IRF4 addiction in multiple myeloma
By A. Shaffer, N. Emre, L. Lamy, Vu N. Ngo, George E. Wright, Wenming Xiao, J. Powell, S. Dave, Xin Yu, Hong Zhao and 4 more. Nature, 2008
706 citations recorded by the source corpus.
Subfields: Hematology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/defc39685095c2c8b6dc5a88ae3f1e0aaaca10f3
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In Hematology
In Molecular Biology
- Richard A. Young
- James E. Bradner
- Tong Ihn Lee
- Charles Y. Lin
- David A. Orlando
- Heather A. Hoke
- K. Honda
- E. Stanley
Citations in the corpus
- Selective Inhibition of Tumor Oncogenes by Disruption of Super-Enhancers (2013, background): “The IRF4 gene encodes a key plasma cell transcription factor that is frequently deregulated in MM (Shaffer et al., 2008).”
- BET bromodomain inhibition as a therapeutic strategy to target c-Myc (2011, neutral): “…factors features prominently in the biology of MM, including NF-kB (Keats et al., 2007), c-Maf (Hurt et al., 2004), XBP1 (Claudio et al., 2002), HSF1 (Mitsiades et al., 2002), GR (Gomi et al., 1990), IRF4 (Shaffer et al., 2008), Myb (Palumbo et al., 1989), and, notably, c-Myc (Dean et al., 1983).”
- Widespread genetic heterogeneity in multiple myeloma: implications for targeted therapy (2014, neutral): “IRF4 has previously been reported as a MM survival factor, wherein a loss-of-function RNAi screen showed that IRF4 inhibition results in loss of viability of MM cell lines (Shaffer et al., 2008).”
- Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction (2009, positive): “of myelomas lacking IRF4 translocations or overexpression (Shaffer et al., 2008).”
- Targeting MYC dependence in cancer by inhibiting BET bromodomains (2011, background): “BET inhibitors have been shown, in stimulated macrophages, to suppress genes in the NF-κB transcriptional pathway (7) that contribute to the pathogenesis of multiple myeloma (10, 11).”
- IRF4 Transcription Factor-Dependent CD11b+ Dendritic Cells in Human and Mouse Control Mucosal IL-17 Cytokine Responses (2013, result): “This finding is in agreement with a study reporting that IRF4-inhibited apoptosis in myeloid cells (Shaffer et al., 2008).”
- Project DRIVE: A Compendium of Cancer Dependencies and Synthetic Lethal Relationships Uncovered by Large-Scale, Deep RNAi Screening. (2017, neutral): “Finally, IRF4 expression is detectable across multiple lymphoma subtypes whereas IRF4 dependency is uniquely detected in multiple myeloma as previously described (Shaffer et al., 2008).”