Proliferation, and carcinogenesis

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Cattley RC, Roberts RA. 2000. Peroxisome proliferators and carcinogenesis editorial perspectives. MutatRes 448 117-119. 

Williams GM, Iatropoulos MJ, Wang CX, Ali N, Rivenson A, et al. 1996. Diethylnitrosamine exposure-responses for DNA damage, centri lobular cytotoxicity, cell proliferation and carcinogenesis in rat liver exhibit some non-linearities. Carcinogenesis 17 2253—58... 

Blum, C.A. et al., F romotion versus suppression of rat colon carcinogenesis by chlorophyllin and chlorophyll Modnlation of apoptosis, cell proliferation, and 3-catenin/Tcf signaling, Mutat. Res., 523, 217, 2003. 

Palozza, P. Serini, S. Di Nicuolo, R et al. 2004a. Beta-carotene exacerbates DNA oxidative damage and modifies p53-related pathways of cell proliferation and apoptosis in cultured cells exposed to tobacco smoke condensate. Carcinogenesis 25 1315-1325. 

The control of cell numbers is regulated by cell proliferation, differentiation and apoptosis. Increased proliferation and/or decreased apoptosis result in neoplasia. In addition to inhibition of proliferation or induction of differentiation, the modulation of apoptosis can be employed for treatment for cancer. Several anticancer agents in use are potent inducers of apoptosis (Dive and Hickman, 1991 Fisher, 1994). Tumor promotion may result in decreased apoptosis. Because PKC activation by TPA induces carcinogenesis, it seems that PKC may be involved in apoptosis. There are many reports on the effects of PKC on apoptosis. However, the results are very controversial. Here an overview of these data is presented. 

Columbano A, Ledda-Columbano GM, Ennas MG, et al. 1990. Cell proliferation and promotion of rat liver carcinogenesis different effect of hepatic regeneration and mitogen induced hypoerplasia on the development of enzyme- altered foci. Carcinogenesis 11 4771-776. 

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Cattley, R.C. Glover, S.E. (1993) Elevated 8-hydroxydeoxyguanosine in hepatic DNA of rats following exposure to peroxisome proliferators relationship to carcinogenesis and nuclear localization. Carcinogenesis, 14, 2495-2499 Cattley, R.C., Conway, J.G Popp, J.A. (1987) Association of persistent proliferation and oxidative injury with hepatocarcinogenicity in female F-344 rats fed di(2-ethylhexyl)-phthalate for 2 years. Cancer Lett., 38, 15-22... 

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Clearly, the mechanism(s) underlying the carcinogenesis of acetylaminofluorene is very complex, and sometimes apparently conflicting and confusing data may reflect the fact that several different metabolic pathways are involved, which are more or less predominant in different tissues and in different animal species. It has been suggested, for instance, that the sulfate ester of N-hydroxyacetylaminofluorene is responsible for cytotoxicity and cell death, cell proliferation, and therefore promotion, whereas an N-hydroxyaminofluorene metabolite is responsible for initiation. Thus, both pathways would be necessary (Fig. 7.1). 

Hoivik DJ, Qualls CW, Mirabile RC, et al. Fibrates induce hepatic peroxisome and mitochondrial proliferation without overt evidence of cellular proliferation and oxidative stress in cynomologous monkeys. Carcinogenesis 2004 25 1757-1769. 

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