Cutting off the hormones that some cancers, especially breast and prostate, need to grow.
Hormonal therapy groups the treatments that cut off the hormones some cancers, especially breast and prostate, need to grow. It spans aromatase inhibitors, SERMs, SERDs including fulvestrant, oral SERDs and PROTAC degraders such as vepdegestrant, ovarian suppression, androgen deprivation and AR pathway inhibitors, combined with CDK4/6, PI3K/AKT or PARP inhibitors depending on the tumour. Technologies linking here include endocrine therapy, CDK4/6 inhibitors, androgen deprivation and AR pathway inhibitors, and fertility-sparing hormonal treatment of early endometrial cancer. Companies such as Sumitomo Pharma, ESSA Pharma, Eli Lilly and Menarini, the person Bernard Fisher, and ideas on primary endocrine therapy for the frail elderly and low-dose tamoxifen also point here.
Joint pain and stiffness are the main reason women stop aromatase-inhibitor tablets early. In a large randomised trial, twelve weeks of acupuncture reduced that pain more than sham needling or no treatment, and the benefit lasted after the sessions ended.
Hot flushes on tamoxifen or aromatase inhibitors are common and hormone replacement is off the table. Acupuncture reduced flushes in several randomised trials, in one about as well as the drug gabapentin and with fewer side effects, though sham-controlled results are mixed.
Androgen deprivation lowers testosterone or blocks its receptor, and has been the foundation of prostate cancer treatment since 1941 (Nobel Prize 1966).
Because hair thinning on endocrine therapy follows the pattern of androgenetic alopecia, the drugs used for that pattern are sometimes added. The evidence in cancer survivors cannot separate them from minoxidil, the one guideline that addresses spironolactone says not to use it routinely, and an expert panel advised against finasteride and dutasteride in breast cancer.
Hormone treatments, chemotherapy that stops the ovaries and long courses of steroids all thin the bones, fast enough to measure within a year. Some of it comes back when the treatment stops, and the drugs that prevent fracture while it is going on are well proven.
Pills that stop the cell-division engine, added to hormone therapy for the most common type of breast cancer.
Being overweight after breast cancer is linked with more recurrence, so a 3,000-woman trial tested a two-year telephone weight-loss programme. Women lost weight, but the trial did not clearly show fewer recurrences.
Pills that block or remove oestrogen signalling, the mainstay of treatment for hormone-driven breast cancer for 50 years.
Male survivors were about half as likely as their brothers to father a child, and the causes are specific: testicular radiotherapy above 7.5 gray, and high cumulative cyclophosphamide, ifosfamide, procarbazine or cisplatin. A young man with none of those was no less likely than his brother. Sperm banking works; tissue banking before puberty has produced no births.
Most female survivors treated with chemotherapy and no radiotherapy to the pelvis or brain can become pregnant: the large cohort that asked found chemotherapy-specific effects were few. The exceptions are busulfan, high-dose lomustine, pelvic and cranial radiotherapy and transplant conditioning. Before puberty, freezing ovarian tissue is the only option.
For young women with the earliest, low-grade endometrial cancers, progestin pills or a hormonal IUD can clear the cancer and allow pregnancy before a later hysterectomy.
Radiotherapy that reaches the pituitary stops the growth hormone signal, and radiotherapy to the spine stops the spine growing. In a Dutch cohort of 573 survivors, 8.9 per cent ended up more than two standard deviations below mean adult height, the largest losses after total body irradiation and craniospinal radiotherapy. Replacement restores some height.
Treatment can bring on menopause in a week rather than a decade, and the usual answer, hormone replacement, is often unavailable. The non-hormonal options now have real trial evidence: elinzanetant cut moderate to severe hot flushes by three and a half episodes a day more than placebo in women on endocrine therapy, and venlafaxine and oxybutynin also beat placebo.
Most hair grows back after chemotherapy, but a minority, especially after docetaxel, are left with thin hair, and tamoxifen and aromatase inhibitors cause gradual thinning. Minoxidil lotion or low-dose tablets, the same treatment used for pattern hair loss, improved regrowth in most patients in dermatology series and shortened regrowth time in an early randomised trial.
Oral drugs that destroy the oestrogen receptor rather than just blocking it, working even when the receptor has mutated to escape older hormone therapies.
For years women with breast cancer were told to avoid soy because it contains plant oestrogens. Large studies show moderate soy food intake is safe and may slightly reduce recurrence, including on tamoxifen.
Low testosterone is common after cancer treatment and is rarely looked for: it was present in 38.5 per cent of 491 men treated for testicular cancer, in about half of a separate cohort whether or not they had chemotherapy, and in a third of adults given cranial radiotherapy. Replacement is straightforward where it is indicated; men with a prostate cancer history are the uncertain group.
Radiotherapy near the base of the brain damages the gland that runs growth, puberty, the thyroid and the stress response, in that order of sensitivity. In 748 survivors treated with cranial radiotherapy, 46.5 per cent had growth hormone deficiency, 10.8 per cent sex hormone deficiency, 7.5 per cent thyroid deficiency and 4 per cent adrenal deficiency, and most of it had not been treated.
Vaginal dryness and painful sex after cancer treatment are common, lasting and under-treated. Low-dose vaginal oestrogen is the usual answer outside cancer, and for women on an aromatase inhibitor the guidance disagrees: American and British bodies read the same cohort studies differently. A reader deserves to be told that rather than given one confident answer.
The first randomised evidence that the order in which prostate cancer treatments are given changes how long they work, independently of which treatments they are. It is also a rare trial in which quality of life pointed one way and the primary endpoint pointed nowhere.
A demonstration that a drug that has stopped working can be made to work again by changing the environment the tumour has adapted to, rather than by changing the drug. It is the strongest clinical evidence in prostate cancer for treating resistance as something reversible.
The answer to a question three individual trials could not answer on their own, and the reason docetaxel with androgen deprivation became standard for metastatic hormone-sensitive disease. It also stopped a widely used bone drug being credited with a survival effect it does not have.
For women at raised risk, a 5-year course of tamoxifen offers long-lasting protection against the commonest kind of breast cancer. Uptake is low because of side effects and fear of rare serious harms; low-dose tamoxifen (TAM-01) is now being tested to improve the balance. It has not been shown to save lives.
The first predictive resistance biomarker in prostate cancer, and a mechanism rather than a correlation: a receptor with no ligand-binding domain cannot be blocked by a drug that binds the ligand-binding domain. It is also the origin of the case for androgen receptor degraders, which destroy the protein rather than blocking a site the protein no longer has.
The trial that made an androgen receptor inhibitor the usual first treatment for castration-resistant prostate cancer, and that delayed chemotherapy by a long margin for most men. Its effect sizes are why later trials in this setting are judged against a hazard ratio near 0.7 for survival.
One of the most cited trial reports Europe PMC returns for Abiraterone acetate in Prostate cancer, so it is a natural first reading for anyone weighing the idea it is linked from. The record was linked automatically by title and abstract; read the abstract above and the paper itself before relying on any figure.
A negative trial that was later overturned, and a standing argument for pooling individual trials rather than acting on the first one to report. It is also the reason the distinction between high-volume and low-volume metastatic disease is written into guidelines.