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Bill Sugden, Ph.D.

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B. Sugden photo James A. Miller Professor of Oncology
American Cancer Society Research Professor


A.B., 1967, Organic Chemistry, Harvard University
M.S., 1968, Physical Chemistry, Columbia University
Ph.D., 1973, Molecular Biology, Columbia University
Postdoctoral research: Karolinska Institute, Stockholm, Sweden

Office: 814 McArdle Laboratory
Telephone:
Office - (608) 262-1116; Lab - (608) 262-6697
Email: sugden@oncology.wisc.edu

Lab Home Page

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Research Interests: Molecular biology of the human tumor virus, Epstein-Barr virus

Research Description: We work with Epstein-Barr Virus (EBV) because it causes several different cancers in people. EBV is a herpesvirus that causes the common, benign infectious mononucleosis, as well as lymphomas such as Burkitt's Lymphoma, most B-cell lymphomas in immunocompromised hosts, and carcinomas such as nasopharyngeal carcinoma. We study EBV both to understand its contributions to these diseases molecularly and to develop rational means to treat them.

Our research focuses on two facets of EBV pivotal to its inducing and maintaining human tumors. One gene product of EBV, LMP1, mimics cellular signaling pathways but in a ligand-independent manner. Its signaling drives proliferation of EBV-infected B-cells, but at high levels inhibits that proliferation. We are dissecting the mechanisms by which LMP1 regulates its host cell both positively and negatively. A second gene product of EBV, EBNA1, binds several elements of EBV's origin of plasmid synthesis, oriP, to mediate the synthesis and maintenance of the viral replicon in proliferating cells. EBV's replicon replicates once per S-phase and uses the cell's DNA synthetic machinery to do so. We study EBNA1 and oriP to elucidate the mechanisms by which EBV DNA is synthesized and segregated to daughter cells. We also study this viral replicon to gain insights into how EBV subverts its host's synthetic machinery to support extrachromosomal DNA synthesis. Finally we are studying EBNA1 which not only mediates replication of EBV's replicon, but also inhibits apoptosis in infectious B-cells to understand its roles in supporting survival of EBV-associated tumors. We want to target EBNA1's survival functions to develop treatments for tumors caused by EBV.

Selected recent publications

Vereide, D. T., Seto, E., Chiu, Y.-F., Hayes, M., Tagawa, T., Grundhoff, A., Hammerschmidt, W., and Sugden, B.  Epstein-Barr Virus Maintains Lymphomas Via Its miRNAs.  Oncogene, 33(10): 1258-1264, 2014.

Chiu, Y.-F., Sugden, A. U., and Sugden, B.  Epstein-Barr Viral Productive Amplification Reprograms Nuclear Architecture, DNA Replication, and Histone Deposition.  Cell Host Microbe, 14(6):  607-618, 2013.

Hammerschmidt, W., and Sugden, B.  Replication of Epstein-Barr Viral DNA.  Cold Spring Harb. Perspect. Biol., 5(1):  pii: a013029, 2013.

Westhoff Smith, D., and Sugden, B.  Potential Cellular Functions of Epstein-Barr Nuclear Antigen 1 (EBNA1) of Epstein-Barr Virus.  Viruses, 5(1):  226-240, 2013.

Chiu, Y.-F., Sugden, B., Chang, P.-J., Chen, L.-W., Lin, Y.-J., Lan, Y.-C., Lai, C.-H., Liou, J.-Y., Liu, S.-T., and Hung, C.-H.  Characterization and Intracellular Trafficking of Epstein-Barr Virus BBLF1, a Protein Involved in Virion Maturation.  J. Virol., 86: 9647-9655, 2012.

Kuzembayeva, M., Chiu, Y.-F., and Sugden, B.  Comparing Proteomics and RISC Immunoprecipitations to Identify Targets of Epstein-Barr Viral miRNAs.  PLoS One, 7(10):e47409, 2012. 

Norby, K., Chiu, Y.-F., and Sugden, B.  Monitoring Plasmid Replication in Live Mammalian Cells over Multiple Generations by Fluorescence Microscopy.  J. Vis. Exp., (70):e4305, 2012.

Pratt, Z. L., and Sugden, B.  How Human Tumor Viruses Make Use of Autophagy.  Cells, 1:  617-630, 2012.

Pratt, Z. L., Zhang, J., and Sugden, B.  The Latent Membrane Protein 1 (LMP1) Oncogene of Epstein-Barr Virus Can Simultaneously Induce and Inhibit Apoptosis in B Cells.  J. Virol., 86: 4380-4393, 2012.

Perform a PubMed search for additional Sugden publications