Hormone therapy for cancer, also called endocrine therapy or hormonal therapy, is treatment that slows or stops the growth of cancers whose cells depend on particular hormones. It is especially important in hormone-sensitive breast and prostate cancers. Rather than directly damaging DNA like many chemotherapy drugs, hormone therapy changes the hormonal environment on which certain tumour cells rely.
Some treatments reduce the amount of a hormone available to the cancer, while others block the hormone receptor or otherwise prevent the hormone from exerting its biological effect. Hormone therapy can be used to treat established cancer, reduce the risk of recurrence after initial treatment, shrink a tumour before surgery or radiotherapy, or control cancer that has returned or spread.
Hormone dependence arises because some cancer cells retain receptors and signalling systems that respond to hormones involved in normal tissue growth. In hormone-receptor-positive breast cancer, for example, oestrogen signalling can stimulate tumour-cell growth. In many prostate cancers, androgen signalling promotes growth and survival. Endocrine therapy interferes with these signals. The presence of a hormone receptor is therefore clinically important because it can indicate that hormonal manipulation may be useful.
Hormone receptor testing is generally performed on tumour tissue, and treatment decisions incorporate the cancer's receptor status, stage, subtype, previous treatments and other clinical factors. A hormone-sensitive tumour is not necessarily cured by endocrine therapy alone; rather, the treatment exploits a specific dependency of the malignant cells.
Hormone therapy can act through two broad mechanisms. One approach reduces the body's production of a hormone that the cancer requires. Another blocks the hormone from binding to or activating its receptor. For breast cancer, endocrine treatments can include drugs that interfere with oestrogen signalling or reduce oestrogen production, while prostate-cancer treatment commonly reduces androgen production or blocks androgen-receptor signalling. Surgical removal of hormone-producing organs, such as the ovaries or testicles, can also reduce hormone production and is a form of permanent endocrine suppression. The exact drug or procedure depends on the cancer, hormonal pathway involved, patient's circumstances and treatment objective.
Hormone therapy is often combined with other treatments because hormone-sensitive cancer can exist at different stages of disease. In early breast cancer, endocrine therapy may be given after surgery and other indicated local treatments to reduce the risk of recurrence. It can sometimes be used before surgery to shrink or control a tumour. In advanced breast or prostate cancer, endocrine treatment can suppress systemic tumour growth and relieve symptoms while maintaining cancer control for variable periods. It may be combined with surgery, radiotherapy, chemotherapy or targeted agents depending on the disease. The timing and combination are determined by tumour biology, previous treatment, stage and evidence for benefit rather than by hormone sensitivity alone.
Hormone therapy differs from hormone replacement therapy. Hormone replacement supplies hormones to compensate for inadequate physiological production, whereas cancer endocrine therapy deliberately reduces, blocks or alters hormone signalling to deprive hormone-dependent tumour cells of a growth stimulus. This distinction is particularly important because the effects of endocrine cancer treatment can resemble the physiological consequences of reduced sex-hormone activity. Depending on the treatment, patients may experience hot flushes, sweating, sexual or reproductive changes, changes in bone density, fatigue, mood or cognitive symptoms, weight changes and metabolic effects. The precise adverse effects vary substantially between drug classes and between individuals.
Hormone therapy is generally a systemic treatment because hormonal signals circulate throughout the body and endocrine medicines can act throughout the body. Oral tablets are common, while some treatments are administered by injection. Certain endocrine treatments require regular administration over months or years, particularly when the goal is to reduce recurrence after initial treatment. Surgical hormone suppression is less commonly used in some settings because medication can provide reversible suppression, although surgery remains an option in selected circumstances. Monitoring depends on the cancer and treatment and can include clinical examinations, imaging and disease-specific biomarkers. For prostate cancer, PSA levels are commonly followed, and a rising PSA during treatment can indicate that the cancer may no longer be responding adequately.
Hormone resistance is an important limitation. A cancer that initially depends strongly on a hormone pathway can adapt so that it continues growing despite hormonal suppression. Mechanisms can include changes in hormone receptors, amplification or mutation of receptor genes, activation of alternative growth pathways, increased local hormone production and selection of tumour cells that are less dependent on the original hormonal signal.
This explains why treatment may progress from one endocrine strategy to another or be combined with other systemic therapies. In prostate cancer, for example, advanced disease may eventually become resistant to androgen-deprivation strategies, requiring additional treatments directed at androgen signalling or other cancer pathways. Resistance therefore reflects cancer evolution rather than simply a failure of the patient to receive enough treatment.
Hormone therapy is an important example of treatment selected according to tumour biology. Its usefulness depends on whether the cancer actually uses the relevant hormonal pathway, which is why receptor and other pathological information are important. It can be highly effective in appropriately selected cancers because suppressing a major growth signal can control malignant cells without using conventional cytotoxic chemotherapy.
However, it is not appropriate for cancers that do not depend on the targeted hormone pathway, and it does not eliminate all tumour cells in every hormone-sensitive cancer. Current cancer care often integrates endocrine therapy with targeted medicines and other treatments to address both hormonal dependence and additional mechanisms of tumour growth. The central principle is to deprive hormone-dependent cancer cells of the signals they need to survive and proliferate, while balancing cancer control against the systemic effects of altering normal endocrine physiology.
