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Notch signaling: switching an oncogene to a tumor suppressor

Blood. 2014 Apr 17;123(16):2451-9. doi: 10.1182/blood-2013-08-355818. Epub 2014 Mar 7.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Erythrocytes / physiology
  • Genes, Switch
  • Genes, Tumor Suppressor / physiology*
  • Hematologic Neoplasms / drug therapy
  • Hematologic Neoplasms / metabolism
  • Hematopoiesis / genetics
  • Hematopoietic Stem Cells / physiology
  • Humans
  • Megakaryocytes / physiology
  • Oncogenes / physiology*
  • Receptors, Notch / physiology*
  • Signal Transduction / physiology

Substances

  • Receptors, Notch