Reflecting on 25 years with MYC

By Natalie Meyer, Linda Z. Penn. Nature Reviews. Cancer, 2008

1,624 citations recorded by the source corpus.

Subfields: Cancer Research, Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/322bd16892bfe09a5633ae7bdba3aaa2829d6a6c

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In Pulmonary and Respiratory Medicine

Citations in the corpus

The Metabolic Profile of Tumors Depends on both the Responsible Genetic Lesion and Tissue Type (2012, background): “One of the well-known consequences of MYC overexpression is the induction of apoptosis by shifting the balance between prosurvival and prodeath signals (Meyer and Penn, 2008).”
Transcriptional Amplification in Tumor Cells with Elevated c-Myc (2012, neutral): “…Hanahan and Weinberg, 2011; Herold et al., 2009; Hoffman and Liebermann, 2008; Hurlin and Dezfouli, 2004; Kuttler and Mai, 2006; Lin et al., 2009; Meyer and Penn, 2008; Nieminen et al., 2007; Nilsson and Cleveland, 2003; Peterson and Ayer, 2011; Prochownik, 2008; Ruggero, 2009; Secombe et al.,…”
Myc and cell cycle control. (2015, background): “(reviewed in [32,93,94]).”
Quantitative interaction proteomics and genome-wide profiling of epigenetic histone marks and their readers. (2010, background): “Since c-Myc is expressed in a broad spectrum of proliferating cell types (Eilers and Eisenman, 2008; Meyer and Penn, 2008), and has been shown to bind P-TEFb and stimulate elongation at a set of genes in tumor cells (Eberhardy and Farnham, 2001, 2002; Gargano et al.”
Cancer epigenetics: from mechanism to therapy. (2012, background): “MYC is a master regulator of cell proliferation and survival; it is also one of the most common genes dysregulated in cancer (Meyer and Penn, 2008).”
c-Myc and Cancer Metabolism (2012, neutral): “(24), DNA microarray (25), and subtractive hybridization (3, 26).”
c-Myc regulates transcriptional pause release (2010, background): “Since c-Myc is expressed in a broad spectrum of proliferating cell types (Eilers and Eisenman, 2008; Meyer and Penn, 2008), and has been shown to bind P-TEFb and stimulate elongation at a set of genes in tumor cells (Eber-hardy and Farnham, 2001, 2002; Gargano et al., 2007; Kanazawa et al., 2003),…”
Targeting oncogenic Myc as a strategy for cancer treatment (2018, background): “Excess Myc expression can be induced upon retroviral promoter insertion, chromosomal translocation/amplification, activation of super-enhancers within the MYC gene, and/or mutation of upstream signaling pathways that enhance Myc stability.(5) Studies in transgenic mouse models have demonstrated that”