Sustained Loss of a Neoplastic Phenotype by Brief Inactivation of MYC

By Meenakshi Jain, Constadina Arvanitis, K. Chu, W. Dewey, E. Leonhardt, Maxine Trinh, Christopher D. Sundberg, J. Bishop, Dean W. Felsher. Science, 2002

685 citations recorded by the source corpus.

Subfields: Hematology, Neurology, Oncology

View Paper: https://www.semanticscholar.org/paper/eda2a723b3bb09f26fda419accaf1039a82a527e

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Citations in the corpus

c-MYC: more than just a matter of life and death (2002, background): “Further to these findings, it was recently shown that transient, rather than sustained, inactivation of c-MYC is sufficient for the full reversal of malignant osteogenic sarcoma in transgenic mic”
BET bromodomain inhibition as a therapeutic strategy to target c-Myc (2011, positive): “In addition, conditional transgenic models featuring tunable transcriptional suppression have shown that even transient inactivation ofMYC is capable of promoting tumor regression (Jain et al., 2002; Soucek et al., 1998; Soucek et al., 2002).”
Liquid-Liquid Phase Separation in Disease. (2019, background): “Many human cancers, for example, exhibit defects that lead to transcriptional dysregulation of the MYC oncoprotein (18, 49, 77).”
MYC on the Path to Cancer (2012, background): “In some cases, a brief suppression ofMYC is sufficient to reverse in vivo tumorigenesis (Jain et al., 2002), but not in other cases (Boxer et al.”
c-Myc controls the balance between hematopoietic stem cell self-renewal and differentiation. (2004, background): “…of division, apoptosis, cellular growth, angiogenesis, and differentiation (Amati et al. 1998; Schuhmacher et al. 1999; Grandori et al. 2000; Jain et al. 2002; Pelengaris et al. 2002b; Bellmeyer et al. 2003; Watnick et al. 2003). c-Myc dimerizes in the cell with the ubiquitous protein Max,…”
Androgen-Induced Differentiation and Tumorigenicity of Human Prostate Epithelial Cells (2004, background): “Moreover, this addictive phenotype (58) is reminiscent of other oncogenes such as RAS (59), MYC (60, 61), and Bcr-Abl (62), whose continued expression are required for tumor maintenance and help explain the salutatory effects of androgen ablation in patients with metastatic prostate cancer.”
Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction (2009, methodology): “For example, mouse models using an inducible MYC oncogene have shown that MYCdriven skin papillomas, lymphomas, and osteosarcomas can all be reversed upon MYC withdrawal (Felsher and Bishop, 1999; Jain et al., 2002; Pelengaris et al., 1999).”
Reflecting on 25 years with MYC (2008, background): “Following differentiation, reactivation of the MYC allele did not lead to new tumours; instead, the MYC-expressing cells were eliminated through apoptosi”
MYC inactivation uncovers pluripotent differentiation and tumour dormancy in hepatocellular cancer (2004, background): “, indicating that, at least in some cases, oncogene inactivation may result in the permanent loss of a neoplastic phenotyp”
Selective Inhibition of Tumor Oncogenes by Disruption of Super-Enhancers (2013, background): “Tumor cells frequently become addicted to oncogenes, thus becoming unusually reliant on high-level expression of these genes (Cheung et al., 2011; Chin et al., 1999; Felsher and Bishop, 1999; Garraway and Sellers, 2006; Garraway et al., 2005; Jain et al., 2002; Weinstein, 2002).”
Differential requirements for Runx proteins in CD4 repression and epigenetic silencing during T lymphocyte development. (2002, background): “…and repress carcinogene-Runx3 transcript levels between cells of the helper and cytotoxic lineage, indicating that expression of Runx sis, as temporal inactivation of Myc resulted in the sustained loss of a neoplastic phenotype (Jain et al., 2002).genes is not sufficient to induce CD4 silencing.”
Transcriptional Amplification in Tumor Cells with Elevated c-Myc (2012, positive): “MYC is a potent oncogene that can promote tumorigenesis in a wide range of tissues (Felsher and Bishop, 1999; Flores et al., 2004; Jain et al., 2002; Pelengaris et al., 1999; Sodir et al., 2011; Soucek et al., 2008; Verbeek et al., 1991).”