ArticleBlood2024
Transcriptional control of leukemogenesis by the chromatin reader SGF29.
Article in Blood, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Disrupting a Convergent Acetylation Circuit Collapses Leukemic Identity Across AML Subtypes.bioRxiv : the preprint server for biology · 2026Article
- Sgf29 regulates pluripotency by maintaining chromatin accessibility and promoting the expression of core transcription factors.Science China. Life sciences · 2026Article
- Disruption of the SAGA CORE triggers collateral degradation of KAT2A.Nature communications · 2026Article
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- Stem Cell for Cancer Immunotherapy: Current Approaches and Challenges.Stem cell reviews and reports · 2025Review
- Systematic decoding of functional enhancer connectomes and risk variants in human glioma.Nature cell biology · 2025Article
- Targeting SUMO2 reverses aberrant epigenetic rewiring driven by SS18::SSX fusion oncoproteins and impairs sarcomagenesis.The EMBO journal · 2025Article
- Review
- Epigenetic dysregulation in acute myeloid leukemia.Seminars in hematology · 2025Review
- Review
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Authors and funding
21 authors at 8 institutions in 4 countries.
Funding
Abstract
abstractAberrant expression of stem cell-associated genes is a common feature in acute myeloid leukemia (AML) and is linked to leukemic self-renewal and therapy resistance. Using AF10-rearranged leukemia as a prototypical example of the recurrently activated "stemness" network in AML, we screened for chromatin regulators that sustain its expression. We deployed a CRISPR-Cas9 screen with a bespoke domain-focused library and identified several novel chromatin-modifying complexes as regulators of the TALE domain transcription factor MEIS1, a key leukemia stem cell (LSC)-associated gene. CRISPR droplet sequencing revealed that many of these MEIS1 regulators coordinately controlled the transcription of several AML oncogenes. In particular, we identified a novel role for the Tudor-domain-containing chromatin reader protein SGF29 in the transcription of AML oncogenes. Furthermore, SGF29 deletion impaired leukemogenesis in models representative of multiple AML subtypes in multiple AML subtype models. Our studies reveal a novel role for SGF29 as a nononcogenic dependency in AML and identify the SGF29 Tudor domain as an attractive target for drug discovery.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.