Carcinogenesis expression

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FIGURE 20.2 The involvement of RARE on apo-lO -lycopenoic acid-transactivated RARp expression. Upper panel Diagram of the RARp reporter vector with wild type and mutated R AREs. Lower panel HeLa cells transfected with the RARp reporter vector and an internal control vector were treated with 5 pmol/I. of apo-lO -lycopenoic acid or 1 pmol/L of all-trans retinoic acid for 24h. Luciferase activities were measured by dual-luciferase reporter system. Values are means of SEM of three replicate assays., statistically significantly different, as compared with control in the same group, P < 0.05. (Adapted from Lian, F. et al., Carcinogenesis, 28, 1567, 2007. With permission.)... 

Xing, N, Y Chen, SH Mitchell, and CYF Young. 2001. Quercetin inhibits the expression and function of the androgen receptor in LNCaP prostate cancer cells. Carcinogenesis 22(3) 409 414. 

Ponnamperuma, R.M., Shimizu, Y., Kirchhof, S.M., and De Luca, L.M. 2000. Beta-carotene fails to act as a tumor promoter, induces RAR expression, and prevents carcinoma formation in a two-stage model of skin carcinogenesis in male Senear mice. Nutr Cancer 37 82-88. 

Richardson FC et al. Dose responses in rat hepatic protein modification and expression following exposure to the rat he-patocarcinogen methapyrilene. Carcinogenesis 1994 15 325-329. 

Stegelmeier, B.L., N.A. Gillett, A.H. Rebar, and G. Kelly. 1991. The molecular progression of plutonium-239-induced rat lung carcinogenesis Ki-ras expression and activation. Molecul. Carcinogen. 4 43-51. 

Hayashi, S., et. al., Expression of Ah receptor (TCDD receptor) during human monocytic differentiation, Carcinogenesis. 16, 1403, 1995. 

The other way to express a relative dose in animals or humans is to do so in terms of body surface area. There are many reasons for believing that the surface area approach is more accurate for relating doses between species (Schmidt-Nielson, 1984), and especially between test animals and humans, but this is still a less common approach in safety assessment, although it is the currently accepted norm in several areas carcinogenesis and chemotherapy, for example. 

Regulation of programmed cell death (apoptosis) is not only important in normal cell development and homeostasis [1, 2], but also during the process of carcinogenesis [3], Apoptosis is suppressed in most cancer cells and induction of apoptosis is one cancer treatment strategy [4], There are many processes and factors that can be modulated to induce cancer cell apoptosis, such as regulation of factors involved in cell cycle arrest [5], protein kinase modulation [6], caspase family activation [7], and the balance in expression between Bcl-2 family members [8],... 

Vondracek M, Xi Z, Larson P, Baker V, Mace K, Pfeifer A, Tjalve H, Donato MT, Gomez-Lechon MJ, and Grafstrom C (2001) Cytochrome P450 expression and related metabolism in human buccal mucosa. Carcinogenesis 22 481-488. 

Crawford EL, Weaver DA, DeMuth JP, Jackson CM, Khuder SA, Frampton MW, Utell MJ, Thilly WG, Willey JC (1998) Measurement of cytochrome P450 2A6 and 2E1 gene expression in primary human bronchial epithelial cells. Carcinogenesis 19(10) 1867—1871. 

Carcinogenesis involves a complex series of genetic and biochemical events that enable transformed cells to proliferate, metastasize, migrate to secondary sites, and, sometimes, acquire resistance to chemotherapy. In Sect. 25.4.1, we will discuss how caveolin-1 expression correlates with cancerous growth, a potential mechanism of chemotherapy drug resistance, and how caveolae may be particularly exploited for cancer therapeutic strategies. 

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