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Alternatively, T can be elevated by the more risky use of anabolic steroids (AAS) or testosterone replacement therapy (TRT)or can be suppressed by prescription of a growth hormone (GH) agonist. All three modes of hormone suppression are known to have increased cancer risk when the treatment is used after the age of 50 years. T has both anti-androgens and estrogen action; it can exert its effects via many routes. It appears that T also can cause estrogenic activity via the binding of estrogens to the androgen receptor. A mechanism by which T binds these estrogens has not been established. This may have the potential to produce adverse side effects, including increased breast cancer risk. It was recently shown that estrogen receptor-activating antibodies (ARAs) were present in women with breast cancer. T binds to estrogen receptors to increase the risk of breast cancer; in this trial, the antibody antibodies were found in both the active patients and the control patients. The role of T in mammary cancer risk is unknown. A common way to increase risk of cancer in adults and young women is through low-grade inflammation (the primary cause of most cancers). Low-grade inflammation also occurs in cancers of the uterus and cervix. The presence of anti-inflammatory prostaglandins (PGs) in the cervix is a strong predictor of early pregnancy loss, and women with low-grade prostaglandins have increased risk. PGE2 is produced by large tumors, and it is produced primarily by carcinomas of the uterus and cervix. These tumors have the highest rate of survival among women with early pregnancy loss. PGs increase progestational pain, and low-grade prostaglandin production is associated with poor prognosis in women with cancer of the uterus and cervix. The use of anti-PG drugs (e.g. albuterol and phentermine) in the treatment of high-grade inflammation in pregnancy has shown to be associated with an increased risk of miscarriage, low birth weight, perinatal depression, abnormal fetal development, and premature delivery. Drugs that stimulate T production can have adverse adverse cardiovascular, neurodevelopmental, immunological, and metabolic effects. Such drugs include, benzodiazepine compounds (anti-anxiety drugs); antimalarial medications; radiological drugs; steroids; anti-inflammatory agents; antineoplastic drugs; anti-estrogens. Cancer Research UK, UK Similar articles: