期刊
CANCER CELL
卷 20, 期 6, 页码 755-767出版社
CELL PRESS
DOI: 10.1016/j.ccr.2011.10.019
关键词
-
资金
- DFG [SFB TR36]
- European Community
- HGF [HA-202]
The genetic instability of cancer cells frequently causes drug resistance. We established mouse cancer models, which allowed targeting of an oncogene by drug-mediated inactivation or monospecific CD8(+) effector T (T-E) cells. Drug treatment of genetically unstable large tumors was effective but selected resistant clones in the long term. In contrast, T-E cells completely rejected large tumors (>= 500 mm(3)), if the target antigen was cancer-driving and expressed in sufficient amounts. Although drug-mediated oncogene inactivation selectively killed the cancer cells and left the tumor vasculature intact, which likely facilitated survival and growth of resistant clones, T-E cell treatment led to blood vessel destruction and probably bystander elimination of escape variants, which did not require antigen cross-presentation by stromal cells.
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