Tumor antigen-derived peptide

“Tumor antigen-derived peptide” is a generic category term for short antigenic peptides derived from tumor antigens—either tumor-associated antigens (self-antigens aberrantly or overexpressed in tumors) or tumor-specific antigens/neoantigens (peptides arising from tumor mutations, splicing errors, post-translational changes, or viral oncoproteins in virus-driven cancers).[2][1] These peptides are not a single molecule, receptor, enzyme, or defined gene product; rather, they are used as vaccine epitopes or experimental reagents to elicit anti-tumor T cell responses when presented on MHC molecules by antigen-presenting cells or tumor cells.[2][3] Personalized neoantigen peptide vaccines have shown induction of robust CD4+ and CD8+ T cell responses and intratumoral cytotoxicity, particularly when combined with PD-1 blockade (e.g., nivolumab), with acceptable safety in early clinical studies.[2] Peptide immunogenicity can be enhanced via sequence modifications (heteroclitic peptides), optimized delivery systems and adjuvants, including cationic polymers that improve peptide uptake and presentation by APCs.[3][4] Tumor immune evasion through impaired antigen processing/HLA-I loss is a challenge; a class of targets termed TEIPP (T cell epitopes associated with impaired peptide processing) represent unmutated peptides from housekeeping proteins that can be leveraged to target TAP-deficient/HLA-I-low tumors.[1]

Other names

Tumor antigen-derived peptideTumor-derived antigenic peptideTumor antigenic peptideTumor-associated antigen peptide (TAA-derived peptide)Tumor-specific antigen peptide (TSA/neoantigen peptide)

Vaccine antigen that, when presented on MHC molecules, induces CD8+ and CD4+ T cell responses against tumor cells expressing the source antigen[2][3] Neoantigen or TSA peptides exploit tumor-specific mutations or aberrant products to generate highly specific T cell responses, avoiding central tolerance[1][2] Use of peptide modifications/heteroclitic peptides to increase MHC binding or TCR recognition and enhance immunogenicity[3] Combination with immune checkpoint blockade (e.g., PD-1 inhibitors) to augment vaccine-induced T cell responses and intratumoral killing[2]