triple negative breast cancer

[Molecular Therapy-Oncolytics] Scientists identified the transcriptional landscape associated with TNBC resistance to neoadjuvant chemotherapy at the single cell level by analyzing publicly-available transcriptome data from more than 5,000 single cells derived from four extinction and four persistence patients, revealing remarkable tumor heterogeneity.

[Journal of Biological Chemistry] The authors utilized TNBC as a model to discern mechanisms of resistance as it has been previously shown to be highly responsive to CDK7 inhibitors. After generating cell lines with acquired resistance, high throughput RNA-sequencing revealed significant upregulation of genes associated with efflux pumps and transforming growth factor-beta (TGF-β) signaling pathways.

[Scientific Reports] Investigators identified how circulating low-density lipoprotein (LDL) cholesterol and tumor LDL receptor (LDLR) may have accelerated oncogenic processes by determining whether increased LDLR expression and cholesterol uptake were associated with the activation of the epidermal growth factor receptor (EGFR) signaling pathway in TNBC cell lines.

[Molecular Cancer Research] To elucidate the underlying mechanisms that drive breast cancer stem cells (BCSCs) tumorigenicity in TNBC, scientists identified the long noncoding RNA BMP/OP-Responsive Gene (BORG) as an enhancer of BCSC phenotypes.

[British Journal of Cancer] Ubiquitin carboxyl terminal hydrolase L1 (UCHL1), a ubiquitin C-terminal hydrolase belonging to the deubiquitinase family of enzymes, is highly expressed in metastatic estrogen receptor negative breast cancer and TNBC, and several key reports have revealed emerging and important roles for UCHL1 in breast cancer.

[British Journal of Cancer] Scientists used a xenograft model of spontaneous metastasis to the liver from an ectopic tumour employing a metastatic TNBC cell line. Atorvastatin was provided to sensitise metastatic cells, followed by chemotherapy.