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논문 기본 정보

자료유형
학술저널
저자정보
저널정보
한국환경성돌연변이발암원학회 한국환경성돌연변이·발암원학회지 한국환경성돌연변이·발암원학회지 제22권 제4호
발행연도
2002.12
수록면
312 - 318 (7page)

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Dioxin represents a group of halogenated aromatic hydrocarbons of which 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is well known for its extremely toxic properties as well as ubiquitous presence in our environment and ecosystems. In order to better assess the carcinogenic mechanism of dioxin, we should utilize the reliable biomarkers that can precisely and correctly reflect multi-stage carcinogenesis. When MCF10A cells were exposed to TCDD (10 nM), expression of both CYP1A1 and CYP1B1 was induced in a time-related
manner. The expression as well as activity of ornithine decarboxylase was transiently induced by TCDD treatment. In contrast, the induction of COX-2 that is implicated in carcinogenesis as well as inflammation, was not induced by TCDD. In another study, gap-junctional intercellular communication (GJIC) was attenuated by TCDD treatment as revealed by the dye-transfer assay. Based on these findings, TCDD has both tumor initiating
and promoting potential in human breast epithelial cells in culture. Also, treatment of MCF10A cells with the carcinogen 7,12-dimethylbenz[a]anthracene plus TCDD resulted in malignant cell transformation as revealed by increased anchorage-independent growth of exposed cells. Additional studies may be necessary to
assess the effects of TCDD on multi-stage carcinogenesis in vivo.

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