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10.1182/blood-2013-08-355818

http://scihub22266oqcxt.onion/10.1182/blood-2013-08-355818
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C3990910!3990910!24608975
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suck abstract from ncbi


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pmid24608975      Blood 2014 ; 123 (16): 2451-9
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  • Notch signaling: switching an oncogene to a tumor suppressor #MMPMID24608975
  • Lobry C; Oh P; Mansour MR; Look AT; Aifantis I
  • Blood 2014[Apr]; 123 (16): 2451-9 PMID24608975show ga
  • 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 hyperactivation 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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