In this study, we sought to explore the effect of most active ligands against different normal and breast cancer cell lines that represent different breast cancer subtypes with distinguished expression levels in HER2 and HER1.
In conclusion, CD32A<sup>131R</sup> -CR T cells are efficiently redirected by cetuximab or panitumumab against breast cancer cells overexpressing EGFR.
Suppression of epidermal growth factor receptor-mediated β-catenin nuclear accumulation enhances the anti-tumor activity of phosphoinositide 3-kinase inhibitor in breast cancer.
In addition, expression of drug-resistance genes such as ATP binding cassette (ABC) transporter, the breast cancer gene family (BCRA1 and BCRA2), and the ErbB gene family were significantly decreased in OD-EXO-treated CSCs.
Controlled Epidermal Growth Factor Receptor Ligand Display on Cancer Suicide Enzymes via Unnatural Amino Acid Engineering for Enhanced Intracellular Delivery in Breast Cancer Cells.
Here, we report on epidermal growth factor receptor and CD44 dual-targeted hyaluronic acid nanogels (EGFR/CD44-NGs) that afford enhanced targetability and protein therapy for metastatic 4T1 breast cancer in vivo.
These data suggest that ER blockade leads to reactivation of ERBB RTKs and thus extended ERBB blockade is necessary to achieve durable clinical outcomes in patients with ER<sup>+</sup>/HER2<sup>+</sup> breast cancer.
The proposed framework is applied to a well-known BRNs of <i>Bacteriophage</i> λ and ERBB Receptor-regulated G1/S transition involved in the breast cancer to demonstrate the viability of our approach.
Western blot analysis along with the confocal imaging of EGFR-overexpressing breast cancer cells (MDA-MB-231) demonstrated the targeting functionality of scFvB10 after conjugation to the GQDs, as well as the potential application of GQDs-scFvB10 in targeted bioimaging.
Overexpressed MYO1D increases colorectal and breast cancer cell motility and viability through upregulating EGFR level, and thereby promotes colorectal tumor progression in a syngeneic mouse model.
4-cholesten-3-one decreases breast cancer cell viability and alters membrane raft-localized EGFR expression by reducing lipogenesis and enhancing LXR-dependent cholesterol transporters.
Previous studies have documented that PTPH1-associated breast cancers exhibit enhanced sensitivity to tamoxifen and tyrosine kinase inhibitors through dephosphorylation of ER and epidermal growth factor receptor, respectively.
Some of the important mutations include epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) mutations in small cell lung cancer, human epidermal growth factor receptor (HER2) mutation in breast cancer, and BRAF mutation in melanoma.
By comparing the TReD results with the gene expression profiles, we found a clear negative correlation between the EGFR diffusivities and the breast cancer luminal differentiation scores (r = -0.75).
Afatinib has improved the prognosis of epidermal growth factor receptor-positive advanced non-small cell lung cancer and has been explored in the treatment of human epidermal growth factor receptor 2 (HER2)-amplified breast cancer.