Lori Frappier (University of Toronto, Canada) “New Functions for EBV Proteins in Manipulating Cellular Processes Important for Cancer” EBV lytic infection and cancer EBV encodes ~ 80 proteins, ~70 of which are only expressed in lytic infection EBV induced cancers are considered to be latent infections but lytic infection is also important because: 1 High […]
Shannon Kenney (McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, USA) “Differentiation-Dependent Lytic EBV Reactivation in Epithelial Cells” Two models of herpesvirus infection (B cell and epithelials) Latent —> Lytic Latent/B cells Few viral genes expressed Replicated by host cell DNA polymerase Episomal viral DNA helps viruses evade immune response EBV genome is methylated in
Lin Feng (Sun Yat-sen University Cancer Center, China)–”Nasopharyngeal Carcinoma Susceptibility Gene TNFRSF19 Inhibits TGFβ Signaling and Promotes Tumorigenesis” TNFRSF19 susceptibility gene. Nat Genet 2010. Bei JX et al A orphan receptor , no ligand found yet by IHC, TFNRSF19 is highly expressed in NPC tissues, possibly an oncogene Survival TNF receptors noncanonical TNFR of TNFRSF19
Bo Zhao (Brigham and Women’s Hospital / Harvard Medical School, USA) –”NPC Epigenetic Landscapes and Super-Enhancers” Chromatin modifying enzymes are frequently altered in NPC (Lin D et al Nature Genetics 2014) exome-seq results Epigenetic changes are reversible and druggable Super-enhancers are recently discovered enhancers with (1). Extraordinarily wide and tall signals for H3K27ac, BRD4 etc
Rebecca Skalsky (Oregon Health and Science University, USA)“Regulation of Host Signaling Pathways by EBV miRNAs” EBV encodes 25 precursor miRNAs ~100-200 different target sites on mRNAs> 44 EBV miRNAs =significan tregulatory potential MiRNAs are great toools for viruses:– non-immunogenicity– -require limited encoding capacity (only 22 not)-can rapidly evolve; have Lymphocryptoivirus muRNAs are highly conserves Circular
Bill Sugden (McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, USA) “How EBV Prevails During Productive Infection” Hybrid of P3HR1 and D98. (Endogenous P3HR1 cells) EBV’s lyticv phase commandeers the cell much as do a-herpesviruses Determining when vEBV DNA amplifies following induction off the productive cycle (treated cells with tamoxifen —> BZLF 1 expression) Tamoxifen was
Paul Farrell (Imperial College London, United Kingdom) –”EBV Genome Sequence Variation: Geography, Function and Disease” J Virol. 2017 Jul 12;91(15). Natural Variation of Epstein-Barr Virus Genes, Proteins, and Primary MicroRNA. (PubMed Link) 138 new EBV genomes, 125 of these combined with 116 others = 241 Analysis of 241 aligned EBV genomes in multiple sequence alignment Type1/Type2
Irving Weissman (Stanford University School of Medicine, USA) “Normal and Neoplastic Stem Cells” Marrow or MPB (mobilized peripheral blood) Mixture of cells: HSCs, T cells, cancer cells Deplete mature blood cells by labeling with magnetic antibodies Pure HSCs for transplantation 250,000 fold depletion an ever cells or T cells Unwanted cells : cancer cells, T
Patrick Moore (University of Pittsburgh, USA) “Why Do Viruses Cause Cancer?” PubMed Link (pdf 2803) Viruses do not “mean” to cause cancer • Cancer endangers virus as well as host • Viruses non-transmissible in tumors (eg latency, pseudo-latency) • Virus populations Limited resource hypothesis: enhancing lyric virus replication tumor virus targets at G1 phase Infection is