<b>Methods</b>: A novel biocompatible linear copolymer poly[<i>bis</i>(ε-Lys-PEI)Glut-PEG] (PLEGP) was developed to deliver VEGF siRNA for TNBC therapy.
<b>Methods:</b> E-cadherin, Slug, Twist and Vimentin levels were detected by immunohistochemistry in 167 TNBC tumors, including 145 invasive carcinomas of no special type (ICONSTs), 14 spindle cell carcinomas (SpCCs) and 8 matrix-producing carcinomas (MPCs).
<b>Purpose:</b> Both PARP inhibitors (PARPi) and sacituzumab govitecan (IMMU-132) are currently under clinical evaluation in triple-negative breast cancer (TNBC).
<b>Purpose:</b> Both PARP inhibitors (PARPi) and sacituzumab govitecan (IMMU-132) are currently under clinical evaluation in triple-negative breast cancer (TNBC).
<b>Purpose:</b> The EGFR is frequently overexpressed in TNBC, and the EGFR-overexpressing TNBC presumably escapes EGFR inhibitor therapy by upregulating autophagy and inhibiting apoptosis.
<b>Rationale:</b> Triple-negative breast cancer (TNBC) is characterized by the absence of estrogen receptor alpha (ER-α), human epidermal growth factor receptor 2 (HER2) and progesterone receptor (PR) expression, but the effect of lacking the three factors on TNBC is unclear.
<b>Rationale:</b> Triple-negative breast cancer (TNBC) is characterized by the absence of estrogen receptor alpha (ER-α), human epidermal growth factor receptor 2 (HER2) and progesterone receptor (PR) expression, but the effect of lacking the three factors on TNBC is unclear.
<b>Rationale:</b> Triple-negative breast cancer (TNBC) is characterized by the absence of estrogen receptor alpha (ER-α), human epidermal growth factor receptor 2 (HER2) and progesterone receptor (PR) expression, but the effect of lacking the three factors on TNBC is unclear.
<b>Results:</b> Head-to-head comparison showed that <sup>89</sup>Zr-transferrin targets TNBC tumors significantly better (<i>P</i> < 0.05-0.001) than <sup>18</sup>F-FDG through PET imaging and biodistribution studies in MDA-MB-231 and MDA-MB-157 xenografts and a patient-derived xenograft model of TNBC. c-Myc and <i>TfR</i> gene expression was decreased upon treatment with BRD4 inhibitors and <i>c-MYC</i> small interfering RNA (<i>P</i> < 0.01-0.001 for responding cell lines), compared with vehicle treatment.
<i>IL1A</i>, <i>IL1B</i>, <i>IL8</i>/<i>CXCL8</i>, <i>IL32</i> and <i>IL27RA</i> in IL superfamily and <i>CD70</i>, <i>TNFSF9</i> and <i>TNFRSF21</i> in TNF superfamily were highly expressed in TNBC compared to other subtypes.
<i>In silico</i> analysis suggested that <i>OTUD7B</i> regulation, probably owing to miR-1180 downregulation, may negatively regulate the NF-κB-Lin28 axis which in turn triggers Let-7 microRNA-mediated caspase-3 downregulation, thereby conferring paclitaxel resistance in TNBCs.
<i>In silico</i> analysis suggested that <i>OTUD7B</i> regulation, probably owing to miR-1180 downregulation, may negatively regulate the NF-κB-Lin28 axis which in turn triggers Let-7 microRNA-mediated caspase-3 downregulation, thereby conferring paclitaxel resistance in TNBCs.
<i>In silico</i> analysis suggested that <i>OTUD7B</i> regulation, probably owing to miR-1180 downregulation, may negatively regulate the NF-κB-Lin28 axis which in turn triggers Let-7 microRNA-mediated caspase-3 downregulation, thereby conferring paclitaxel resistance in TNBCs.
<i>In vitro</i> and <i>in vivo</i> experiments indicated that circEPSTI1 binds to miR-4753 and miR-6809 as a miRNA sponge to regulate BCL11A expression and affect TNBC proliferation and apoptosis.
<i>Objective</i>.In the current study, we measured the expression status of melanoma antigen gene c2 (MAGE-C2) in triple-negative breast cancer (TNBC) and analyzed its prognostic with the clinical pathological features of patients with TNBC.<i>Methods</i>.
<sup>99m</sup>Tc-labeled LyP-1 showed high radiochemical purity and stability and could be used as a probe for targeted SPECT imaging of TNBC cells in vitro and in a TNBC tumor-bearing mouse model.