Abstract
MacMahon (1), Lemon (2) and Smith and Smith (3) have emphasized that abnormal ovarian function or steroid metabolism not modified by pregnancy in early life, may well be implicated in human breast cancer etiology. Wynder (4) and Dao (5) have pointed toward an etiological role for estrogen metabolism and nutritionally-conditioned alteration of estrogen metabolism in breast cancer, as also have Stocks (6) and Hems (7). The study of steroid excretion patterns in women with breast cancer (or prior to the onset of the disease) is further recommended by Bulbrookâs observations in the women of Guernsey (8). Furthermore, there is some evidence (9) that at least part of the genetic predisposition of certain mouse strains is the result of genetically-determined ovarian function. These are but a few of the reports, published in the past decade, that pertain to steroid hormone metabolism in mammary cancer. However, before reappraising the data in this field it may be helpful to summarize what is now known of the fate of steroid hormones in the mammal.
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Brooks, S.C. (1976). The Metabolism of Steroid Hormones in Breast Cancer: A Reappraisal. In: Menon, K.M.J., Reel, J.R. (eds) Steroid Hormone Action and Cancer. Current Topics in Molecular Endocrinology, vol 4. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-2601-4_4
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DOI: https://doi.org/10.1007/978-1-4684-2601-4_4
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