The Intersection of HPV Epidemiology, Genomics and Mechanistic Studies of HPV-Mediated Carcinogenesis
Lisa Mirabello,
Megan A. Clarke,
Chase W. Nelson,
Michael Dean,
Nicolas Wentzensen,
Meredith Yeager,
Michael Cullen,
Joseph F. Boland,
NCI HPV Workshop,
Mark Schiffman,
Robert D. Burk
Affiliations
Lisa Mirabello
Division of Cancer Epidemiology and Genetics (DCEG), National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA
Megan A. Clarke
Division of Cancer Epidemiology and Genetics (DCEG), National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA
Chase W. Nelson
Division of Cancer Epidemiology and Genetics (DCEG), National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA
Michael Dean
Division of Cancer Epidemiology and Genetics (DCEG), National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA
Nicolas Wentzensen
Division of Cancer Epidemiology and Genetics (DCEG), National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA
Meredith Yeager
Division of Cancer Epidemiology and Genetics (DCEG), National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA
Michael Cullen
Division of Cancer Epidemiology and Genetics (DCEG), National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA
Joseph F. Boland
Division of Cancer Epidemiology and Genetics (DCEG), National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA
NCI HPV Workshop
NCI HPV Workshop, DCEG, