Hormonal Etiology of Epithelial Ovarian Cancer, With a Hypothesis Concerning the Role of Androgens and Progesterone

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ID: 304808
1998
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Abstract
In the United States, ovarian cancer is the fourth most frequent cause of cancer death among women, following lung, breast, and colorectal cancers. Each year, approximately 26 000 women are diagnosed with ovarian cancer and 14 000 die of it. Germline mutations in BRCA1, BRCA2, or other genes have been implicated in a small fraction of cases. However, it has been suggested that, for the great majority of patients, the risk of epithelial ovarian cancer could be related to "incessant ovulation" (i.e., to the chronically repeated formation of stromal epithelial clefts and inclusion cysts following ovulation) or to some type of hormonal stimulation of ovarian epithelial cells, either on the surface of the ovary or within ovarian inclusion cysts, possibly mediated through excessive gonadotropin secretion. From the evidence to date, the relative importance of these two hypotheses— incessant ovulation and gonadotropin stimulation— cannot be distinguished. While either or both may play a role in the development of ovarian cancer, it appears that an additional major factor must also be involved. The purpose of this review is to evaluate evidence for and against the incessant ovulation and gonadotropin hypotheses, as well as to consider the possibility that risk of ovarian cancer may be increased by factors associated with excess androgenic stimulation of ovarian epithelial cells and may be decreased by factors related to greater progesterone stimulation. Many features of the evidence bearing on the pathophysiology of ovarian cancer appear to support a connection with androgens and progesterone.
Reference Key
openalex_W2137849078 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors H. A. Risch
Journal JNCI Journal of the National Cancer Institute
Year 1998
DOI
10.1093/jnci/90.23.1774
URL
Keywords Keywords not found

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