AUG 20, 2014 08:00 AM PDT
High-resolution genomic analysis reveals genetic impacts of human papillomavirus in human cancers
Presented at the Genetics and Genomics Virtual Event
CONTINUING EDUCATION (CME/CE/CEU) CREDITS: CE | CEU
4 42 1942

Speakers:
  • Assistant Professor Department of Molecular Virology, Immunology and Medical Genetics, Assistant Professor, Division of Hematology, Department of Internal Medicine, Human Cancer Genetics Prog
    Biography
      Dr. David Symer is an assistant professor in the Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics and Department of Internal Medicine, Division of Hematology at the Ohio State University Comprehensive Cancer Center - James Cancer Hospital. Recently, Dr. Symer also was named interim director of the core laboratory offering shared resources in genomics at Ohio State, the Nucleic Acids / Microarray Shared Resource. Dr. Symer has ongoing research interests in molecular biology and in cancer genetics and genomics. His primary clinical interest is chronic lymphocytic leukemia. He graduated with an AB degree in mathematics from Dartmouth College, earned his MD and PhD degrees at Johns Hopkins University School of Medicine, did his residency at Brigham and Women's Hospital (Harvard Medical School), and completed his fellowship training at Brigham and Women's Hospital and Johns Hopkins Oncology Center. Dr. Symer was a principal investigator at the National Cancer Institute prior to moving to Ohio State in 2009.

    Abstract:
    One of the hallmarks of human cancers is genetic instability. My colleagues and I recently identified a remarkable association between human papillomavirus (HPV) and genomic structural variation in flanking host genomic DNA, both in human cancer cell lines and primary tumors. A combination of whole-genome sequencing and other molecular assays revealed HPV integrants frequently adjacent to and bridging extensively amplified and rearranged genomic sequences, including deletions, inversions, and chromosomal translocations. We developed a model of looping to explain these data. Our model suggests that HPV integrant-mediated DNA replication and recombination may result in viralhost DNA concatemers, frequently disrupting genes involved in oncogenesis and amplifying the HPV oncogenes E6 and E7. Using innovative new long-range deep sequencing methods, we currently are characterizing in detail these genomic structural variants, induced by HPV integration in primary human cancers. Use of such high-resolution genomics methods has shed new light on a catastrophic process, distinct from chromothripsis and other mutational processes, by which HPV can induce genomic instability and disrupt candidate cancer-causing genes.

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