Genetically engineered mouse models of cancer reveal new insights about the antitumor immune response

被引:68
作者
DuPage, Michel [1 ,2 ]
Jacks, Tyler [1 ,2 ,3 ]
机构
[1] MIT, Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA
[2] MIT, Dept Biol, Cambridge, MA 02139 USA
[3] MIT, Howard Hughes Med Inst, Cambridge, MA 02139 USA
关键词
TUMOR-SPECIFIC ANTIGENS; T-CELL RESPONSES; INFLAMMATION; MICROENVIRONMENT; SURVEILLANCE; CHEMOTHERAPY; PROMOTES; XENOGRAFTS; INHIBITION; EXPRESSION;
D O I
10.1016/j.coi.2013.02.005
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Cancer is a complex disease that can originate in virtually all the tissues of the body, and tumors progress through many different stages during their development. While genetic mutations in the emerging cancer cells drive this disease, it has become increasingly clear that cancer development is strongly influenced by the surrounding microenvironment. Cells of the immune system are critical components of this extrinsic network of cancer regulators, contributing significantly to the microenvironment of most cancers and either promoting or inhibiting the initiation and progression of this disease. Genetically engineered mouse (GEM) mouse models of spontaneous cancer are starting to shape our understanding of how antitumor T cells may act to prevent or inhibit cancer progression in some settings and not others. Lessons learned from investigating spontaneous mouse cancer models have important implications for directing clinical efforts that attempt to direct a cancer patient's immune system to eradicate their disease.
引用
收藏
页码:192 / 199
页数:8
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