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P1A and Mastocytoma Growth
Gene P1A (P1CTL)，a mouse cancer-germline gene encoding a tumor antigen that represents the best mouse model for human MAGE-type tumor antigens, and encodes the major tumor rejection antigen of mastocytoma P815 which is composed of a peptide (LPYLGWLVF, P1A35–43) derived from the P1A protein and presented to cytotoxic T lymphocytes (CTL) by MHC class I molecule H-2 Ld. P1A is activated in several tumors but silent in normal cells except in placental trophoblasts and male germline cells, and these cells do not bear surface MHC class I molecules. They do not present the P1A peptide, so antigen P815A is strictly tumor-specific, and immunization against this peptide does not induce autoimmune side-effects. According to Gaëlle Vandermeulen’ studies, immunization with a plasmid coding for the full-length P1A significantly delayed tumor growth, mice failed to reject tumor and even delay tumor growth.
P1A And Photodynamic Therapy
Photodynamic therapy (PDT) is a two-step procedure which involves the administration of a photosensitizing drug followed by activation of the drug with nonthermal light of a specific wavelength. PDT is thought to be particularly effective at activating an immune response against a locally treated tumor. Among various tumor antigens discovered to date, P1A is the best-described nonmutated mouse cancer-testis tumor antigen and has been used for many immunotherapy studies, and is expressed in cancers, but not at all or at very low levels in other tissues. In Pawel Mroz et al. Studies, PDT does indeed induce recognition of MHC class I-bound epitope derived from the P1A antigen and provide additional evidence to support the notion that the expression of tumor antigen makes a significant difference in the outcome of PDT.
P1A And Immune Evasion
Tumor evasion of T-cell immunity remains a significant obstacle to adoptive T-cell therapy, but the mode of immune evasion is dictated by the cancer cells or by the tumor antigens. Although P1CTL conferred partial protection, tumors recurred in almost all mice. And the ability of Meth A to cause T-cell death alleviated the need for P1A antigen downregulation in cancer cells.
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