Triple-negative breast cancer (TNBC), which lacks expression of estrogen receptor (ER), progesterone receptor (PgR), and epidermal growth factor receptor 2 (HER2), currently has no effective hormonal or molecular target therapy.
Cell viability assay findings indicated that ZER and ZERencapsulated in hydroxypropyl-β-cyclodextrin (ZER-HPβCD) inhibited the growth of estrogen receptor positivebreast cancer cells (ER<sup>+</sup> MCF-7) at 72 h treatment with an inhibitory concentration (IC)<sub>50</sub> of 7.51 ± 0.2 and 5.08 ± 0.2 µg/mL, respectively, and inhibited the growth of triple negative breast cancer cells (MDA-MB-231) with an IC<sub>50</sub> of 14.96 ± 1.52 µg/mL and 12.18 ± 0.7 µg/mL, respectively.
Estrogen receptor (ER)+/progesterone receptor (PR)+, human epidermal‑growth factor receptor 2 (HER2)‑ BRCA and triple‑negative breast cancer (TNBC) are two important subtypes of this disease.
Triple negative breast cancer (TNBC) is a subtype of breast cancer of heterogeneous nature that is negative for estrogen receptor (ER), progesterone receptor (PR) and growth factor human epidermal 2 (HER2) following immunohistochemical analysis.
Triple-negative breast cancer (TNBC), defined by lack of expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), is characterized by early recurrence of disease and poor survival.
No similar trends were evident in East Asian patients; their probability of estrogen receptor positivity at age 40-49 years was statistically significantly higher (odd ratio [OR] = 1.50, 95% confidence interval [CI] = 1.36 to 1.67, P < .001) and of TNBC was statistically significantly lower (OR = 0.79, 95% CI = 0.71 to 0.88, P < .001), whereas the probability of ER positivity at age 50-59 years was statistically significantly lower (OR = 0.88, 95% CI = 0.828 to 0.95, P < .001).
Triple-negative breast cancer (TNBC) lacks the receptor targets estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2, and thus, it does not respond to receptor-targeted treatments.
It is unknown whether the prevalence of triple-negative breast cancer (negative forestrogen receptor, progesterone receptor, and human epidermal growth factor 2 receptor) among black women in the United States differs similarly by birthplace.
The present study aimed to the identification of estrogen receptor (ER)β as a novel mitochondrial target in TNBC cells, together with underlying mechanisms.
The patients in the SNB group had a higher rate of estrogen receptor-positive and triple-negative breast cancers, but a lower rate of human epidermal growth factor receptor 2 (HER2)-positive cancer (p < 0.001).
MSKE also decreased CUX1 binding to ER-α promoter and restored ER-α expression in TNBC cells, while both MSKE and CUX1 siRNA restored sensitivity to estradiol and 4-hydoxytamoxifen as shown by increased cell viability.
Breast cancers that have no expression of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2) are defined as triple negative breast cancers (TNBCs); luminal cancers have different expressions of ER, PR and/or HER2.
A peptide corresponding to part of the hinge region/AF2 domain of the human estrogen receptor α (ERα17p, residues 295-311) exerts anti-proliferative effects in various breast cancer cells including those used as triple negative breast cancer (TNBC) models.
Triple-negative breast cancer (TNBC) refers to cancers that are low in expression of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2).
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.
SIGNIFICANCE: MUC1-C directly interacts with MYC to activate the NuRD complex, mediating regulation of the estrogen receptor in triple-negative breast cancer cells.
Triple negative breast cancer (TNBC) is a more aggressive subtype of breast cancer and is characteristic of the absence of the expressions of estrogen receptor, progesterone receptor, and human epithelial growth factor receptor 2 in breast tumor tissues.
Breast cancer brain metastases (BM) affect younger women disproportionally, including those lacking estrogen receptor (ER), progesterone receptor, and HER2 (known as triple-negative breast cancer; TNBC).
In this review, we highlight important signaling pathways regulated by WWOX and p53 that are related to estrogen receptor signaling, epithelial-to-mesenchymal transition, and genomic instability and how they impact BLBC and TNBC development.
In this study, subcellular fractionation followed by Western blot and immunocytochemistry showed that TRPC3 was over-expressed on the plasma membrane of TNBC line MDA-MB-231 when compared to an estrogen receptor-positive cell line MCF-7.
Triple-negative breast cancer (TNBC) is highly proliferative and metastatic, and because it lacks three major molecular targets for chemotherapy (estrogen receptor, progesterone receptor, and human epidermal receptor 2), it is extremely refractory.
When combined with paclitaxel, bazedoxifene may be a potential small molecule for the treatment of both estrogen receptor positive and triple-negative breast cancer.
The association was more pronounced for estrogen receptor (ER)-negative (HR<sub>highest vs. lowest quartile</sub> : 1.67 [95% CI, 1.07-2.61], p<sub>trend</sub> = 0.03) and triple-negative breast cancer (HR<sub>highest vs. lowest quartile</sub> : 2.20 [95% CI, 1.23-3.95], p<sub>trend</sub> = 0.02).