Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia

By M. Dawson, R. Prinjha, A. Dittmann, George Giotopoulos, Marcus Bantscheff, Wai-In Chan, S. Robson, C. Chung, C. Hopf, Mikhail M. Savitski and 17 more. Nature, 2011

1,525 citations recorded by the source corpus.

Subfields: Hematology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/d77530ae38885c2522f5d00b8b97be263f433b76

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Hematology

1. Richard A. Young
2. James E. Bradner
3. Denes Hnisz
4. M. Dawson
5. Tony Kouzarides
6. Peter A. Jones
7. S. Baylin

In Molecular Biology

1. Richard A. Young
2. Denes Hnisz
3. Peter A. Jones
4. S. Baylin
5. James E. Bradner
6. Tong Ihn Lee
7. Charles Y. Lin
8. David A. Orlando

Citations in the corpus

• Epigenetic Determinants of Cancer. (2016, background): “1; Table 2) (Baylin and Jones 2011; Dawson et al. 2011; You and Jones 2012; Garraway and Lander 2013; Shen and Laird 2013; Timp and Feinberg 2013; Audia and Campbell 2014).”
• Metabolic reprogramming and epigenetic modifications on the path to cancer (2021, background): “JQ-1 or I-BET treatment leads to the transcriptional suppression of MYC target genes, resulting in antitumor effects in MYC-driven models of AML (Dawson et al., 2011; Zuber et al., 2011), Burkitt’s lymphoma (Mertz et al., 2011) and multiple © The Author(s) 2021 895 P ro te in & C e ll myeloma…”
• The mechanisms behind the therapeutic activity of BET bromodomain inhibition (2014, background): “Importantly, overexpression of either MYC or BCL2 from a heterologous promoter can partially alleviate the anticancer effects of JQ1/I-BET, highlighting that suppression of these genes is an important downstream effect of BET inhibition in these malignancies (Dawson et al., 2011; Delmore et al., 201”
• Selective Inhibition of Tumor Oncogenes by Disruption of Super-Enhancers (2013, background): “These BET inhibitors cause selective repression of the potent MYC oncogene in a range of tumors, including multiple myeloma (MM), Burkitt’s lymphoma (BL), acute myeloid leukemia (AML), and acute lymphoblastic leukemia (ALL) (Dawson et al., 2011; Delmore et al., 2011; Mertz et al., 2011; Ott et al., ”
• A CRISPR Dropout Screen Identifies Genetic Vulnerabilities and Therapeutic Targets in Acute Myeloid Leukemia (2016, background): “…mechanistic studies have identified DOT1L as a vulnerability of MLL-rearranged leukemia (Bernt et al., 2011), and both a mechanistic and an RNAi-based epigenetics-focused screen identified BRD4 as a therapeutic target against AMLs of different genotypes (Dawson et al., 2011; Zuber et al., 2011).”