Tumor homing receptor modification

Tumor homing receptor modification is not a discrete molecular target, but a strategy wherein immune cells (such as T cells or stem cells) are engineered to overexpress or otherwise modify specific homing receptors—such as selected chemokine receptors (for example, CCR2), selectin ligands, or integrins—to increase their migration to and accumulation in tumor tissue. This approach aims to overcome one of the major barriers in adoptive cell therapies, where therapeutic cells display poor trafficking and infiltration into solid tumors due to insufficient expression or mismatched repertoire of homing receptors compared to the ligands displayed by tumor vasculature[3][4]. Multiple receptor-ligand pairs involved in homing (such as CCR2/CCL2, CXCR3/CXCL9-10, integrin/VCAM-1, E-selectin/E-selectin ligand) have been targeted by these modifications depending on tumor and disease context[1][3]. 'Tumor homing receptor modification' is therefore a class of modification strategies, not a single molecular entity or therapeutic target.

Enhancement of immune or therapeutic cell trafficking to tumor site by genetic or biochemical modification of cell-surface homing receptors