Progesterone and Glucocorticoid Receptor Modulator Mifepristone (RU-486) as Treatment for Advanced Cancers

Abstract

The fetal placental unit has paternal proteins which would normally result in immune rejection of fetus. Thus, to allow growth to 266 days, the mother must develop immunosuppressive proteins, cytokines, etc. to allow progression to a full-term baby. One of these essential immunomodulatory proteins is called the progesterone induced blocking factor (PIBF). Probably, the mechanism involved allowing the progesterone receptor antagonist mifepristone to cause termination of a pregnancy is by blocking the PIBF protein. There is good evidence that cancerous tumors borrow some of the same mechanisms as the fetus to escape immune surveillance, including the PIBF protein. Research data suggest that this protein is made and excreted by embryonic cells, mesenchymal cells, and trophoblast cells of the fetal placental unit to block the killing effect of natural killer cells and T-cells in the fetal microenvironment. Cancer cells do the same. Indeed, there is good evidence that mifepristone, a drug approved for pregnancy termination, can significantly improve length and quality of life in patients with various advanced cancers.