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The reduced expression of death receptors and elevated levels of c-FLIP in CSCs impede the activation of the death receptor pathway and block apoptosis progression [176, 177]

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Recognizing the likely role that progesterone plays in fibroids and the ability of estrogen to boost progesterone receptor expression, research is now focusing on SPRMs (selective progesterone receptor modulators), sometimes referred to as antiprogestins, that alter PR functionand thus cellular responsivity to progesterone

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