MYC inactivation uncovers pluripotent differentiation and tumour dormancy in hepatocellular cancer

By C. Shachaf, Andrew M. Kopelman, Constadina Arvanitis, Åsa Karlsson, Shelly Beer, S. Mandl, Michael H. Bachmann, A. Borowsky, B. Ruebner, R. Cardiff and 4 more. Nature, 2004

898 citations recorded by the source corpus.

Subfields: Cell Biology, Hepatology, Oncology

View Paper: https://www.semanticscholar.org/paper/d3fc45120340c24918a75bde1fb3435c079390eb

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Citations in the corpus

Targeting cancer stem cell pathways for cancer therapy (2020, background): “119 Studies have also shown that MYC is highly expressed in glioblastoma multiforme stem cells and induces cell proliferation and invasion and inhibits apoptosis.”
MYC activation is a hallmark of cancer initiation and maintenance. (2014, background): “2006), whereas epithelial tumors such as hepatocellular or breast carcinoma do not (Boxeret al. 2004; Shachaf et al. 2004).”
Therapeutic delivery of miR-26a inhibits cancer cell proliferation and induces tumor-specific apoptosis (2009, positive): “To extend these findings to a solid tumor model and to investigate the potential use of these miRNAs as anticancer therapeutics , we studied their expression in a previously described model of liver cancer in which mice harboring a tetracycline (tet)– repressible MYC transgene (tet-o-MYC) are crosse”
MYC on the Path to Cancer (2012, background): “, 2002), but not in other cases (Boxer et al., 2004; Jonkers and Berns, 2004; Shachaf et al., 2004), suggesting that tissue specificity and either other mutagenic events or epigenetic alterations affect the reversibility of tumorigenesis upon Myc suppression.”
The Metabolic Profile of Tumors Depends on both the Responsible Genetic Lesion and Tissue Type (2012, methodology): “In order to compare the effect of two distinct oncogenes, we used well-characterized mouse models of liver cancer induced by tissue-specific overexpression of either humanMYC (Shachaf et al., 2004) or MET (Wang et al.”
The Cancer Stem Cell Niche: How Essential is the Niche in Regulating Stemness of Tumor Cells? (2015, neutral): “Although angiogenic stimulators such as c-Myc, VEGF, and Fibroblast growth factor 2 (FGF-2) (Shachaf et al., 2004; Naumov et al., 2006) may play a role in mediating tumor exit from dormancy.”
Essential metabolic, anti-inflammatory, and anti-tumorigenic functions of miR-122 in liver. (2012, neutral): “…;LAP-tTA mice compared with normal liver from tet-o-MYC littermates (which lack the LAP-tTA transgene and therefore exogenous MYC expression) (Figure 6A). miR-122 levels were not reduced in normal liver tissue in tet-o-MYC ;LAP-tTA mice, where Myc expression is only minimally increased (34).”