25 results for “tnbc”. Showing 25 of 39,449.
Salidroside sensitizes Triple-negative breast cancer to ferroptosis by SCD1-mediated lipogenesis and NCOA4-mediated ferritinophagy.
TNBC, revealing that the potential mechanism of the Sal act on TNBC
Targeted MDM2 Degradation Reveals a New Vulnerability for p53-Inactivated Triple-Negative Breast Cancer.
TNBC cells in two-dimensional/three-dimensional culture and TNBC patient
Integrating network pharmacology, molecular docking and experimental verification to explore the therapeutic effect and potential mechanism of nomilin against triple-negative breast cancer.
TNBC) remains unclear. This study aims to uncover the potential
MiR-526b targets lncRNA SLC16A1-AS1 to suppress cell proliferation in triple-negative breast cancer.
TNBC). Expression of miR-526b and SLC16A1-AS1 in TNBC
Activation of the γ-secretase/NICD-PXR/Notch pathway induces Taxol resistance in triple-negative breast cancer.
TNBC. However, Taxol resistance often develops in the treatment of TNBC
A novel peptide 66CTG stabilizes Myc proto-oncogene protein to promote triple-negative breast cancer growth.
TNBC cells and the tumor growth of TNBC xenograft by stabilizing
Prognosis in different subtypes of metaplastic breast cancer: a population-based analysis.
TNBC) between 2010 and 2014 using the surveillance, Epidemiology, and End Results
VEGFA/NRP-1/GAPVD1 axis promotes progression and cancer stemness of triple-negative breast cancer by enhancing tumor cell-macrophage crosstalk.
TNBC cells. Our study underscores the crosstalk between TNBC cells
Cancer-associated fibroblasts promote doxorubicin resistance in triple-negative breast cancer through enhancing ZFP64 histone lactylation to regulate ferroptosis.
TNBC and its detailed molecular mechanisms. METHODS: TNBC cell lines
S-equol promotes ferroptosis in triple negative breast cancer by coordinating NCOA4-mediated ferritinophagy and PPARγ-mediated lipid metabolism.
TNBC) is a diverse and highly aggressive cancer characterized by a strong
PRMT1 Sustains De Novo Fatty Acid Synthesis by Methylating PHGDH to Drive Chemoresistance in Triple-Negative Breast Cancer.
TNBC. Furthermore, IHC coupled with imaging MS in clinical TNBC
CD19+Ki67+B cells regulated by NAMPT as key modulators in triple-negative breast cancer with brain metastasis.
TNBC) stands out for its aggressiveness and high frequency of brain
Bruceine D suppresses CAF-promoted TNBC metastasis under TNF-α stimulation by inhibiting Notch1-Jagged1/NF-κB(p65) signaling.
TNBC) has a poor prognosis because of its high degree
GLUT1 inhibition blocks growth of RB1-positive triple negative breast cancer.
TNBC, we investigated the vulnerability of TNBC cell lines and patient
SOD1-high fibroblasts derived exosomal miR-3960 promotes cisplatin resistance in triple-negative breast cancer by suppressing BRSK2-mediated phosphorylation of PIMREG.
TNBC cells via exosomes. Within TNBC cells, miR-3960 targets
Low level of ARID1A contributes to adaptive immune resistance and sensitizes triple-negative breast cancer to immune checkpoint inhibitors.
TNBC patients. Low ARID1A expression in TNBC, causing an immunosuppressive
TROP2/claudin program mediates immune exclusion to impede checkpoint blockade in breast cancer.
TNBC progression. A humanized TROP2 syngeneic TNBC model was used
Targeting PRMTs Creates Vulnerability of DNA Double-Stand Break Repair Pathways, and Potentiates Chemotherapy Efficacy in TNBC.
TNBC cells to chemotherapeutic agents inducing DNA double-strand breaks
Chemotherapy Shifts the Balance in Favor of CD8+ TNFR2+ TILs in Triple-Negative Breast Tumors.
TNBC) is primarily treated via chemotherapy; in parallel, efforts are made
Tumour-infiltrating lymphocytes and prognosis in different subtypes of breast cancer: a pooled analysis of 3771 patients treated with neoadjuvant therapy.
TNBC) and HER2-positive breast cancer, but their role in luminal
LncRNA SLC16A1-AS1 regulates the miR-182/PDCD4 axis and inhibits the triple-negative breast cancer cell cycle.
TNBC. METHODS: We observed downregulation of SLC16A1-AS1 expression in TNBC
AKT and EZH2 inhibitors kill TNBCs by hijacking mechanisms of involution.
TNBC) is the most aggressive breast cancer subtype and has the highest
Tetraarsenic hexoxide enhances generation of mitochondrial ROS to promote pyroptosis by inducing the activation of caspase-3/GSDME in triple-negative breast cancer cells.
TNBC) cells. Interestingly, tetraarsenic hexoxide-treated TNBC cells exhibited specific
Single-cell sequencing unveils mitophagy-related prognostic model for triple-negative breast cancer.
TNBC) is an aggressive subtype of breast cancer lacking hormone
Triple-negative breast cancer: challenges and opportunities of a heterogeneous disease.
TNBC) in both the early and advanced-stages of the disease