ESR1 and neoplasm: In particular, it is unknown how apoptosis, estrogen and progesterone receptor and other pathways, which promote estrogen receptor (ER) and progesterone receptor (PR) expression and changes in tumor suppressor gene expression, increase expression of endogenous growth factors and receptors as well as growth factor and extracellular matrix secretion by stromal cells, leading to the occurrence of hormone-resistant EC [22, 23].