Abstract
We have found evidence suggesting that ARF and p53 are essential for tumor regression upon MYC inactivation through distinct mechanisms ARF through p53-independent affect, is required to for MYC to regulate the expression of genes that are required for both the induction of cellular senescence as well as recruitment of innate immune activation. Our observations have possible implications for mechanisms of therapeutic resistance to targeted oncogene inactivation.
Highlights
Division of Oncology, Departments of Medicine and Pathology, Molecular Imaging Program, Stanford University, Stanford, CA 94305, USA; Department of Radiology, Stanford University, Stanford, CA 94305, USA; Current Address: Genitourinary Medical Oncology, The University of Texas, MD Anderson Cancer Center, Houston, TX 77030, USA
We previously reported that p53 loss results in tumor recurrence by maintaining tumor vasculature, despite inactivation, through upregulation of angiogenesis inhibitor TSP1 [3]
We have described that INK4A/ARF loss or RB1 loss results in tumor recurrence through abrogation of cellular senescence
Summary
Division of Oncology, Departments of Medicine and Pathology, Molecular Imaging Program, Stanford University, Stanford, CA 94305, USA; Department of Radiology, Stanford University, Stanford, CA 94305, USA; Current Address: Genitourinary Medical Oncology, The University of Texas, MD Anderson Cancer Center, Houston, TX 77030, USA.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
