Promiscuous mutations activate the noncanonical NF-kappaB pathway in multiple myeloma.
By J. Keats, R. Fonseca, M. Chesi, R. Schop, A. Baker, W. Chng, S. V. Van Wier, R. Tiedemann, C. Shi, M. Sebag and 20 more. Cancer Cell, 2007
1,072 citations recorded by the source corpus.
Subfields: Cancer Research, Hematology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/fdfa00a94449f9f75c4d221afd15e0fdedb260f9
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Citations in the corpus
- BET bromodomain inhibition as a therapeutic strategy to target c-Myc (2011, neutral): “In marked contrast, JQ1 treatment did not exert significant suppression of gene sets for other transcription factors linked to pathophysiology of MM, including NF-kB, AP-1, STAT3, GR, and XBP-1 (Figure 2E and Figure S2).”
- NF‐κB and the link between inflammation and cancer (2012, background): “Clues as to possible alternative functions for IKKa were arrived at through the notice that the aly mouse which is defective in NIK activity, the relb) ⁄ ) mouse and the IKKa) ⁄ ) mouse all suffer from defective secondary lymphoid organ development (80–83).”
- IL-6 in inflammation, autoimmunity and cancer (2020, background): “LOF mutations of TRAF3, a negative regulator of IL-6–STAT3 signaling, are observed in B-cell lymphoma and multiple myeloma patients (122, 273, 274).”
- Targeting NF-κB pathway for the therapy of diseases: mechanism and clinical study (2020, background): “On the other hand, deletion of NIK suppresses tumor formation in mouse model.(392) Besides, rearrangement or mutations of NF-κB2 have also been found in various human malignancies, including multiple myeloma, T-cell and B-cell lymphoma, with constitutive processing of p100, resulting in sequential n”
- IAPs: from caspase inhibitors to modulators of NF-κB, inflammation and cancer (2010, background): “Therefore, depending on cellular context, IAPs seem to have both pro-tumorigenic and anti-tumorigenic role”
- Widespread genetic heterogeneity in multiple myeloma: implications for targeted therapy (2014, neutral): “An additional four genes (BRAF, TRAF3, CYLD, and RB1) have been implicated in the pathogenesis of MM (Annunziata et al., 2007; Chapman et al., 2011; Demchenko et al., 2010; Keats et al., 2007; Walker et al., 2012).”