Bradlow H L, Hershcopf R J, Martucci C P, Fishman J
Proc Natl Acad Sci U S A. 1985 Sep;82(18):6295-9. doi: 10.1073/pnas.82.18.6295.
In this report, we describe our findings on the relationship between estradiol 16 alpha-hydroxylation and mammary tumor incidence. A close correlation between the two has been demonstrated with 16-hydroxylation being elevated in strains with a high incidence of tumors, such as RIII and C3H, and low in strains with a low incidence of cancer, such as C57BL. The extent of reaction is highly reproducible and unaffected by age or presence of overt mammary tumors. Studies on the inheritance of estradiol 16 alpha-hydroxylase showed that it is inherited as an autosomal dominant and is not correlated with estradiol 2-hydroxylase or androgen and progestin 16 alpha-hydroxylases. In addition, the reaction was shown to be markedly enhanced by the presence of murine mammary tumor virus and diminished in the absence of the virus. These studies establish a relationship between genetics, hormonal factors, and murine mammary tumor virus, the three key factors in mammary tumorigenesis.
在本报告中，我们描述了关于雌二醇16α-羟基化与乳腺肿瘤发生率之间关系的研究结果。已证实二者密切相关，在肿瘤发生率高的品系（如RIII和C3H）中，16-羟基化水平升高，而在癌症发生率低的品系（如C57BL）中则较低。反应程度具有高度可重复性，且不受年龄或明显乳腺肿瘤存在与否的影响。关于雌二醇16α-羟化酶遗传的研究表明，它作为常染色体显性遗传，与雌二醇2-羟化酶或雄激素及孕激素16α-羟化酶无关。此外，该反应在鼠乳腺肿瘤病毒存在时显著增强，而在无病毒时减弱。这些研究确立了遗传学、激素因素和鼠乳腺肿瘤病毒这三个乳腺肿瘤发生的关键因素之间的关系。
