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• W3042477647 abstract "Notch activation is highly prevalent among cancers, in particular T-cell acute lymphoblastic leukemia (T-ALL). However, the use of pan-Notch inhibitors to treat cancers has been hampered by adverse effects, particularly intestinal toxicities. To circumvent this barrier in T-ALL, we aimed to inhibit ETS1, a developmentally important T-cell transcription factor previously shown to co-bind Notch response elements. Using complementary genetic approaches in mouse models, we show that ablation of Ets1 leads to strong Notch-mediated suppressive effects on T-cell development and leukemogenesis, but milder intestinal effects than pan-Notch inhibitors. Mechanistically, genome-wide chromatin profiling studies demonstrate that Ets1 inactivation impairs recruitment of multiple Notch-associated factors and Notch-dependent activation of transcriptional elements controlling major Notch-driven oncogenic effector pathways. These results uncover previously unrecognized hierarchical heterogeneity of Notch-controlled genes and points to Ets1-mediated enucleation of Notch-Rbpj transcriptional complexes as a target for developing specific anti-Notch therapies in T-ALL that circumvent the barriers of pan-Notch inhibition." @default.
• W3042477647 created "2020-07-23" @default.
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• W3042477647 date "2020-07-14" @default.
• W3042477647 modified "2023-10-16" @default.
• W3042477647 title "Combinatorial ETS1-Dependent Control of Oncogenic NOTCH1 Enhancers in T-cell Leukemia" @default.
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• W3042477647 doi "https://doi.org/10.1158/2643-3230.bcd-20-0026" @default.
• W3042477647 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7482717" @default.
• W3042477647 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32924017" @default.
• W3042477647 hasPublicationYear "2020" @default.
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