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HER2, EGFR, and HER4 are members of the human epidermal growth factor receptor family, which are cell surface receptor tyrosine kinases that regulate signaling pathways involved in cell proliferation, differentiation, and survival. These receptors can form homo- or heterodimers, activating phosphorylation cascades that mediate various biological functions. Dysregulation of these receptors—by overexpression, amplification, or mutation—is associated with multiple tumor types, most notably breast and lung cancers. They are high-priority therapeutic targets, with several clinically approved drugs designed to inhibit their signaling, but therapeutic challenges remain, including the development of resistance and on-target toxicities, especially cardiac side effects due to interference with physiological signaling in heart tissue[1][2][3][4][5].
Monoclonal antibodies (block ligand binding, promote receptor internalization, induce ADCC) Tyrosine kinase inhibitors (block intracellular kinase activity, prevent downstream signaling) Antibody–drug conjugates (target and deliver cytotoxic molecules) Dimerization inhibitors (blocking receptor–receptor interactions, especially HER2/HER3, HER2/HER4)
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