ArticleCancer discovery2017
Targeting HDAC3 in CREBBP-Mutant Lymphomas Counterstrikes Unopposed Enhancer Deacetylation of B-cell Signaling and Immune Response Genes.
Article in Cancer discovery, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Review
- Targeting AURKA to induce synthetic lethality in CREBBP-deficient B-cell malignancies via attenuation of MYC expression.Oncogene · 2024Article
- The Role of CREBBP/EP300 and Its Therapeutic Implications in Hematological Malignancies.Cancers · 2023Review
- Preclinical Evaluation of the HDAC Inhibitor Chidamide in Transformed Follicular Lymphoma.Frontiers in oncology · 2021Article
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Abstract
The cellular phenotype of B-cell lymphomas arising from B cells undergoing germinal center reactions, such as follicular lymphoma and diffuse large B-cell lymphoma, is strongly shaped by mutations in chromatin-modifying genes. The work presented by Jiang and colleagues addresses how somatic mutations in CREBBP disable acetylation and cause unopposed deacetylation by BCL6/SMRT/HDAC3 complexes on enhancers of B-cell signaling and immune response genes. This opens a therapeutic avenue toward targeted inhibition of CREBBP-mutant lymphomas by HDAC inhibitors. Cancer Discov; 7(1); 14-6. ©2017 AACRSee related article by Jiang et al., p. 38.
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