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• W2094448610 abstract "Activating mutations of NOTCH1 and deletion of the INK4A-ARF (CDKN2A) tumor suppressor locus are two of the most frequent genetic alterations in T cell acute lymphoblastic leukemia (T-ALL). In a murine model of T-ALL induced by the intracellular domain of Notch1 (ICN1), the genetic interaction between ICN1 signaling and Arf inactivation is developmentally stage-specific, with a more pronounced requirement for Arf deletion in thymocytes than in bone marrow precursors targeted for transformation. In the thymus, the target cell for transformation is a CD4 and CD8 double-negative progenitor that undergoes T cell receptor beta-chain rearrangement, a cell type in which polycomb silencing of Ink4a-Arf is normally requisite. Epigenetic remodeling during tumor progression licenses Arf as a tumor suppressor and in turn provides the selective pressure for Ink4a-Arf deletion in clonal T-ALLs that emerge." @default.
• W2094448610 created "2016-06-24" @default.
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• W2094448610 date "2013-04-01" @default.
• W2094448610 modified "2023-09-28" @default.
• W2094448610 title "Epigenetic regulation of the Ink4a-Arf (Cdkn2a) tumor suppressor locus in the initiation and progression of Notch1-driven T cell acute lymphoblastic leukemia" @default.
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• W2094448610 doi "https://doi.org/10.1016/j.exphem.2012.11.006" @default.
• W2094448610 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3860824" @default.
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