Targeting MYC dependence in cancer by inhibiting BET bromodomains

By J. Mertz, A. Conery, Barbara Bryant, P. Sandy, S. Balasubramanian, Deanna A. Mele, L. Bergeron, R. Sims. Proceedings of the National Academy of Sciences of the United States of America, 2011

1,130 citations recorded by the source corpus.

Subfields: Hematology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/0ade9a2c2bc9863cb5464a53a742d68adabb982a

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. M. Dawson
4. Tony Kouzarides

In Molecular Biology

1. Richard A. Young
2. James E. Bradner
3. Tong Ihn Lee
4. C. V. Dang
5. C. Crews
6. Ping Gao
7. Huafeng Zhang
8. Charles Y. Lin

Citations in the corpus

• Discovery and Characterization of Super-Enhancer Associated Dependencies in Diffuse Large B-Cell Lymphoma (2013, positive): “…has recently identified a role for BET bromodomains in supporting the transcription of known DLBCL oncogenes (MYC and BCL2) in studies of acute leukemia, multiple myeloma and Burkitt lymphoma (Dawson et al., 2011; Delmore et al., 2011; Mertz et al., 2011; Ott et al., 2012; Zuber et al., 2011).”
• Selective Inhibition of Tumor Oncogenes by Disruption of Super-Enhancers (2013, background): “Although BRD4 is widely expressed in mouse tissues, mice are reasonably tolerant of the levels of BET bromodomain inhibition that inhibit certain tumors in mouse models (Dawson et al., 2011; Delmore et al., 2011; Filippakopoulos et al., 2010; Mertz et al., 2011; Zuber et al., 2011).”
• The PI3K pathway in human disease (2017, neutral): “Finally, primaryoracquiredresistancecanalsoarisebyactivationofheterologous pathwaysleadingtocommonendpoints;forinstance,MYC-dependent transcriptional activation or ERK activity (in pink, ‘‘4’’). mTORC2 and PDK1 and shares with AKT the ability to phosphorylate TSC2, leading to mTORC1 activation.”
• Histone Recognition and Large-Scale Structural Analysis of the Human Bromodomain Family (2012, background): “Recent data strongly suggested that targeting BET BRDs will be beneficial for many diverse cancer types due to downregulation of oncogenes such as c-Myc (Dawson et al., 2011; Delmore et al., 2011; Mertz et al., 2011).”
• MYC on the Path to Cancer (2012, background): “Inhibition of the BET BRD4 protein, thus, proves effective in an in vivo preclinical mode, suggesting that targeting MYC expression is feasible in selected cancers (Delmore et al., 2011; Mertz et al., 2011).”
• Drugging the ‘undruggable’ cancer targets (2017, neutral): “Although the bromodomain and extraterminal (BET) inhibitors have been touted to target MYC, their pleiotropic effect complicates matters and in some instances their activities are independent of an effect on MYC 28 .”
• Hijacking the E3 Ubiquitin Ligase Cereblon to Efficiently Target BRD4. (2015, background): “…in multiple cancer types, including midline carcinoma, acute myeloid leukemia (AML), multiple myeloma (MM), Burkitt’s lymphoma (BL), and prostate cancer (Asangani et al., 2014; Delmore et al., 2011; French et al., 2008; Loven et al., 2013; Mertz et al., 2011; Wyce et al., 2013; Zuber et al., 2011).”
• Cancer epigenetics: from mechanism to therapy. (2012, background): “…the expression of MYC was noted to be substantially decreased in a variety of malignant hematopoietic cell lines, including MLL-translocated acute myeloid leukemia (Dawson et al., 2011; Zuber et al., 2011), multiple myeloma (Delmore et al., 2011), and Burkitt's lymphoma (Mertz et al., 2011).”