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An Embryonic Diapause-like Adaptation with Suppressed Myc Activity Enables Tumor Treatment Persistence
Authors:Eugen Dhimolea  Ricardo de Matos Simoes  Dhvanir Kansara  Aziz Al’Khafaji  Juliette Bouyssou  Xiang Weng  Shruti Sharma  Joseline Raja  Pallavi Awate  Ryosuke Shirasaki  Huihui Tang  Brian J. Glassner  Zhiyi Liu  Dong Gao  Jordan Bryan  Samantha Bender  Jennifer Roth  Michal Scheffer  Constantine S. Mitsiades
Affiliation:1. Department of Medical Oncology, Dana-Farber Cancer Institute Boston, MA, USA;2. Harvard Medical School, Boston, MA, USA;3. Broad Institute of MIT and Harvard, Cambridge, MA, USA;4. Ludwig Center at Harvard, Boston, MA, USA;5. Department of Biomedical Engineering, Tufts University, Medford, MA, USA;6. Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA;7. Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT, USA;8. Department of Medicine, Weill Cornell Medicine, New York, NY, USA;9. Cancer Signaling and Epigenetics Program, Institute for Cancer Research, Cancer Epigenetics Institute, Fox Chase Cancer Center, Philadelphia, PA, USA;10. Albert Einstein College of Medicine, Bronx, NY 10461, USA;11. Department of Data Sciences, Dana-Farber Cancer Institute & Harvard T.H. Chan School of Public Health, Boston, MA, USA
Abstract:
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  • Keywords:cancer  drug persistence  residual tumor  MYC  diapause  adaptation to stress  breast cancer  prostate cancer  CRISPR  CDK9
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