Breast cancer (BC) is the most common cancer in women, where hormone receptor-positive (HR+; estrogen receptor and/or progesterone receptor) BC comprises the majority (>50%) and has better prognosis, while a minority (<20%) are triple negative BC (TNBC), which has an aggressive phenotype.
Cytotoxic activity was studied over a panel of estrogen-receptor-positive (ER+) and negative (ER-) human cancer cell lines by means of both 2D and 3D cell viability studies.
Prospective cohort studies of Cd and breast cancer risk suggest a significant relationship between increased Cd intake and cancer incidence, with more pronounced effects for estrogen receptor α (ERα)-positive breast cancers.
This study aimed to evaluate the prognostic significance of the Oncotype DX recurrence score (RS) in T<sub>1-2</sub>N<sub>1</sub>M<sub>0</sub> estrogen receptor (ER)-positive, human epidermal growth factor receptor 2 (HER2)-negative breast cancer based on the prognostic stage in the updated American Joint Commission on Cancer, 8th edition.
Tumor size and vascular invasion were top-ranked predictors of all three end-points, followed by estrogen receptor status and lobular cancer for prediction of N2.
Stratification analysis showed that rs13293512 CC genotype was associated with an increased risk of BC in patients with negative estrogen receptor (adjusted OR = 2.39; 95% CI: 1.32-4.30; <i>P=</i>0.004), patients with negative progesterone receptor (adjusted OR = 1.92; 95% CI: 1.11-3.33; <i>P=</i>0.02), patients with T1-2 stage cancer (adjusted OR = 1.77; 95% CI: 1.07-2.93; <i>P=</i>0.03), and patients with N1-3 stage cancer (adjusted OR = 1.89; 95% CI: 1.13-3.17; <i>P=</i>0.015).
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).
The combination of overweight/obesity and elevated breast density in premenopausal women is associated with a higher risk of ER-negative compared with ER-positive cancer.
Our data reveal a non-canonical function of YAP1 and TEAD4 as ERα cofactors in regulating cancer growth, highlighting the potential of YAP/TEAD as possible actionable drug targets for ERα<sup>+</sup> breast cancer.
To investigate autophagy regulation in YAP signaling in the context of cancer metastasis, we performed profiling analysis of YAP signaling, YAP subcellular localization, autophagosome formation and cell invasiveness in TNBC cell lines (MDA-MB-231 and Hs 578T) versus estrogen receptor (ER) positive breast cancer cell line MCF7.
Long non‑coding RNA (lncRNA)‑mediated transcriptional dysregulation triplets (lncTDTs) may contribute to the development of cancer; however, the precise functional roles of lncTDTs in ER+/PR+, HER2‑ BRCA and TNBC require further investigation.
The Cancer Genomics Data Server was interrogated for mutational and clinical data of all ER+ breast cancers with information on PR status from The Cancer Genome Atlas (TCGA), Memorial Sloan Kettering (MSK), and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) projects.
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.
Previous comprehensive genomic studies have revealed prevalent estrogen receptor 1 (ESR1) mutations in breast cancer, which are rare in certain other types of cancer.
We found that CD163<sup>+</sup> macrophages were the dominant macrophages in atypical endometrial hyperplasia and cancer, and their infiltration was positively associated with ERα expression.
In vitro studies revealed the potential of the total sub-classes of the synthesized analogs to show anti-proliferative activity against estrogen receptor-dependent cancer cell lines at IC<sub>50</sub> ranging from 28.23 to 57.13 μM.
In this review, we provide an overview of NR-based drug discovery in cancer and related resistance mechanisms, focusing on novel strategies for targeting well-established NR targets, including ERα, the AR, the glucocorticoid receptor, and the progesterone receptor, as well as opportunities to target other NRs that are attracting interest in immuno-oncology, such as liver X receptors, retinoic acid-related orphan receptors, and farnesoid X receptors.