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Patient-specific lung tumor-associated antigens (TAAs) represent a personalized repertoire of proteins or peptides expressed by lung cancer cells that serve as targets for the host immune system. This category encompasses both shared TAAs, which are overexpressed in many patients (such as MAGE-A3, NY-ESO-1, or MUC1), and neoantigens, which are unique to an individual patient's tumor resulting from non-synonymous somatic mutations [1][2]. These antigens are processed and presented on the cell surface via Major Histocompatibility Complex (MHC) molecules, where they can be recognized by T-cell receptors (TCRs) to trigger a cytotoxic response [3]. In therapeutic contexts, these antigens are utilized to develop personalized cancer vaccines, such as mRNA-based platforms, or adoptive cell therapies designed to elicit a robust, tumor-specific cytotoxic T-lymphocyte response [4]. By focusing on antigens specific to the patient's malignancy, these strategies aim to maximize therapeutic efficacy while minimizing the risk of systemic toxicity associated with non-specific treatments [5]. However, the clinical success of targeting these antigens is often challenged by tumor heterogeneity and immune evasion mechanisms, such as the loss of antigen expression by the tumor [6].
Induction of a specific T-cell mediated immune response against tumor cells through the presentation of antigenic peptides on Major Histocompatibility Complex (MHC) molecules.
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