Senescence and the tumor-immune landscape: Implications for cancer immunotherapy.
Senescence and the tumor-immune landscape: Implications for cancer immunotherapy.
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DOI：
10.1016/j.semcancer.2022.02.005
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发表时间：
2022-11
影响因子：
14.5
通讯作者：
Ruscetti, Marcus
中科院分区：
文献类型：
--
作者：
Chibaya, Loretah;Snyder, Jarin;Ruscetti, Marcus
关键词：
癌症治疗，包括常规化疗、放疗和分子靶向药物，可以通过多种机制根除肿瘤。除了对肿瘤细胞生长和存活的影响外，这些方案还可以影响周围的肿瘤免疫微环境，最终影响治疗反应。癌症治疗的独特生物学结果是诱导细胞衰老。衰老是一种损伤诱导的应激程序，其通过激活一系列多效性细胞因子、趋化因子、生长因子和蛋白酶（称为衰老相关分泌表型（SASP）），导致肿瘤细胞的持久停滞和肿瘤免疫微环境的重塑。根据癌症背景和治疗的作用机制，治疗诱导衰老（TIS）后产生的SASP可以促进抗肿瘤免疫，增强治疗效果，或者促进导致治疗失败和肿瘤复发的慢性炎症。因此，更深入地了解调节SASP的机制以及在不同癌症和治疗背景下强大的抗免疫监视所必需的组分是利用衰老控制肿瘤的关键。在这里，我们绘制了一个路线图，以调节TIS及其免疫刺激功能，用于癌症免疫治疗。
Cancer therapies, including conventional chemotherapy, radiation, and molecularly targeted agents, can lead to tumor eradication through a variety of mechanisms. In addition to their effects on tumor cell growth and survival, these regimens can also influence the surrounding tumor-immune microenvironment in ways that ultimately impact therapy responses. A unique biological outcome of cancer therapy is induction of cellular senescence. Senescence is a damage-induced stress program that leads to both the durable arrest of tumor cells and remodeling the tumor-immune microenvironment through activation of a collection pleiotropic cytokines, chemokines, growth factors, and proteinases known as the senescence-associated secretory phenotype (SASP). Depending on the cancer context and the mechanism of action of the therapy, the SASP produced following therapy-induced senescence (TIS) can promote anti-tumor immunity that enhances therapeutic efficacy, or alternatively chronic inflammation that leads to therapy failure and tumor relapse. Thus, a deeper understanding of the mechanisms regulating the SASP and components necessary for robust anti-immune surveillance in different cancer and therapy contexts are key to harnessing senescence for tumor control. Here we draw a roadmap to modulate TIS and its immune-stimulating features for cancer immunotherapy.
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影响因子：
64.8
作者：
Baker DJ;Childs BG;Durik M;Wijers ME;Sieben CJ;Zhong J;Saltness RA;Jeganathan KB;Verzosa GC;Pezeshki A;Khazaie K;Miller JD;van Deursen JM
通讯作者：
van Deursen JM
影响因子：
9
作者：
通讯作者：
--
DOI：
10.1083/jcb.201608026
发表时间：
2016-11-07
期刊：
The Journal of cell biology
影响因子：
--
作者：
Aird KM;Iwasaki O;Kossenkov AV;Tanizawa H;Fatkhutdinov N;Bitler BG;Le L;Alicea G;Yang TL;Johnson FB;Noma KI;Zhang R
通讯作者：
Zhang R
影响因子：
5.9
作者：
Andersson A;Bergenstråhle J;Asp M;Bergenstråhle L;Jurek A;Fernández Navarro J;Lundeberg J
通讯作者：
Lundeberg J
影响因子：
11.5
作者：
Angevin, Eric;Tabernero, Josep;Kurzrock, Razelle
通讯作者：
Kurzrock, Razelle