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Forkhead box protein M1 (FOXM1) is a master regulator transcription factor that plays a pivotal role in the cell cycle, specifically governing the expression of genes required for the G1/S and G2/M transitions (UniProt P14854) [1]. While FOXM1 expression is minimal in most differentiated adult tissues, it is highly upregulated in a broad spectrum of cancers, including breast, lung, and gastrointestinal malignancies, where it drives oncogenic processes such as proliferation, metastasis, and drug resistance (PubMed: 30103734) [4]. The FOXM1 tumor-associated antigen epitope refers to specific peptide fragments derived from the FOXM1 protein that are presented by Human Leukocyte Antigen (HLA) molecules on the surface of cancer cells. These epitopes, such as FOXM1-235 (YLIPIPRAL) and FOXM1-362 (LMDLSTTPL), are recognized by the T-cell receptors (TCRs) of cytotoxic T lymphocytes, marking the cancer cells for destruction (PubMed: 21159633) [2]. Therapeutic interventions targeting these epitopes include cancer vaccines and T-cell receptor (TCR) engineered T-cell therapies, which aim to harness the immune system to specifically target FOXM1-overexpressing tumors (PubMed: 24583792) [3]. Because FOXM1 is considered a "universal" cancer antigen with limited expression in normal tissues, these epitopes represent promising targets for broad-spectrum immunotherapy with a potentially favorable safety profile.
Induction of peptide-specific cytotoxic T lymphocytes (CTLs) that recognize and lyse tumor cells presenting FOXM1 epitopes via MHC class I molecules.
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