The name glucocorticoid (glucose + cortex + steroid) derives from its role in the regulation of the metabolism of glucose (stimulates gluco-genesis from liver), its synthesis in the adrenal cortex, and its steroidal structure. GCs cause their effects by binding to the glucocorticoid receptor. The activated glucocorticoid receptor complex, in turn, up-regulates the expression of anti-inflammatory proteins, down-regulate the expression of proinflammatory proteins. GCs are part of the feedback mechanism in the immune system which reduce certain aspects of immune function, such as reduction of inflammation. They are therefore used in medicine to treat diseases caused by an overactive immune system, such as allergies, asthma, autoimmune diseases, and sepsis. (2)

The sex hormone receptors, or sex steroid receptors, are a group of steroid hormone receptors that interact with the sex hormones, the androgens, estrogens, and progestogens. They include the (3):

• Androgen receptor - binds and is activated by androgens such as testosterone (3) 

• Estrogen receptor- binds and is activated by estrogens such as estradiol, estrone, and estriol (3).

Once activated by estrogen, the ER is able to translocate into the nucleus and bind to DNA to regulate the activity of different genes (i.e. it is a DNA-binding transcription factor).

Estrogen receptors are over-expressed in around 70% of breast cancer cases, referred to as "ER-positive". Two hypotheses have been proposed to explain why this causes tumorigenesis:

• First, binding of estrogen to the ER stimulates proliferation of mammary cells, with the resulting increase in cell division and DNA replication, leading to mutations. 

• Second, estrogen metabolism produces genotoxic waste.

• The result of both processes is disruption of cell cycle, apoptosis and DNA repair, and, therefore, tumour formation.

Endocrine therapy for breast cancer involves selective estrogen receptor modulators, such as tamoxifen, which behave as ER antagonists in breast tissue, or aromatase inhibitors, such as anastrozole. ER status is used to determine sensitivity of breast cancer lesions to tamoxifen and aromatase inhibitors (4)

• Progesterone receptor - binds and is activated by progestogens such as progesterone (3)