| Literature DB >> 28314854 |
Giulia Fabbri1, Antony B Holmes1, Mara Viganotti1, Claudio Scuoppo1, Laura Belver1, Daniel Herranz1, Xiao-Jie Yan2, Yasmine Kieso2, Davide Rossi3,4, Gianluca Gaidano5, Nicholas Chiorazzi2, Adolfo A Ferrando1,6,7, Riccardo Dalla-Favera8,6,9,10.
Abstract
Activating mutations of NOTCH1 (a well-known oncogene in T-cell acute lymphoblastic leukemia) are present in ∼4-13% of chronic lymphocytic leukemia (CLL) cases, where they are associated with disease progression and chemorefractoriness. However, the specific role of NOTCH1 in leukemogenesis remains to be established. Here, we report that the active intracellular portion of NOTCH1 (ICN1) is detectable in ∼50% of peripheral blood CLL cases lacking gene mutations. We identify a "NOTCH1 gene-expression signature" in CLL cells, and show that this signature is significantly enriched in primary CLL cases expressing ICN1, independent of NOTCH1 mutation. NOTCH1 target genes include key regulators of B-cell proliferation, survival, and signal transduction. In particular, we show that NOTCH1 transactivates MYC via binding to B-cell-specific regulatory elements, thus implicating this oncogene in CLL development. These results significantly extend the role of NOTCH1 in CLL pathogenesis, and have direct implications for specific therapeutic targeting.Entities:
Keywords: NOTCH1; chronic lymphocytic leukemia; transcriptional network
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Year: 2017 PMID: 28314854 PMCID: PMC5389283 DOI: 10.1073/pnas.1702564114
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN: 0027-8424 Impact factor: 11.205