Moderate supplemental vitamin D intake was associated with decreased risk of TNBC, and increased sun exposure was associated with reduced risk of ER+, ER-, and TNBC among black women.
Studies have shown that androgen receptor (AR) signaling activation may be one of the mechanisms, and targeting AR showed some promising results in AR-positive triple-negative breast cancer.
These results demonstrate a significant impact of ERβ in TNBC genome activity mediated by its cooperation with regulatory multiprotein chromatin remodelling complexes, providing novel ground to devise new strategies for the treatment of these diseases based on ligands affecting the activity of this nuclear receptor or some of its protein partners.
Consistent with this data, PTEN-null TNBC tumors expressed higher levels of STING, and PTEN-null TNBC cell lines were hyperresponsive to STING agonists.
Triple negative breast cancer (TNBC) refers to breast cancer that lacks progesterone receptor (PR), estrogen receptor (ER) and human epidermal growth factor receptor 2 (HER2).
Triple negative breast cancer (TNBC) refers to breast cancer that lacks progesterone receptor (PR), estrogen receptor (ER) and human epidermal growth factor receptor 2 (HER2).
In this study, we evaluated the characteristics, clinical behaviour and role of biomarkers (androgen receptor (AR), oestrogen receptor beta (ERβ) and p53) in metastatic TNBC.
TNBC lacks of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2), so there are still no effective treatment methods for TNBC.
Supporting this genetic interaction, CD44 positively correlated with PD-L1 expression at the mRNA and protein levels in primary tumor samples of TNBC and NSCLC patients.
Neoadjuvant chemotherapy (NAC) is a standard treatment for locally advanced breast cancer, especially for HER2-positive or triple negative breast cancer which shows good response to chemotherapy.
Triple negative breast cancer (TNBC) refers to breast cancer that lacksprogesterone receptor (PR), estrogen receptor (ER) and human epidermal growth factor receptor 2 (HER2).
The AKT inhibitor capivasertib has shown preclinical activity in TNBC models, and drug sensitivity has been associated with activation of PI3K or AKT and/or deletions of PTEN.
Crosslinking of CD32A<sup>131R</sup> -CR on T cells by cetuximab or panitumumab and CD16<sup>158F</sup> -CR T cells by cetuximab induced elimination of triple negative breast cancer (TNBC) MDA-MB-468 cells, and the secretion of interferon gamma and tumor necrosis factor alpha.
High in vivo anticancer efficiency against the MDA-MB-231 triple-negative breast cancer (TNBC) model is obtained due to the combination of genetic regulation of miR-21i and the photokilling effect of ICG.
We have recently shown that the combined inhibition of EGFR and ROCK in TNBC cells results in cell death, however, the underlying mechanisms remain unclear.
CSCs with high epithelial specific antigen (ESA), high CD44 and low CD24 expression levels were derived from the TNBC cancer cells, MDA-MB-231 and MDA-MB-468.
Interestingly, a novel link between BRCA1 status and miRNA expression level was identified through miR-96 and miR-10b that were very important discriminators between TNBC with mutated BRCA1 and TNBC with wild type BRCA1.