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triple negative breast cancer

Simultaneous CK2/TNIK/DYRK1 Inhibition by 108600 Suppresses Triple Negative Breast Cancer Stem Cells and Chemotherapy-Resistant Disease

[Nature Communications] Scientists described a novel multi-kinase inhibitor, 108600, that suppressed growth, colony and mammosphere forming capacity of breast cancer stem cell-like cells and induced G2M arrest and apoptosis of TNBC cells.

CRYβB2 Enhances Tumorigenesis through Upregulation of Nucleolin in Triple Negative Breast Cancer

[Oncogene] Researchers reported that the expression of CRYβB2 in breast cancer cells increased stemness, growth, and metastasis. Transcriptomics data revealed that CRYβB2 upregulated genes that were functionally associated with unfolded protein response, oxidative phosphorylation, and DNA repair, while down-regulating genes related to apoptosis.

Carrick Therapeutics Announces Collaboration with Roche to Evaluate Novel Samuraciclib Combination to Treat HR+ Breast Cancer

[Carrick Therapeutics (Globe Newswire, Inc.)] Carrick Therapeutics announced a clinical collaboration with Roche to evaluate a novel combination of Carrick’s samuraciclib and Roche’s giredestrant in CDK4/6i resistant HR+, HER2- metastatic breast cancer.

Lactate Consumption via Cascaded Enzymes Combined VEGF siRNA for Synergistic Anti-Proliferation and Anti-Angiogenesis Therapy of Tumors

[Advanced Healthcare Materials] A codelivery strategy that combined the cascaded enzymes lactate oxidase/catalase and vascular endothelial growth factor siRNA to suppress tumor proliferation and angiogenesis synergistically was proposed.

The Efficacy of Indoximod upon Stimulation with Pro-inflammatory Cytokines in Triple-Negative Breast Cancer Cells

[Immunopharmacology and Immunotoxicology] Scientists determined the effects of indoximod as an indoleamine 2,3-dioxygenase inhibitor on triple-negative breast cancer and to assess the link between the efficacy of indoximod and IFN-γ or TNF-α stimulation.

DIF-1 Inhibits Growth and Metastasis of Triple-Negative Breast Cancer through AMPK-Mediated Inhibition of the mTORC1-S6K Signaling Pathway

[Oncogene] Scientists found that DIF-1 induced phosphorylation of AMPK and Raptor and dephosphorylation of p70S6K in multiple TNBC cell lines.

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