| Abstract: | The polypeptide hormone prolactin (PRL), ubiquitous and multifunctional in vertebrates, always interested biologists, was of restricted concern to clinicians and researched little compared to insulin and growth hormone. PRL in lactation initially aroused relatively little interest, but it rose when with ovarian steroids and chemical carcinogens, it was implicated in rodent mammary carcinoma. It declined when PRL suppression did not counter breast cancer. Meanwhile, long-known, estrogen-related cancers in the ovary and breast did not deter wide estrogen use for contraception and supplementation despite risk, and estrogen blockers and inhibitors have improved treatment and are on trial for prophylaxis, despite serious short and long term side-effects. Despite the great differences between steroid and polypeptide, research on PRL and breast cancer mirroring that on estrogens is now growing. This is mainly negative, much due to recent prospective research reporting minor rises in plasma levels as a basis, together with some recent laboratory research, for a hypothesis that PRL induces post-menopausal breast cancer. That view contradicts a reproductive biology that evolved to benefit women and offspring. Elevated PRL in pregnancy and probably that in lactation, reduce risk. Many exogenous chemical and physical PRL-stimulants also do not increase risk. It has not been shown that PRL increases risk of breast cancer and some older and recent cell and tissue data suggest it may be the key, two-sided, in human breast tissue homeostasis. Excessive disturbance of this is unlikely to originate in PRL itself. The natural biology of PRL, the reproductive woman's hormone par excellence, and research in various fields, suggest a positive potential in the PRL family for direct prevention and treatment of breast cancer, possibly greater than that in the estrogens. It is time to debate and research this. |
