title: ARF: connecting senescence and innate immunity for clearance.
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.
authors.affiliation: Division of Oncology, Departments of Medicine and Pathology, Molecular Imaging Program, Stanford University, Stanford, CA 94305, USA.|Current Address: Genitourinary Medical Oncology, The University of Texas, MD Anderson Cancer Center, Houston, TX 77030, USA.
authors.forename: Alper Y
authors.initials: AY
authors.lastname: Kearney
authors.affiliation: Department of Radiology, Stanford University, Stanford, CA 94305, USA.
authors.forename: Benedict
authors.initials: B
authors.lastname: Anchang
authors.affiliation: Department of Radiology, Stanford University, Stanford, CA 94305, USA.
authors.forename: Sylvia
authors.initials: S
authors.lastname: Plevritis
authors.affiliation: Division of Oncology, Departments of Medicine and Pathology, Molecular Imaging Program, Stanford University, Stanford, CA 94305, USA.
authors.forename: Dean W
authors.initials: DW
authors.lastname: Felsher
mesh_terms: D020823:ADP-Ribosylation Factor 1 / Q000235:genetics*; D000375:Aging / Q000235:genetics*; D000818:Animals; D016158:Genes, p53; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics*; D009857:Oncogenes / Q000235:genetics
chemical_list: D020823:ADP-Ribosylation Factor 1
keywords: Myc inactivation; innate immunity; p19arf; senescence