| Literature DB >> 16166587 |
Jennifer O'Neil1, Jennifer Calvo, Keith McKenna, Veena Krishnamoorthy, Jon C Aster, Craig H Bassing, Frederick W Alt, Michelle Kelliher, A Thomas Look.
Abstract
Recent studies have demonstrated that most patients with T-cell acute lymphocytic leukemia (T-ALL) have activating mutations in NOTCH1. We sought to determine whether these mutations are also acquired in mouse models of T-ALL. We sequenced the heterodimerization domain and the PEST domain of Notch1 in our mouse model of TAL1-induced leukemia and found that 74% of the tumors harbor activating mutations in Notch1. Cell lines derived from these tumors undergo G(0)/G(1) arrest and apoptosis when treated with a gamma-secretase inhibitor. In addition, we found activating Notch1 mutations in 31% of thymic lymphomas that occur in mice deficient for various combinations of the H2AX, Tp53, and Rag2 genes. Thus, Notch1 mutations are often acquired as a part of the molecular pathogenesis of T-ALLs that develop in mice with known predisposing genetic alterations.Entities:
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Year: 2005 PMID: 16166587 PMCID: PMC1895623 DOI: 10.1182/blood-2005-06-2553
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113