| First Author | Höpken UE | Year | 2017 |
| Journal | Cancer Discov | Volume | 7 |
| Issue | 1 | Pages | 14-16 |
| PubMed ID | 28062671 | Mgi Jnum | J:238052 |
| Mgi Id | MGI:5818057 | Doi | 10.1158/2159-8290.CD-16-1285 |
| Citation | Hopken UE (2017) Targeting HDAC3 in CREBBP-Mutant Lymphomas Counterstrikes Unopposed Enhancer Deacetylation of B-cell Signaling and Immune Response Genes. Cancer Discov 7(1):14-16 |
| abstractText | 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. (c)2017 AACRSee related article by Jiang et al., p. 38. |
