• Microbiology and Biotechnology Letters
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• v.51 no.2
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• pp.135-146
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• 2023

Viral oncology is focused on understanding the relationship between cancer and viruses, which are known to play a role in the development of certain types of cancer. Approximately 15-20% of human cancers are believed to be caused by oncogenic viruses, and as a result, there is significant interest in understanding how these viruses contribute to cancer development. There are several viruses that have been linked to cancer, including human papillomavirus, hepatitis B and C virus, Epstein-Barr virus, human T-cell lymphotropic virus type 1, Kaposi's sarcoma-associated herpesvirus, and Merkel cell polyomavirus. Each of these viruses is associated with different types of cancer, and the mechanisms by which they contribute to cancer development are diverse. This article discusses these mechanisms as well as current and future strategies for preventing and treating virus-associated cancers with the goal of presenting a thorough review of the current state of knowledge in viral oncology and to highlight the importance of continued research in this field.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.3
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• pp.1219-1225
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• 2014

Epigallocatechin-3-gallate (EGCG) is the most abundant polyphenol molecule from green tea and is known to exhibit antioxidative as well as tumor suppressing activity. In order to examine EGCG tumor invasion and suppressing activity against adult T-cell leukemia (ATL), two HTLV-1 positive leukemia cells (HuT-102 and C91-PL) were treated with non-cytotoxic concentrations of EGCG for 2 and 4 days. Proliferation was significantly inhibited by 100 ${\mu}M$ at 4 days, with low cell lysis or cytotoxicity. HTLV-1 oncoprotein (Tax) expression in HuT-102 and C91-PL cells was inhibited by 25 ${\mu}M$ and 125 ${\mu}M$ respectively. The same concentrations of EGCG inhibited NF-kB nuclearization and stimulation of matrix metalloproteinase-9 (MMP-9) expression in both cell lines. These results indicate that EGCG can inhibit proliferation and reduce the invasive potential of HTLV-1-positive leukemia cells. It apparently exerted its effects by suppressing Tax expression, manifested by inhibiting the activation of NF-kB pathway and induction of MMP-9 transcription in HTLV-1 positive cells.

• The Korean Journal of Food And Nutrition
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• v.10 no.1
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• pp.74-81
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• 1997

In this study, we tried to figure out how phenol effects on cancer prevention, and for this purpose we focused on phenol effects on TBARS and the relationship between TBARS(thiobarbituric acid-reactive substances) and cancer. A protocol using a nutritionally adequate amino acid-based diet and a transgenic mouse model of neurofibromatosis was used to evaluate the effect of dietary phenols on body tissue oxidation and tumor onset. The mice carry the human T-lymphotropic virus type-1 transactivator(texl) gene and spontaneously develop externally visible tumors. Twenty-five male transgenic mice were systematically assigned into five groups, control group, 2 mmol, 4 mmol, 8 mmol catechin/kg diet groups and wine solid group. Mice in control group were without catechin, Mice in wine solid group received red wine 750 mL/kg diet, Mice were examined daily, and the age at which a first tumor appeared was recorded. Transgenic mice consuming catechin and wine solid were older when a first tumor appeared. No tumor was found in one mouse of 4 mmol catechin/kg diet and one mouse of 8 mmol catechin diet group. Levels of TBARS in brain and spleen of 8 mmol catechin group and wine solid group were significantly decreased as compared to the same tissue in control group. TBARS levels in tissues were significantly correlated with tumor onset. Results from this study suggest that dietary phenol effects on cancer prevention through tissue antioxidation in spite of different kinds of phenols.