<b>Conclusions:</b> For premenopausal women with ER-positive cancer who have completed adjuvant tamoxifen, another 5 years of tamoxifen is the preferable extended endocrine strategy.
Estrogen receptor alpha (ERα) plays a pivotal role in hormone-dependent cancer development and the status of ERα is used for designing treatment strategy and for prognosis.
Estrogen receptor α in cancer-associated fibroblasts suppresses prostate cancer invasion via modulation of thrombospondin 2 and matrix metalloproteinase 3.
Estrogen receptor (ER) antagonist, tamoxifen has been universally used for the treatment of the ER-positive breast cancer; however, the inevitable emergence of resistance to tamoxifen obstructs the successful treatment of this cancer.
A methyl deviation index (MDI) was calculated for each lesion relative to terminal ductal-lobular unit baseline, and group comparisons revealed that high-grade and short-survival estrogen receptor-positive (ER(+)) cancers manifest a significantly higher MDI than low-grade and long-survival ER(+) cancers.
A recent genome-wide association study (GWAS) has identified a single nucleotide polymorphism (SNP) rs11249433 in the 1p11.2 region as a novel genetic risk factor for breast cancer, and this association was stronger in patients with estrogen receptor (ER)+ versus ER- cancer.
A set of investigations came to the world in AD 2000 to show that: a) A total of 50 genes of the estrogen receptor positive (ER+) human breast cancer cell line MCF-7 in their gene expressions were found to undergo stimulation from a physiological concentration of 17beta-estradiol. b) Comparison of estrogen-responsiveness among a number of estrogen-responsive genes, among cancer cell lines of both the breast and endometrium with and without active ER, and among cell lines of normal tissues revealed that association between the presence of active ER and estrogen-responsive genes is quantitative rather than qualitative including some exceptions, and that none of the estrogen-responsive genes tested was classified as of breast cancer specific.
A switch in receptor status was identified for ER in 17% of tumors (p = 4 × 10(-3)), PR in 29% of cancers (p < 4 × 10(-4)), and HER2 in 4% of lesions (p = .16).
About 75% of breast cancer cases are diagnosed as ER-positive; however, nearly half of these cancers are either intrinsically or inherently resistant to the current anti-estrogen therapies.
According to hormone receptor, later age at menarche and later age at last birth were positively associated with the risk of all-cause death among patients with ER- and PR- cancer (menarche, HR = 2.18 for ≥ 15 vs. ≤ 12 years, p<sub>trend</sub> = 0.03; last birth, HR = 3.10 for ≥ 35 vs. ≤ 29 years, p<sub>trend</sub> = 0.01).
Acquisition of epithelial-mesenchymal transition phenotype in the tamoxifen-resistant breast cancer cell: a new role for G protein-coupled estrogen receptor in mediating tamoxifen resistance through cancer-associated fibroblast-derived fibronectin and β1-integrin signaling pathway in tumor cells.