Molecular Mechanisms of Viruses Linked to Human Cancers

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Molecular Mechanisms of Viruses Linked to Human Cancers

Monday, January 24, 2011

The New York Academy of Sciences

This mini-symposium will focus on recent advances in our molecular knowledge of two viruses that play a role in the etiology of human cancers by distinctly different mechanisms. Hepatitis C viruses (HCV) and the immunopathology they induce are an important cause of liver cancers. Human papillomaviruses (HPVs) directly inactivate tumor suppressor pathways and are causally involved in anogenital and oropharyngeal cancers.

Agenda

The Role of Human Papillomaviruses in Anogenital and Oropharyngeal Cancers
Denise A. Galloway, PhD, Fred Hutchinson Cancer Research Center

Chronic Hepatitis C Infection and Liver Cancer:  Breaking the Link
Charles M. Rice, PhD, The Rockefeller University and Center for the Study of Hepatitis C

Networking Reception To Follow

This event will also be broadcast as a webinar.

Please note: Transmission of presentations via the webinar is subject to individual consent by the speakers. Therefore, we cannot guarantee that every speaker's presentation will be broadcast in full via the webinar. To access all speakers' presentations in full, we invite you to attend the live event in New York City, where possible.

 

Speakers

Organizers

S. Marvin Friedman, PhD

Hunter College, CUNY

Jennifer S. Henry, PhD

The New York Academy of Sciences

Speakers

Denise A. Galloway, PhD

Fred Hutchinson Cancer Research Center

Denise A. Galloway was born and educated in New York City, receiving her PhD in 1975 from the City University of New York. She did post-doctoral work on DNA tumor viruses at Cold Spring Harbor Laboratory. In 1979 she joined the faculty at the Fred Hutchinson Cancer Research Center in Seattle, WA. She is currently a Member of the Divisions of Human Biology and Public Health Sciences, and Head of the Cancer Biology Program at the FHCRC. She is also a Research Professor in the Departments of Microbiology and Pathology at the University of Washington School of Medicine. Dr. Galloway has served on and chaired NIH study sections, and is an associate editor and editorial board member of several journals. From 2000-2010 she had a prestigious MERIT award, and continues to have PO1 and RO1 grants. She is a Fellow of the Academy of Microbiology, the Infectious Disease Society and the American Association for the Advancement of Science.

Charles M. Rice, PhD

The Rockefeller University and Center for the Study of Hepatitis C

Dr. Rice is the Maurice R. and Corinne P. Greenberg Chair in Virology and serves as Head of the Laboratory for Virology and Infectious Disease at Rockefeller University. He is one of the world’s most accomplished virologists and a prominent figure in research on members of the Flaviviridae including hepatitis C virus (HCV). Dr. Rice received his bachelor’s degree from University of California Davis in 1974 and earned his PhD from California Institute of Technology in 1981. From 1986-2000, Dr. Rice was a faculty member at Washington University in St. Louis. His research team has helped to understand the biogenesis and structure of HCV-encoded proteins, discovered a highly conserved RNA element at the 3’ terminus of HCV genome RNA, and produced the first infectious molecular clone of the virus—an essential tool for future studies on this important human pathogen. His laboratory has established efficient cell culture systems for studying HCV replication and evaluating antiviral efficacy. Dr. Rice has co-authored over 300 articles in the field of virology, serves as a reviewer for numerous journals, is a former editor of Journal of Virology, is a past President of the American Society for Virology, a Fellow of the American Association for the Advancement of Science, and a Member of the National Academy of Sciences. For more specific information about Dr. Rice’s research, please go to http://www.hepccenter.org


Supporters

For sponsorship opportunities, please contact Cristine Barretto at cbarreto@nyas.org or 212.298.8652.

Grant Support

This program is supported by an educational grant from Gilead Sciences.

This event is funded in part by the Life Technologies™ Foundation.

This program is supported by an educational grant from Merck & Co., Inc.

This program is supported through a medical education grant from Vertex Pharmaceuticals Incorporated.

Academy Friend

Abstracts

The Role of Human Papillomaviruses in Anogenital and Oropharyngeal Cancers

Denise A. Galloway, PhD, Fred Hutchinson Cancer Research Center

Human papillomaviruses (HPVs) are a large family of epithelial tropic viruses; approximately 130 have been molecularly cloned and partial sequences suggest at least another hundred exist. Of these, a group of 15 are called high risk (HR-HPV) because they are found in 100% of cervical cancers, the majority of other of other anal and genital tract cancers, and 25-50% of cancers of the oropharynx. Several lines of evidence support a causative role for HPVs in the etiology of these cancers. First, the precursor lesions to cervical cancer are well understood, and the HR-HPVs are expressed in these lesions. Vaccination to prevent infection with the two most common HR-HPVs, HPV 16 and HPV 18, prevents the development of the precursors. Second, two viral genes, E6 and E7 are invariably expressed in these cancers. HR-HPV E6 and E7 inactivate tumor suppressor pathways, block apoptosis and promote genetic instability. The subsequent accumulation of mutations that are related to tumor invasiveness and metastasis may not be directly mediated by HPVs, but rather due to ongoing genetic instability. Consistent with this view is the observation that E6 and E7 together immortalize primary epithelial cells in culture, but additional oncogenes are required to convert the HPV immortalized cells to tumorigenicity. Also consistent with this model is the long time lag between infection and the median age of anogenital cancer.

This talk will focus on how molecular mechanisms by which HR E6 and E7 cause genetic instability. E7 promotes cell cycle entry of normally quiescent cells by targeting the Rb family of proteins for degradation, and disrupts the regulation of centrosome duplication. E6 targets p53 for degradation leading to inactivation of several cell cycle checkpoints. E6 also blocks apoptosis by several means, and induces the expression of telomerase. Together these activities contribute to HPVs oncogenic role in cancer.

Chronic Hepatitis C Infection and Liver Cancer:  Breaking the Link

Charles M. Rice, PhD, The Rockefeller University and Center for the Study of Hepatitis C

Hepatitis C virus is a worldwide health problem with chronic infection often leading to liver cirrhosis and cancer. Over the last two decades, research has focused on trying to establish tractable systems for studying virus replication and drug development. I will highlight recent work on HCV entry, RNA replication, virus assembly and emerging therapies. In addition, I will describe new tools for studying HCV biology, including HCV-permissive human hepatocyte micropatterned co-cultures, reporter systems that allow real time imaging of infectious processes, and new animal models.


 

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