期刊
BLOOD
卷 123, 期 16, 页码 2451-2459出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2013-08-355818
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资金
- Research Project Grant Program of the National Cancer Institute [RO1CA173636, RO1CA133379, RO1CA105129, RO1CA149655]
- Leukemia & Lymphoma Society
- V Foundation for Cancer Research
- William Lawrence and Blanche Hughes Foundation
- St. Baldrick's Foundation for Cancer Research
- New York University Medical Scientist Training Program
- Helen and Martin Kimmel Center for Stem Cell Research
- Kay Kendall Leukaemia Fund of the United Kingdom
- Claudia Adams Barr foundation of the Dana Farber Cancer Institute
- National Cancer Institute [5P01CA109901, 1R01CA176746, P30CA06516]
- Alex's Lemonade Stand
- Team Path To the Cure grant
- MRC [G0500389] Funding Source: UKRI
- Medical Research Council [G0500389] Funding Source: researchfish
The Notch signaling pathway is a regulator of self-renewal and differentiation in several tissues and cell types. Notch is a binary cell-fate determinant, and its hyper-activation has been implicated as oncogenic in several cancers including breast cancer and T-cell acute lymphoblastic leukemia (T-ALL). Recently, several studies also unraveled tumor-suppressor roles for Notch signaling in different tissues, including tissues where it was before recognized as an oncogene in specific lineages. Whereas involvement of Notch as an oncogene in several lymphoid malignancies (T-ALL, B-chronic lymphocytic leukemia, splenic marginal zone lymphoma) is well characterized, there is growing evidence involving Notch signaling as a tumor suppressor in myeloid malignancies. It therefore appears that Notch signaling pathway's oncogenic or tumor-suppressor abilities are highly context dependent. In this review, we summarize and discuss latest advances in the understanding of this dual role in hematopoiesis and the possible consequences for the treatment of hematologic malignancies.
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