期刊
CANCER CELL
卷 22, 期 4, 页码 438-451出版社
CELL PRESS
DOI: 10.1016/j.ccr.2012.09.015
关键词
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资金
- Swedish Foundation
- Wennergren Foundation
- NIH [R01 CA083688, P01 CA080111, P01 CA109901]
- Claudia Adams Barr grant
- Novartis
- National Cancer Institute [1K99CA157951]
- William Lawrence and Blanche Hughes Foundation
- Children's Leukemia Research Association
- Japan Society for the Promotion of Science
D-cyclins represent components of cell cycle machinery. To test the efficacy of targeting D-cyclins in cancer treatment, we engineered mouse strains that allow acute and global ablation of individual D-cyclins in a living animal. Ubiquitous shutdown of cyclin D1 or inhibition of cyclin D-associated kinase activity in mice bearing ErbB2-driven mammary carcinomas triggered tumor cell senescence, without compromising the animals' health. Ablation of cyclin D3 in mice bearing Notch 1-driven T cell acute lymphoblastic leukemias (T-ALL) triggered tumor cell apoptosis. Such selective killing of leukemic cells can also be achieved by inhibiting cyclin D associated kinase activity in mouse and human T-ALL models. Inhibition of cyclin D-kinase activity represents a highly-selective anticancer strategy that specifically targets cancer cells without significantly affecting normal tissues.
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