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Studies of the growth behaviour and hormone receptor contents of GR-mouse mammary tumours suggest that the hormone responsive tumours are mixed populations of hormone-dependent cells and autonomous cells. The hormone-dependent moiety of these tumours contains high levels of progesterone receptor and oestrogen receptor. The autonomous moiety has a low but probably significant oestrogen receptor level, and is practically devoid of progesterone receptor. Androgen receptor levels in both moieties are low. Endocrine ablation prevents growth of the hormone-dependent moiety of the tumours, but not of the autonomous moiety.

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Somatically generated mutations in the estrogen receptor (ER) have been found at the mRNA/cDNA level in human breast cancer biopsies and in established breast cancer cell lines. Aberrantly spliced ER mRNA causes the appearance of truncated or internally deleted ER protein forms. Studies on the functional activity of the ER variants in expression systems have revealed dominant-positive receptors that are transcriptionally active in the absence of estrogen, and dominant-negative receptors that are themselves transcriptionally inactive but that prevent the action of the normal receptor. The ER variants are believed to confer resistance to endocrine therapy in breast cancer patients. Abnormally spliced forms of ER, similar to those in breast cancer, have been reported in human meningiomas.