ArticleBlood2022
Tcf1 is essential for initiation of oncogenic Notch1-driven chromatin topology in T-ALL.
Article in Blood, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Enhancers in T Cell development and malignant lesions.Cell death discovery · 2024Review
- Baf155 controls hematopoietic differentiation and regeneration through chromatin priming.Cell reports · 2024Article
- Cdc73 protects Notch-induced T-cell leukemia cells from DNA damage and mitochondrial stress.Blood · 2023Article
- Review
- Three-dimensional genome organization in immune cell fate and function.Nature reviews. Immunology · 2023Review
- The Interplay of Transcription and Genome Topology Programs T Cell Development and Differentiation.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- TCF-1 promotes chromatin interactions across topologically associating domains in T cell progenitors.Nature immunology · 2022Article
- Firing up chromatin to forge T-ALL.Blood · 2022Article
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19 authors.
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Abstract
NOTCH1 is a well-established lineage specifier for T cells and among the most frequently mutated genes throughout all subclasses of T cell acute lymphoblastic leukemia (T-ALL). How oncogenic NOTCH1 signaling launches a leukemia-prone chromatin landscape during T-ALL initiation is unknown. Here we demonstrate an essential role for the high-mobility-group transcription factor Tcf1 in orchestrating chromatin accessibility and topology, allowing aberrant Notch1 signaling to convey its oncogenic function. Although essential, Tcf1 is not sufficient to initiate leukemia. The formation of a leukemia-prone epigenetic landscape at the distal Notch1-regulated Myc enhancer, which is fundamental to this disease, is Tcf1-dependent and occurs within the earliest progenitor stage even before cells adopt a T lymphocyte or leukemic fate. Moreover, we discovered a unique evolutionarily conserved Tcf1-regulated enhancer element in the distal Myc-enhancer, which is important for the transition of preleukemic cells to full-blown disease.
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