• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.188-188
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• 2003

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a prototype of halogenated aromatic hydrocarbons, is a persistent environmental contaminant and one of the most powerful tumor promoters. The molecular mechanism underlying induction of tumor promotion by TCDD has not been elucidated.(omitted)

• Maxillofacial Plastic and Reconstructive Surgery
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• v.30 no.5
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• pp.465-472
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• 2008

We experienced a rare case of oral squamous cell carcinoma arisen from gingival tissues overlying prolonged chronic osteomyelitis of the mandible. A 66 years old man complained of unhealed extraction sockets of left mandibular second premolar and first molar, and showed extensive leukoplakia in the gingival tissues of the same area. The inflammation of the socket granuloma became severe and extended into adjacent mandibular proper, resulted in diffuse suppurative chronic osteomyelitis of mandibular body, exhibiting irregular osteolytic changes of mandibular trabecular patterns in mottled radiolucent appearance. The leukoplakia was initially diagnosed under microscope, and the involved gingival tissues were radically removed. Thereafter, the gingival soft tissue inflammation involving the mandibular osteomyelitis was hardly healed for two years. During the period of repeated surgical treatments for the inflamed lesion, nine biopsies were taken sequentially. Until the eighth biopsy, there consistently showed the suppurative osteomyelitis with ingrowing gingival tissues into the bony inflammatory lesion. The gingival epithelium showed the features of leukoplakia but no evidence of malignant changes. However, the ninth biopsy, taken about 2 years after initial diagnosis, showed the early carcinomatous changes of the gingival epithelium. The neoplastic epithelial cells were relatively well differentiated with many keratin pearls, and infiltrated only into underlying connective tissues. So, we presumed that the present case of squamous cell carcinoma was caused by the persistent inflammatory condition of the mandibular osteomyelitis, and also suggest that the leukoplakia should be carefully removed in the beginning to prevent the neoplatic promotion of the chronic inflammation.

• Environmental Mutagens and Carcinogens
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• v.25 no.2
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• pp.66-70
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• 2005

Telomerase, a specialized RNA-directed DNA polymerase that extends telomeres of eukaryotic chromosomes, has activity in most malignant tumors and provides a mechanism for the unlimited potential for division of neoplastic cells. Although telomerase is known to be a regulated enzyme, the factors and mechanisms involved in telomerase regulation are not well understood. In the present study, we compared the effect of 12-O­tetradecanoyl-phorbol-13-acetate (TPA) and non-phorbol ester tumor promoters such as okadaic acid, anthralin and benzoyl peroxide on the expression of telomerase in the mouse skin carcinogenesis system, a well characterized model for studying pre-malignant and malignant progression. We found that most early papillomas harvested after 10 weeks of TPA promotion showed telomerase activity. Other papillomas harvested after 10 weeks of okadaic acid, anthralin and benzoyl peroxide promotion and after single treatment of DMBA only also showed telomerase activity, respectively. On the other hand, normal and all skins surrounded by papillomas harvested after 10 weeks of these promoters has no telomerase activity. Taken together these results, there appears to be no clear association between the level of telomerase activity and protein phosphorylation in mouse skin papillomas and telomerase may be useful as bio-markers in early detection of tumors.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.9
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• pp.4815-4822
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• 2012

Invasion and metastasis are the major causes of cancer-related death. Pharmacological or therapeutic interventions such as chemoprevention of the progression stages of neoplastic development could result in substantial reduction in the incidence of cancer mortality. (-)-Epigallocatechin-3-gallate (EGCG), a promising chemopreventive agent, has attracted extensive interest for cancer therapy utilizing its antioxidant, anti-proliferative and inhibitory effects on angiogenesis and tumor cell invasion. In this study, we assessed the influence of EGCG on the proliferative potential of HeLa cells by cell viability assay and authenticated the results by nuclear morphological examination, DNA laddering assay and cell cycle analysis. Further we analyzed the anti-invasive properties of EGCG by wound migration assay and gene expression of MMP-9 and TIMP-1 in HeLa cells. Our results indicated that EGCG induced growth inhibition of HeLa cells in a dose- and time-dependent manner. It was observed that cell death mediated by EGCG was through apoptosis. Interestingly, EGCG effectively inhibited invasion and migration of HeLa cells and modulated the expression of related genes (MMP-9 and TIMP-1). These results indicate that EGCG may effectively suppress promotion and progression stages of cervical cancer development.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.15
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• pp.6439-6444
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• 2015

Background: In India smokeless tobacco users account for 25.9% of total tobacco use, Gutkha being the most common form. This study evaluated the association between serum lipid profile and Gutkha use as an early diagnostic and/or prognostic indicator for oral submucous fibrosis (OSMF) and oral cancer (Oral Ca) in non-smokers and non-alcohol consumers. Materials and Methods: A total of 163 participants were recruited from two sites in India. Participants were divided into four groups: individuals without any Gutkha chewing habit and without any oral lesions (control group), individuals with Gutkha chewing habit but without any oral lesions (GWL), patients with a confirmed clinical diagnosis of OSMF, and patients with a confirmed diagnosis of Oral Ca. Mixed linear modelling (MLM) was conducted to detect the change in mean serum lipid levels among four groups. Results: The sample consisted of 69% males and 31% females. Results of MLM show an inverse relationship between serum lipid levels in OSMF, and Oral Ca groups when compared to the control group. Conclusions: The results of our study demonstrated that GWL, OSMF and Oral Ca patients had lower serum lipid levels. Low serum lipid levels could be an indicator of initial neoplastic changes in oral cancer.

