This analysis demonstrates how nanotechnology improves anti-EGFR drug delivery in cancer, suggesting better outcomes against drug resistance.
The EGFR, a major receptor tyrosine kinase in the HER family, controls cell growth and division via its extracellular and intracellular tyrosine kinase domains. Ligand binding and receptor dimerization stimulate downstream pathways such as KRAS-BRAF-MEK-ERK, which are critical for cell proliferation, survival, and angiogenesis. Dysregulation of EGFR is linked to cancer development by encouraging uncontrolled cell proliferation, resistance to apoptosis, and metastases. Anti-EGFR medicines, including monoclonal antibodies (e.g., cetuximab) that prevent ligand binding and tyrosine kinase inhibitors (e.g., gefitinib), suppress abnormal EGFR signaling to slow cancer growth. Their usefulness is, however, constrained by issues, such as drug resistance, off-target effects, and limited potency in specific tumors. By using nanoparticles, including liposomes, polymeric nanoparticles, and quantum dots, for accurate drug administration, decreased systemic toxicity, and circumvention of resistance mechanisms, nanotechnologybased techniques have been developed to improve EGFR-targeted therapy. Functionalized nanoparticles improve effectiveness and make combo treatments possible by permitting regulated drug release and active targeting. These developments hold promise for addressing present constraints and offering individualized treatment choices. Comprehending EGFR signaling and using nanotechnology continue to be essential for creating more potent, focused cancer treatments.
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Islam et al. (2025) studied this question.
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