Identification of essential molecules and elucidation of the mechanism for novel cancer immune evasion system: Research for biomarker for immunological response

我们首次发现，一个新的克隆，获得了免疫逃避能力，出现从原来的肿瘤克隆，这是敏感的肿瘤相关抗原特异性T细胞反应。肿瘤克隆的出现依赖于T细胞应答。新生肿瘤细胞的MHC I类分子、TRP 2、Gp 100、IFN-γ（包括对IFN-γ的功能反应）和Fas的表达无明显变化，但上调了syt 12、GATA 1和2的表达，下调了NGFR的表达，提示这些分子可能是肿瘤免疫逃避的潜在生物标志物。

We firstly found that a new clone, which have acquired the immune evasion potentials, emerges from the original neoplastic clone, which is susceptible to the tumor associated antigens-specific T cell response. This emergence of neoplastic clone is dependent on the T cell response. The new neoplastic cells have no change in the expression of MHC class I, TRP2, Gp100, IFN-γ (including functional response to IFN-γ), and Fas, but upregulate the expressions of sytl2, GATA1 and 2, and downregulate NGFR, suggesting that the molecules may be potential biomarkers in the immune evasion of neoplasm.