Targeting MYCN in neuroblastoma by BET bromodomain inhibition.
By A. Puissant, Stacey M. Frumm, G. Alexe, Christopher F. Bassil, J. Qi, Yvan H. Chanthery, Erin A Nekritz, Rhamy Zeid, W. Gustafson, Patricia Greninger and 7 more. Cancer Discovery, 2013
628 citations recorded by the source corpus.
Subfields: Hematology, Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/82c53a0ebad41acaff1e2ed06bb83013fa14db03
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Hematology
In Molecular Biology
- Richard A. Young
- Denes Hnisz
- James E. Bradner
- C. Crews
- Charles Y. Lin
- P. Rahl
- Stefano Monti
- John G Doench
Citations in the corpus
- Discovery and Characterization of Super-Enhancer Associated Dependencies in Diffuse Large B-Cell Lymphoma (2013, positive): “Consistent with prior studies of BET bromodomain function and inhibition, HEXIM1 was markedly up-regulated by JQ1 in all DLBCL cell lines (Figure S2B) (Bartholomeeusen et al., 2012; Puissant et al., 2013).”
- Hijacking the E3 Ubiquitin Ligase Cereblon to Efficiently Target BRD4. (2015, background): “Also, not surprisingly, high sensitivity to BRD4 inhibitors, such as JQ1, has been associated with high level of either c-MYC or n-MYC in different tumor types, including c-MYC-driven BL (Baratta et al., 2015; Loosveld et al., 2014; Mertz et al., 2011; Puissant et al., 2013).”
- The mechanisms behind the therapeutic activity of BET bromodomain inhibition (2014, background): “Neuroblastomas that harbor NMYC amplifications are also sensitive to JQ1, correlating with suppression of NMYC transcription (Puissant et al., 2013).”
- Targeting oncogenic Myc as a strategy for cancer treatment (2018, background): “Neuroblastomas and other MYCN-driven cancers are also sensitive to BET inhibitors.(23) GSK525762, a specific BET inhibitor, is currently in early-phase clinical trials for treating these hematopoietic malignancies and solid tumors (ClinicalTrials.”
- Neuroblastoma and MYCN (2013, background): “Mice treated with JQ1 showed a significant increase in overall survival, and tumors showed increased apoptosis and decreased proliferation as well as decreased expression of MYCN itself (Puissant et al. 2013).”
- Transcriptional Addiction in Cancer (2017, positive): “Moreover, BRD4 function has emerged as a transcriptional addiction in MYCN-amplified neuroblastomas (Puissant et al., 2013), a positive regulator of anti-apoptotic gene expression in AMLs (Dawson et al.”