University of Pittsburgh Cancer Institute (UPCI)

Viral Oncology (VO)

This group of scientists performs cutting-edge research at the forefront of some of the most exciting areas of cancer biology. Viruses have long been used as tools to understand basic mechanisms of cancer development and progression. Many cellular proteins crucial in oncogenesis and tumor suppression were first discovered by studying tumor viruses. UPCI is building on this foundation and has gathered an extremely strong and interactive group of tumor virologists who use viruses to understand how cancers arise or progress. Although members of this interest area use traditional approaches to investigate viral interactions with cancer cell signaling pathways, Viral Oncology faculty members are also building approaches to understanding virus-host cell interactions in new areas such as microRNA (miRNA) perturbations, innate immune evasion, and genomic instability caused by viruses.

Selected Publications

• Terminal small noncoding cellular RNAs are extensively processed in both mouse and human cells (Li et. al., Nucleic Acids Res. 2012).
• Focal adhesion kinase is an early activator of cell defenses against viral infection (Borzym et. al., Cell Host Microbe 11:153-66 2012).
• Merkel cell polyomavirus (MCV) small T antigen is a human oncoprotein targeting cap-dependent translation (Shuda et. al., J Clin Invest 121:3623-34, 2011).
• Differences in microRNA (miRNA) expression may affect their clinical outcomes of human papilloma virus (HPV)-infected head and neck carcinoma (SCCHN) (Wald et. al., Head Neck. 33:504-512, 2011).
• The Kaposi sarcoma herpesvirus LANA1 and Epstein Barr Virus EBNA1 proteins, which are involved in maintaining virus latency, appear to use different mechanisms to evade host immune surveillance (Kwun et. al., Virology. 412:357-65, 2011).
• The tumor suppressor WWOX is linked to NF-kB activation during HTLV-I tumorigenesis (Fu et. al., Blood 117:1652, 2011).
• A significant number of immune response genes were found to be upregulated by SV40 TAg including many interferon-stimulated genes (ISGs) such as ISG56, OAS, Rsad2, Ifi27 and Mx1 (Rathi et. al., Virology. 406(2):202-11, 2010).
• Crystal structure of the Src family kinase Hck regulatory region supports an SH3-dominant activation mechanism (Alvarado et. al., J Biol Chem 285:35455-61, 2010).

Members

Section Leader: Saumendra Sarkar