Journal
TRENDS IN BIOCHEMICAL SCIENCES
Volume 44, Issue 12, Pages 991-993Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tibs.2019.10.007
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Funding
- University of Michigan Center for Gastrointestinal Research Pilot Feasibility Program [P30DK034933]
- National Cancer Institute (NCI) National Research Service Award (NRSA) Award [F32CA228328]
- Taubman Institute
- Forbes Institute for Cancer Discovery
- Clinician Scientist Development Award from the American Cancer Society (ACS)
- Career Development award from the NCI [K08CA234416]
- 2017 American Association for Cancer Research (AACR) NextGen Grant for Transformative Cancer Research [17-20-01-LYSS]
- ACS Research Scholar Grant [RSG-18-18601]
- Cancer Center Core Grant [P30CA46592]
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Senescence is engaged in response to oncogenes to suppress proliferation. Cancers rewire metabolism to facilitate proliferation; however, it is not well appreciated how this enables senescence bypass. Recent work by Buj et al. demonstrates that loss of the tumor suppressor p16 engages a mTORC1-dependent increase in nucleotide pools to override senescence.
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