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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Lack of an effect of dietary retinoids in chemical carcinogenesis of the mouse mammary gland: inverse relationship between mammary tumor cell anaplasia and retinoid efficacy.

Feeding of retinyl acetate (0.2 mM) or N-(4-hydroxyphenyl) retinamide (4-HPR) (1.0 mM) for 27 weeks to female BD2F1 mice previously treated with a series of gastric intubations of 7,12-dimethylbenzanthracene (DMBA), did not significantly affect the incidence of mammary tumors. In the retinyl acetate study, 75 retinyl acetate fed mice developed 31 mammary adenocarcinomas and 19 mammary adenoacanthomas (50 total mammary tumors) while 75 control mice developed 22 mammary adenocarcinomas and 20 mammary adenoacanthomas (42 total mammary tumors). In the 4-HPR study, 74 4-HPR fed mice developed 45 mammary adenocarcinomas and 41 mammary adenoacanthomas (86 total mammary tumors) while 74 control mice developed 29 mammary adenocarcinomas and 44 mammary adenoacanthomas (73 total mammary tumors). Retinoid treatments did not significantly affect body weight gains or mortality rates. These results provide evidence that carcinogen induced mouse mammary gland tumorigenesis in vivo is not influenced by hyperalimentation of dietary retinoids.[1]

References

  1. Lack of an effect of dietary retinoids in chemical carcinogenesis of the mouse mammary gland: inverse relationship between mammary tumor cell anaplasia and retinoid efficacy. Welsch, C.W., DeHoog, J.V., Moon, R.C. Carcinogenesis (1984) [Pubmed]
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