Estrogen dependency in uterine endometrial cancers involves complicated tumor biology. A transformed phenotype of uterine endometrial cancers is supported by estrogen-dependent oncogene (c-Ha-ras, c-fos and c-jun) expressions. The relative overexpression of estrogen receptor exon 5 splicing variant and the damaged expression of progesterone receptor A, which belong to a lack of estrogen dependency, are related to metastatic potential. The estrogen-related metastatic processes, detachment, invasion and angiogenesis in some uterine endometrial cancers can be inhibited by progestins.
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Fujimoto et al. (1998) studied this question.
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