Myc proto-oncogene is a gene that generally plays a central role in cell cycle progression, apoptosis, and cellular transformation in humans. And unsurprisingly, due to its involvement in cell cycle progression, Myc is often tied to the development and maintenance of some types of cancerous tumors. But in a new study published in Cell Reports, researchers at the Department of Pediatrics in the Division of Genetic and Genomic Medicine, among other collaborators, have found that the full picture of Myc involvement may be more complicated than that. 
In a study titled, “Premature aging and reduced cancer incidence associated with near-complete body-wide Myc inactivation,” collaborative researchers, led by Edward V. Prochownik, MD, PhD, the Paul C. Gaffney Professor of Pediatrics and Professor of Microbiology and Molecular Genetics, discovered an interesting relationship between Myc inactivation and aging in mouse models. Specifically, their work showed that in mice with functioning Myc proto-oncogenes, remain comparatively healthier and longer-lived than mice with body-wide Myc inactivation initiated postnatally. Inversely, those Myc knockout mice, while generally experiencing higher levels of metabolic dysfunction, hepatic steatosis, and other dysregulation of gene sets related to regular aging, demonstrated extended lifespans correlated to a 3-4 times lower incidence of lifetime cancer occurrence.
This work was recently featured in more detail in The Scientist, which can be found here.
Other participating researchers included Huabo Wang, PhD, Jie Lu, MS, Taylor Stevens, Alexander Roberts, Jordan Mandel, Raghunandan Avula, Yijen Wu, PhD, Jinglin Wang, Clinton Van’t Land, PhD, Toren Finkel, MD, PhD, Jerry E Vockley, MD, PhD, FACMG, Merlin Airik, PhD, Rannar Airik, PhD, Radhika Muzumdar, PhD, and Zhenwei Gong, PhD.
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