c-Myc can induce DNA damage, increase reactive oxygen species, and mitigate p53 function: a mechanism for oncogene-induced genetic instability.

By O. Vafa, M. Wade, S. Kern, M. Beeche, T. Pandita, G. Hampton, G. Wahl. Molecules and Cells, 2002

956 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/d55d400f188013bbe34eb00381f51dd1f310bc16

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In Cell Biology

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3. F. Colotta
4. C. Garlanda
5. C. V. Dang
6. Ruixue Huang
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8. P. Storz

In Molecular Biology

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In Oncology

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6. L. Brown-Swigart
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Citations in the corpus

• MYC on the Path to Cancer (2012, background): “Myc induction of reactive oxygen species (ROS), presumably through its induction of mitochondrial biogenesis and increased metabolism, has been implicated in genomic instability (Egler et al., 2005; Gao et al., 2007; Vafa et al., 2002; Zhang et al., 2007).”
• Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability. (2009, background): “Finally, c-Myc delays prometaphase inducing chromosomal missegregation by direct transactivation of the spindle checkpoint proteins Mad2 and BubR1 [171] and mitigates p53 function [168].”
• Reactive oxygen species in tumor progression. (2005, background): “With respect to sod2 gene regulation, it was recently demonstrated that expression of the c-myc gene in normal human fibroblasts raises the levels of intracellular ROS and that this is sufficient to induce DNA damage (187).”
• Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “However, the expression of the four Yamanaka factors in human fibroblasts leads to accumulation of 8-oxoguanine adducts (Figure 3.4B) which are commonly the result of oxidative stress, and c-MYC induces DNA damage in a ROS-dependent (Vafa et al., 2002) rather than DNA replication-dependent manner (E”
• Inference of radio-responsive gene regulatory networks using the graphical lasso algorithm (2014, background): “It has been known that MYC is a key regulator of cell proliferation and apoptosis [16-19].”
• Mitochondrial reactive oxygen species and cancer (2014, background): “Exogenous expression of Myc increased ROS production, leading to the transformation in some cells, but ROS induced apoptosis in others [70,71].”