c-MYC: more than just a matter of life and death

By S. Pelengaris, Michael Khan, G. Evan. Nature Reviews. Cancer, 2002

1,230 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/5407fa6f999ede58458954b7df6843a10892ff7f

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Citations in the corpus

MicroRNA let-7a down-regulates MYC and reverts MYC-induced growth in Burkitt lymphoma cells. (2007, neutral): “41, 42) as have several other laboratories (43, 44).”
dMyc transforms cells into super-competitors. (2004, background): “Hence Among the candidate genes involved in the initial the heritable increase in dMyc levels causes cells to steps of tumor formation, the myc family has a prominent behave as “super-competitors” and reveals a novel position (Pelengaris et al., 2002).”
Control of apoptosis by p53 (2003, background): “Conversely, the ability of oncogenes such as Myc to sensitize cells to chemotherapy may explain, in part, the therapeutic index of certain chemotherapeutic agents to begin with (Lowe and Lin, 2000; Pelengaris et al., 2002).”
CIP2A inhibits PP2A in human malignancies. (2007, neutral): “Moreover, by focusing on a tumor-specific protein, such as CIP2A, the controversy surrounding the inability to directly regulate PP2A and/or c-Myc in normal tissue due to their requirement for normal cellular function would be alleviated (Gotz et al., 1998; Pelengaris et al., 2002).”
Myc Stimulates Nuclearly Encoded Mitochondrial Genes and Mitochondrial Biogenesis (2005, background): “MYC, which encodes a transcription factor, c-Myc (herein termed Myc), plays a central role in the regulation of cell size, cell proliferation, and apoptosis (6, 11, 28, 40, 41) through its regulation of RNA polymerase I-, II-, and III-dependent genes (2, 17, 18, 39).”
c-Myc and Cancer Metabolism (2012, neutral): “The oncogenic properties of c-Myc are counterbalanced by its ability to induce apoptosis through several pathways (13, 14).”
The ERK1/2 mitogen-activated protein kinase pathway as a master regulator of the G1- to S-phase transition (2007, background): “…of the Myc family of transcription factors that plays a central role in regulating cell growth, cell cycle progression and apoptosis (reviewed in Pelengaris et al., 2002). c-Myc heterodimerizes with its obligate partner Max to activate or repress transcription of a vast array of target genes…”
Reflecting on 25 years with MYC (2008, background): “Soucek and colleagues have shown that the recruitment and degranulation of mast cells is essential for the subsequent maintenance of angiogenesis during tumour expansio”
Elucidation of a universal size-control mechanism in Drosophila and mammals. (2007, background): “The dual function of YAP in promoting cell proliferation and suppressing apoptosis distinguishes it from a conventional oncogene such as c-myc, whose mitogenic activity is coupled with a proapoptotic activity (Pelengaris et al., 2002).”
c-Myc controls the balance between hematopoietic stem cell self-renewal and differentiation. (2004, background): “c-Myc-induced apoptosis has been previously shown to be blocked by expression of BCL-2 (Pelengaris et al. 2002a; Nilsson and Cleveland 2003).”
The circadian gene per1 plays an important role in cell growth and DNA damage control in human cancer cells. (2006, background): “Per1 Overexpression Induces c-Myc and Represses p21Waf1/Cip1 in Response to Ionizing Radiation Activation of the oncoprotein c-Myc is a frequent event in human cancer and has been associated with almost every aspect of tumorigenesis (Pelengaris et al., 2002; Adhikary and Eilers, 2005).”