一般认为细胞衰老是阻止肿瘤发生的一道重要天然屏障，有利于控制肿瘤。但随衰老研究加深，发现衰老并非一定导致细胞永久、不可逆性停止增殖，或走向凋亡，衰老过程中修复异常基因时的不稳定性和重编，及肿瘤细胞在接受放化疗等各种基因损伤压力时，可能为新致癌基因或耐药产生营造机会，乃至衰老瘤细胞复活、增殖力更强，其分泌表型等会干扰机体免疫功能，促进肿瘤免疫逃逸。我们前期发现复发/难治DLBCL与抑制性细胞和细胞因子浸润增多密切相关，药物等刺激后衰老基因SENEX触发的应力性衰老具有抗凋亡和免疫抑制效应，故推测SENEX触发的衰老是促进复发/难治DLBCL免疫逃逸机制之一，拟采用组织病理、细胞培养、分子生物学和基因工程等技术从临床、体外细胞水平和动物模型体内研究予以验证。DLBCL是成人最常见淋巴瘤，复发难治者无有效治疗方法，本研究对防止复发、开发新免疫治疗靶点有意义。未见类似研究报道。

Cellular senescence is generally considered as an important natural tumor barrier, is helpful to control tumor. However, as research deepens, found that aging does not necessarily lead to permanent, irreversible cessation of cell growth or to apoptosis. During repairing the abnormal genes in senescent cells, the Gene unstability and reprogramming and the genetic damage pressure such as radio-chemotherapy may make opportunities for create new oncogenes and drug resistance. This possibly made the senescent cell reviving and more proliferating, and the secreting phenotype can interfere with the immune function and facilitate tumor immune escape. We found previously that the relapsed/refractory DLBCL is closely related to the increased and infiltrated inhibitory immunologic cells and cytokines, and the stress induced cell senescence by SENEX gene triggered after drug stimulation has anti-apoptotic and immune-suppressing effect. So we speculate that the SENEX gene triggering senescence is the one of mechanisms for promoting immune escape in relapsed/refractory DLBCL, and will research it in clinical, cellular and animal models three levels using cell culture, molecular biology techniques, such as. DLBCL is the most common in adults Lymphoma, now the relapsed/refractory type hasn’t specially effective treatment, this study may be useful for preventing relapse and developing new immune-targeted treatment. No similar study has been reported till now.