• Toxicological Research
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• v.14 no.4
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• pp.475-481
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• 1998

This study was performed to investigate the modifying effect of the general (GPA) and the fermented pilose antler (FPA) on experimental hepatocarcinogenesis and Natural Killer cell activity in rats. Specific pathogen free, 5-week male Sprague-Dawley rats were divided into four groups. To induce hepatocarcinogenesis, diethylnitrosamine (DEN, 200 mg/kg, i.p.) was used as a tumor initiator and was given in a single dose at experimental onset. All rats were given a partial hepatectomy (PH) at 3 weeks after experimental onset. Sodium phenobarbital (PB, 0.05% in diet), GPA (0.075% in diet) and FPA (0. 075% in diet) were given from 2 to 8 weeks. Group I of the initiation control group was only given DEN. As initiation-promotion group, Group II was given DEN and then PB. Group III and IV were given DEN-PB-GPA and DEN-PB-FPA, respectively. In hematological analysis, as compared with Group I. the number of white blood cells were significantly increased in the GPA (p<0.01) and the FPA treated group (p<0.05), respectively. Natural killer (NK) cell activity by flow cytometer (FCM) analysis was higher in group of treated with the GPA (35%) than that of the FPA (27.5%), but not significant. Result of the immunohistochemical staining of the glutathione S-transferase placental form (GST-p) indicated that the number of and area of the pre-neoplastic lesions was not significantly changed in Group III and IV compared Group II, respectively. In conclusion, the GPA and the FPA treatment significantly increased the number od WBC in peripheral blood, but the enhancing NK activity and the modifying effect on the experimental hepatocarcinogenesis were not observed.

• Clinical and Experimental Pediatrics
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• v.52 no.2
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• pp.213-219
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• 2009

Purpose:Iron is a critical nutritional element that is essential for a variety of important biological processes, including cell growth and differentiation, electron transfer reactions, and oxygen transport, activation, and detoxification. Iron is also required for neoplastic cell growth due to its catalytic effects on the formation of hydroxyl radicals, suppression of host defense cell activities, and promotion of cancer cell multiplication. Chronic transfusion-dependent patients receiving chemotherapy may have iron overload, which requires iron-chelating therapy. We performed this study to demonstrate whether the iron chelating agent deferoxamine induces apoptosis in Saos-2 osteosarcoma cells, and to investigate the underlying apoptotic mechanism. Methods:To analyze the apoptotic effects of an iron chelator, cultured Saos-2 cells were treated with deferoxamine. We analyzed cell survival by trypan blue and crystal violet analysis, apoptosis by nuclear condensation, DNA fragmentation, and cell cycle analysis, and the expression of apoptotic related proteins by Western immunoblot analysis. Results:Deferoxamine inhibited the growth of Saos-2 cell in a time- and dose-dependent manner. The major mechanism for growth inhibition with the deferoxamine treatment was by the induction of apoptosis, which was supported by nuclear staining, DNA fragmentation analysis, and flow cytometric analysis. Furthermore, bcl-2 expression decreased, while bax, caspase-3, caspase-9, and PARP expression increased in Saos-2 cells treated with deferoxamine. Conclusion:These results demonstrated that the iron chelating agent deferoxamine induced growth inhibition and mitochondrial-dependent apoptosis in osteosarcoma Saos-2 cells, suggesting that iron chelating agents used in controlling neoplastic cell fate can be potentially developed as an adjuvant agent enhancing the anti-tumor effect for the treatment of osteosarcoma.

• The Journal of the Convergence on Culture Technology
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• v.5 no.4
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• pp.431-438
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• 2019

The present study was designed to investigate the chemopreventive effects of supercritical heat radish extracts with anti-constipation acitivity in loperamide-treated rats, on 1,2-dimethylhydrazine(DMH)-induced aberrant crypt foci(ACF) in rat colonic mucosa. Supercritical heat radish extracts was administered in the drinking water(3.2 mg/ml) during the initiation (for 12 weeks) or postinitiation phase(for 9 weeks) of DMH-induced carcicogenesis. Supercritical heat radish extracts coupled with DMH for 12 weeks decreased significantly total number of aberrant crypts(pre-neoplastic lesions) and the number of ACF to 35% and 30%, respectively. The number of ACF with more than four aberrant crypts (crypt multiplicity) was significantly reduced in the colon of rats receiving Supercritical heat radish extracts for 12 weeks. In the group receiving Supercritical heat radish extracts after post-initiation for 9 weeks, only the number of ACF with ${\geq}4$ abberant crypts significantly decreased. Supercritical heat radish extracts, given alone for 12 weeks, did not induced the development of ACF. These results indicate that Supercritical heat radish extracts possess chemopreventive effects on chemically induced rat colon carcinogenesis.