Jornal de Síndromes Genéticas e Terapia Gênica
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Trypsin-antitrypsin Imbalance in Immune Escape and Clonal Proliferation of Pancreatic Cancer

Chen Qing-quan, Gao Feng, Zhuang Ze-hao, Zhang Zhi-bo, Liu Qi-cai and Chen Jin-tong

So far it has been failed to confirm whether trypsinogen (PRSS1) besides its homologous genes and TCRVß gene which are co-localized is a gene linkage, though the process of trypsinogen activation has been loaded into textbooks as a classical theory. At present, researchers mainly focuse on PRSS1/PRSS2 genes mutations themselves without considering the particularities of genes structures and changes, therefore, cannot explain the immune mechanism of pancreatic cancer. It has been verified that trypsin can serve as a signal factor in stimulating tumor cells proliferation and destroying matrix to promote cell transfer and as a stimulator of lymphocytes to combat with its inhibitor (α1-antitrypsin, α1-AT/AAT), so to play an important role in tumor immune surveillance. Therefore, in order to illuminate the pancreatic cancer immune escape, it is necessary to clarify the correlative spatiotemporal expression of PRSS1/PRSS2/AAT genes. It may provide a theoretical basis for TCRVß gene modification or AAT gene treatment of pancreatic cancer to expound the process of trypsinogen gene mutation or abnormal activation leading to AAT gene’s over expression which induced body immune tolerance to cause mutant cells immune escape and clonal proliferation.