Notch signaling: switching an oncogene to a tumor suppressor
Year: 2014
Type: review
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.
Source: Blood
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
Awards: Discovery of New Targets and Pathways for T-ALL Therapy, Medical Scientist Research Service Award, Mechanisms of T cell leukemia induction and maintenance, Modifiers of Notch stability and their role in cancer, The role of the SCF/FBW7 ubiquitin ligase complex in hematopiesis and leukemia., Genetic Dissection of Acute Myeloid Leukemia., Role of TET2 mutations in malignant transformation and acute myeloid leukemia, Molecular Pathways to Thynmic Lymphoma and Leukemia, Regulation of hematopoietic stem cell differentiation, Dana-Farber/Harvard Cancer Center
OpenAlex ID: W2014952486