A prospective randomized phase II trial was conducted to evaluate the time course effects of toremifene (TOR) and letrozole (LET), as adjuvant hormone therapy, on serum lipid profiles and bone metabolism in estrogen receptor (ER)-positive, postmenopausal breast cancer patients.Fifty-four postmenopausal breast cancer patients [ER positive, HER2 negative, T1-2, node metastases (n = 0-3), M0] who had undergone curative resection were enrolled.
On further immunohistochemistry (IHC), all metastases evaluated were diffusely, strongly positive for estrogen receptor (5/5 cases) and GATA3 (4/4 cases).
Chemerin expression was significantly correlated with weight (<i>r</i>=0.256, <i>P</i>=0.04), body mass index (<i>r</i>=0.233, <i>P</i>=0.03), tumor size (<i>r</i>=0.235, <i>P</i>=0.03), lymph node metastasis (<i>r</i>=0.265, <i>P</i>=0.045), distant metastasis (<i>r</i>=0.267, <i>P</i>=0.02), and tumor grading, (<i>r</i>=0.421, <i>P</i>=0.004), while it was inversely significantly correlated with estrogen receptor and progesterone receptor expression in malignant breast tissues (<i>P</i>=0.038, <i>r</i>=-0.437, and <i>P</i>=0.047, <i>r</i>=-0.316), respectively.
Dynamics of the hazard for distant metastases after ipsilateral breast tumor recurrence according to estrogen receptor status: An analysis of 2851 patients.
Body mass index (P = .023) and DACH1 (P = .034) were correlated with MBC prognosis, whereas the expression of AR (P = .049), SIX1 (P = .048), surgery (P < .001), and chemotherapy (P = .001) were important for FBC in addition to already known factors: tumor size and location, TNM stage (lymph nodes and organ metastasis), radiotherapy, and ER and human epidermalgrowth factor receptor-2 (HER2) expression.
Univariate analysis revealed nodal metastasis and the expression of ER beta as factors correlating with a shorter overall survival and disease free survival.
We used general linear models to examine associations of sleep disturbance with markers of tumor aggressiveness among cases: estrogen receptor (ER) status, progesterone receptor (PR) status, and human epidermal growth factor receptor-2 (HER2) status; tumor size, stage, grade, lymph node involvement, and presence of metastasis.
A major risk for patients having estrogen receptor α (ERα)-positive breast cancer is the recurrence of drug-resistant metastases after initial successful treatment with endocrine therapies.
Furthermore, Notch4 expression was inversely associated with estrogen receptor (ER) and/or progesterone receptor positivity, and positively associated with larger tumor size, more lymph node involvement, and more advanced tumor node metastasis stage (P<0.05).
Reduced expression of oestrogen receptor-β is associated with tumour invasion and metastasis in oestrogen receptor-α-negative human papillary thyroid carcinoma.
A genetic model system with three mouse strains, one that develops ER-positive mammary tumors (p18 single deletion) and the others that develop ER-negative tumors (p16;Brca1 and p18;Brca1 compound deletion), human BRCA1 mutant breast cancer patient-derived xenografts, and human BRCA1-deficient and BRCA1-proficient breast cancer cells were used to determine the role of estrogen in activating epithelial-mesenchymal transition (EMT), stimulating cell proliferation, and promoting ER-negative mammary tumor initiation and metastasis.
Knockdown of the E2-inducible UNC5A resulted in altered basal gene expression affecting plasma membrane integrity and ERα signaling, as evident from ligand-independent activity of ERα, altered turnover of phosphorylated ERα, unique E2-dependent expression of genes effecting histone demethylase activity, enhanced upregulation of E2-inducible genes such as BCL2, and E2-independent tumorigenesis accompanied by multiorgan metastases.
Among the 46 cases of ER negative expression in all cores of primary lesions, 39 of them had all the metastatic nodes being ER negative, and ER negative nodes were seen in 95.7% of the metastases.
Here, we show that BAd increased the dissemination of estrogen receptor positive BC cells (BCC) <i>in vivo</i> in the zebrafish model of metastasis, while dissemination of the more aggressive and metastatic BCC such as estrogen receptor negative was unaffected.
In this study, we investigated whether single nucleotide polymorphisms (SNPs) identified by genome-wide association study (GWAS) (MAP3K1, FGFR2, TNRC9, HCN1, and 5p12), and SNPs involved in the metabolism of estrogen (CYP19, COMT, ESR1, and UGT1A1), tamoxifen (CYP2C9, CYP2C19, CYP3A5, and CYP2D6), and chemotherapeutic agents (ABCB1, ALDH3A1, and CYP2B6) are associated with the prognoses of 414 hormone receptor (HR)-positive early breast cancers with negative or 1 to 3 nodal metastases.
Overall, 38% of triple-negative metastases were Sox10 positive, compared to 0% of estrogen receptor (ER)<sup>+</sup> or human epidermal growth factor 2 (HER-2) <sup>+</sup> metastases (P=.045).
Interestingly, CTGF immuno-detection in bioptic specimens from women with estrogen receptor positive (ER<sup>+</sup>) BC correlated with hormone therapy resistance, distant metastases, reduced overall and disease-free survival.
The clinical results showed that ER ≥1% breast cancers showed a positive correlation with bone metastasis, which was found to be the preferred site of metastasis.
Retrospective analyses of ESR1 mutations in baseline plasma circulating tumor DNA from completed clinical trials suggest that these mutations are prognostic and predictive of resistance to aromatase inhibitors in metastatic disease.
Overall, there was discordance between the primary tumor and either the first or second metastases for ER in 27.7%, PR receptor in 40.7%, and HER-2/neu in 19.6% of cases.
In this study, we have examined the mechanism by which ERα regulates β-catenin expression as well as the metastasis ability of hepatocellular cancer HA22T cells.