evaluated. COX-2 and 15-PGDH expression was quantified by real-time polymerase chain reaction. The expression of $PGE_2$ and mPGEs-1 was measured using enzyme-linked immunosorbent assay and Western blotting, respectively. Results: The expression of COX-2, mPGEs-1, and $PGE_2$ did not differ between the adenomas and matched distant normal tissues. 15-PGDH expression was lower in adenomas than in the matched normal colonic tissues (P<0.001). In adenocarcinomas, mPGEs-1 and $PGE_2$ expression was significantly higher (P<0.001 and P=0.020, respectively), and COX-2 expression did not differ from that in normal tissues (P=0.207). 15-PGDH expression was significantly lower in the normal colonic mucosa from adenocarcinoma patients than in the normal mucosa from adenoma patients (P=0.018). Conclusions: Early inactivation of 15-PGDH, followed by activation of COX-2 and mPGEs-1, contributes to $PGE_2$ production, leading to colon carcinogenesis. 15-PGDH might be a novel candidate marker for early detection of field defects in colon carcinogenesis.