Combining cancer immunotherapy and targeted therapy

被引:57
|
作者
Ribas, Antoni [1 ,2 ,3 ,4 ]
Wolchok, Jedd D. [5 ,6 ,7 ]
机构
[1] Univ Calif Los Angeles, Dept Med, Div Hematol Oncol, Los Angeles, CA 90024 USA
[2] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90024 USA
[3] Univ Calif Los Angeles, Dept Surg, Los Angeles, CA 90024 USA
[4] Univ Calif Los Angeles, Dept Med & Mol Pharmacol, Los Angeles, CA USA
[5] Weill Cornell Med Coll, Dept Med, Mem Sloan Kettering Canc Ctr, New York, NY USA
[6] Weill Cornell Med Coll, Ludwig Ctr Canc Immunotherapy, Mem Sloan Kettering Canc Ctr, Program Immunol, New York, NY USA
[7] Ludwig Inst Canc Res, New York, NY USA
关键词
HISTONE DEACETYLASE INHIBITORS; MHC CLASS-I; T-CELL RESPONSES; SUBERIC BISHYDROXAMATE; ANTITUMOR-ACTIVITY; KINASE INHIBITOR; RAS MUTATIONS; TUMOR; BRAF; MELANOMA;
D O I
10.1016/j.coi.2013.02.011
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The ability to pharmacologically modulate key signaling pathways that drive tumor growth and progression, but do not negatively impact the function of lymphocytes, provides avenues for rational combinatorial approaches to improve the antitumor activity of tumor immunotherapies. Novel targeted agents can very specifically block oncogenic events in cancer cells, leading to a pro-apoptotic milieu and a potential increase in sensitivity to recognition and attack by cytotoxic T lymphocytes (CTLs). Furthermore, targeted pathway modulation in lymphocytes may change their function and have activating effects in some instances. When tested together with recently developed powerful tumor immunotherapies, such combinations may exploit the highly specific targeting of oncogenes with small molecule inhibitors to lead to high frequency of tumor regressions, and merge this benefit with the durable responses achievable with effective tumor immunotherapies.
引用
收藏
页码:291 / 296
页数:6
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