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Italo Tempera, PhD

Italo Tempera, PhD

Assistant Professor

Associate Professor, Department of Microbiology and Immunology and Fels Institute for Cancer Research and Molecular Biology, Lewis Katz School of Medicine, Temple University

Education and Training

Educational Background

  • Postdoctoral Fellowship, The Wistar Institute, 2012
  • Visiting Scientist, The Wistar Institute, 2010
  • PhD, Biochemistry, University of Rome "La Sapienza", 2007
  • BS, Molecular Biology, University of Rome "La Sapienza", 2003
Research Profile

Research Interests

  • Chromatin architecture and its implication in gene expression
  • Alteration of the three-dimensional structure of chromatin in cancer
  • Relationship between EBV chromosome structure and the carcinogenic risk of EBV infection
  • Identification of cellular and viral proteins involved in chromatin organization
  • Effect of post-translational modifications of CTCF and the Cohesin complex on chromatin architecture
  • Correlation between metabolism and chromosome conformation

Dr. Tempera’s research focuses on understanding the functional links between epigenetic domains, chromosome conformation and gene expression in the context of cancer. Chromatin composition and organization represent an important element in regulating genome function. The analysis of chromosome conformation in yeast and Drosophila promoted the view of the genome as a set of physical domains that correlate with the epigenetic domains, suggesting a strong link between genome structure and genome function.

Our goal is to understand how the chromatin three-dimensional structure affects gene expression and how cancer can alter this process.

In particular we study the role of epigenetic modifications into the mechanism regulating Epstein-Barr virus (EBV) latency since EBV latent infection has been causally linked to a variety of B-cell and epithelial malignancies. EBV is able to establish a life-long latent infection persisting in memory B-lymphocytes as a chromatin-associated multicopy mini-chromosome adopting different gene expression programs that are referred to as latency types. These different latency types are epigenetically stable and correspond to different promoter utilization and depend on the host cell type and the nature of the tumor from which EBV is isolated. Hence, EBV represents a useful system for gaining a new insight into the basic understanding of the role of chromatin architecture in gene expression regulation in mammals. EBV studies are also instrumental in clarifying how cancer manipulates the epigenome for continued neoplastic growth and adaptability.

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