Relationship of p53 overexpression on cancers and recognition by anti-p53 T cell receptor-transduced T cells - PubMed (original) (raw)

FIG. 4.

Specificity of p53:264 TCR-transduced T cells for tumor and normal cells. Tumor or normal cells (1 × 105) were cultured overnight with 1 × 105 p53:264 TCR-transduced T cells, and supernatants were collected and analyzed for IFN-γ by ELISA. Tumor and normal cell populations are separated by the divided line. Tumor cell lines included HLA-A2− (888, 938, A549, HCC-2998, HOP-92, IGR-OV1, KM12, and OVCAR-8), HLA-A2+, p53264–272 epitope-disrupted (BIC-1, HCT-15, NCI-H522, OVCAR 5, Saos-2, SW 620, TC71, SNB-19, and U251), and HLA-A2+ tumor lines with an intact p53264–272 epitope containing either mutant p53 (BT549, OVCAR 3, RXF-393, Saos2/143, SNB-75, 526, H2087, MDA 231, and 1861) or wild-type p53 (A375, A498, HCT-116, HepG2, MALME-3M, MCF-7, SF 539, SK-MEL-5, 1890, 1994, 2081, 2207, UACC 257, and UACC 62). Normal cell lines included fibroblasts, a renal epithelial line, and an astrocyte line. Peripheral blood stem cells (PBSCs) were obtained freshly from patients after CD34+ cell selection and tested immediately. These data are compiled from 21 experiments using the same p53:264 TCR-transduced effector T cell line, GLp53TCR, that had been previously expanded and cryopreserved, and the average IFN-γ value is reported for targets that were tested in multiple experiments (range, 2 to 18 individual experiments). Recognition of targets tested in one experiment (e.g., PBSCs) was validated with an additional p53:264 TCR-transduced T cell line.