期刊
MOLECULAR BIOLOGY OF THE CELL
卷 23, 期 1, 页码 1-6出版社
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E10-04-0335
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资金
- National Cancer Institute [CA139980]
- NATIONAL CANCER INSTITUTE [P01CA139980, R01CA164448] Funding Source: NIH RePORTER
Cytotoxic cancer chemotherapy drugs are believed to gain selectivity by targeting cells that proliferate rapidly. However, the proliferation rate is low in many chemosensitive human cancers, and it is not clear how a drug that only kills dividing cells could promote tumor regression. Four potential solutions to this proliferation rate paradox are discussed for the microtubule-stabilizing drug paclitaxel: drug retention in tumors, killing of quiescent cells, targeting of noncancer cells in the tumor, and bystander effects. Testing these potential mechanisms of drug action will facilitate rational improvement of antimitotic chemotherapy and perhaps cytotoxic chemotherapy more generally.
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