期刊
CANCER CELL
卷 25, 期 3, 页码 318-334出版社
CELL PRESS
DOI: 10.1016/j.ccr.2014.02.018
关键词
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资金
- National Institutes of Health [1R01CA169784, 1R01CA133379, 1R01CA105129, 1R01CA149655, 5R01CA173636, 1R01CA172560]
- William Lawrence and Blanche Hughes Foundation
- Leukemia & Lymphoma Society (TRP) [6340-11, LLS 6373-13]
- Chemotherapy Foundation
- V Foundation for Cancer Research
- Alex's Lemonade Stand Foundation for Childhood Cancer
- St. Baldrick's Cancer Research Foundation
- Lady Tata Memorial Trust
- American Society for Hematology [118898-RSG-10-071-01-TBG]
- Leukemia & Lymphoma Society [LLS 1029-10]
- A*STAR in Singapore
Since Notch phenotypes in Drosophila melanogaster were first identified 100 years ago, Notch signaling has been extensively characterized as a regulator of cell-fate decisions in a variety of organisms and tissues. However, in the past 20 years, accumulating evidence has linked alterations in the Notch pathway to tumorigenesis. In this review, we discuss the protumorigenic and tumor-suppressive functions of Notch signaling, and dissect the molecular mechanisms that underlie these functions in hematopoietic cancers and solid tumors. Finally, we link these mechanisms and observations to possible therapeutic strategies targeting the Notch pathway in human cancers.
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