Supplementary Figure 6 from Coactivation of AKT and β-Catenin in Mice Rapidly Induces Formation of Lipogenic Liver Tumors
Supplementary Figure 3 from Coactivation of AKT and β-Catenin in Mice Rapidly Induces Formation of Lipogenic Liver Tumors
Supplementary Figure 2 from Coactivation of AKT and β-Catenin in Mice Rapidly Induces Formation of Lipogenic Liver Tumors
Supplementary Figure Legends, Supplementary Tables 1-2 from Coactivation of AKT and β-Catenin in Mice Rapidly Induces Formation of Lipogenic Liver Tumors
Supplementary Figure 4 from Nitric Oxide, a Mediator of Inflammation, Suppresses Tumorigenesis
Supplementary Figure 5 from Nitric Oxide, a Mediator of Inflammation, Suppresses Tumorigenesis
Abstract Inflammation influences the development of cancer. The nitric oxide synthase (NOS2) is induced by inflammatory cytokines, e.g., tumor necrosis factor α and interleukin 1β, and produces nitric oxide (NO·), a critical mediator of the inflammatory response. Because p53 governs NO· production by transcriptionally transrepressing NOS2, we used a genetic strategy to determine whether NO· and p53 cooperatively regulate tumorigenesis. Lymphomas developed more rapidly in p53−/−NOS2−/− or p53−/−NOS2+/− mice than in p53−/−NOS2+/+ mice that were cross-bred into a >95% C57BL6 background and maintained in a pathogen-free condition. Likewise, sarcomas and lymphomas developed faster in p53+/−NOS2−/− or p53+/−NOS2+/− than in p53+/−NOS2+/+ mice. When compared with the double knockout mice, p53−/−NOS2+/+ mice showed a higher apoptotic index and a decreased proliferation index with an increased expression of death receptor ligands, CD95-L and tumor necrosis factor-related apoptosis-inducing ligand, and the cell cycle checkpoint protein, p21waf1, in the spleen and thymus before tumor development. Furthermore, mice deficient in both p53 and NOS2 produced a high level of anti-inflammatory interleukin 10 when compared with p53-deficient mice. These studies provide genetic and mechanistic evidence that NO· can suppress tumorigenesis.
Supplementary Figure 1 from Coactivation of AKT and β-Catenin in Mice Rapidly Induces Formation of Lipogenic Liver Tumors
Supplementary Figure 3 from Nitric Oxide, a Mediator of Inflammation, Suppresses Tumorigenesis
Supplementary Figure 1 from Antigen Presented by Tumors <i>In vivo</i> Determines the Nature of CD8<sup>+</sup> T-Cell Cytotoxicity
Supplementary Figure 6 from Antigen Presented by Tumors In vivo Determines the Nature of CD8+ T-Cell Cytotoxicity
Supplementary Figure 4 from Coactivation of AKT and β-Catenin in Mice Rapidly Induces Formation of Lipogenic Liver Tumors
Supplementary Figure 2 from Nitric Oxide, a Mediator of Inflammation, Suppresses Tumorigenesis
Supplementary Figure 6 from Antigen Presented by Tumors <i>In vivo</i> Determines the Nature of CD8<sup>+</sup> T-Cell Cytotoxicity
Supplementary Figure 9 from Nitric Oxide Is a Key Component in Inflammation-Accelerated Tumorigenesis
Supplementary Figure 8 from Nitric Oxide Is a Key Component in Inflammation-Accelerated Tumorigenesis
Supplementary Figure 6 from Nitric Oxide, a Mediator of Inflammation, Suppresses Tumorigenesis
Supplementary Table 1. Th1 vs. Th2 Cytokine Trend. Supplementary Table 2. Effect of L-NAME on Radiation-induced Cytokine Expression.
Supplementary Figure 3 from Antigen Presented by Tumors In vivo Determines the Nature of CD8+ T-Cell Cytotoxicity
Supplementary Figure 7 from Nitric Oxide, a Mediator of Inflammation, Suppresses Tumorigenesis
Weiss Jonathan M合作论文数42Subleski Jeff J合作论文数29
Curtis C. Harris合作论文数Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health21Anthony J. Scarzello合作论文数17Peijun He合作论文数16S. Perwez Hussain合作论文数16John R. Ortaldo合作论文数15
Victor E Laubach合作论文数Department of Surgery, University of Virginia Health System14
William J. Murphy合作论文数Department of Dermatology, School of Medicine, University of California Davis;Mammalian Comparative Genomics Laboratory, Texas A&M University13Leah E. Mechanic合作论文数13Jimmy K. Stauffer合作论文数13Diana C Haines合作论文数12Draginja Djurickovic合作论文数12Thomas J. Sayers合作论文数12
Lorne Hofseth合作论文数Department of Drug Discovery and Biomedical Sciences, College of Pharmacy, University of South Carolina12Jiang Qun合作论文数11Jacobsen Kristen M合作论文数11
Snorri Thorgeirsson合作论文数National Cancer Institute11J. W. Wine合作论文数11Glennwood E. Trivers合作论文数11
Alan D Brooks合作论文数11
Anil Shanker合作论文数Department of Biochemistry, Cancer Biology, Neuroscience and Pharmacology, School of Medicine, Meharry Medical College11Lynnette Shorts合作论文数11Irfan Shaikh合作论文数10Saira Doja合作论文数10Weidong Jiang合作论文数10
Jesper Bøje Andersen合作论文数Biotech Research and Innovation Centre, Department of Health and Medical Sciences, University of Copenhagen9Rachel L. De Kluyver合作论文数8
Bruce Blazar合作论文数Division of Pediatric Blood and Marrow Transplantation & Cellular Therapy, Department of Pediatrics, Medical School, University of Minnesota;Center for Translational Medicine, University of Minnesota8Veronica L. Hall合作论文数8
Dan L Longo合作论文数Department of Medicine, Brigham and Women's Hospital;Harvard Medical School7Hideo Yagita合作论文数6Alderson Kory L合作论文数6
Gail Sckisel合作论文数6Doug Redelman合作论文数6Hideo Yagita合作论文数Department of Immunology, School of Medicine, Juntendo University6
Howard A. Young合作论文数Cancer Innovation Laboratory, National Cancer Institute, National Institutes of Health6
Timothy Chan合作论文数National Center for Regenerative Medicine, School of Medicine, Case Western Reserve University;Case Comprehensive Cancer Center, Case Western Reserve University;Center for Immunotherapy & Precision Immuno-Oncology, Lerner Research Institute, Cleveland Clinic6Raoul R. Salup合作论文数5Bouchlaka Myriam N合作论文数Department of Microbiology &Immunology, University of Nevada;Department of Microbiology & Immunology, University of Nevada5
Annie Mirsoian合作论文数5
Xiaolin Wu合作论文数5
Arta Monir Monjazeb合作论文数Department of Cancer Biology, Wake Forest University Baptist Medical Center5Thomas B. Wolfe合作论文数4Jonathan Schwank合作论文数4
Julia Tietze合作论文数4
David A. Wink Jr合作论文数Cancer Innovation Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health4Danice E. C. Wilkins合作论文数4Deborah L. Hodge合作论文数4
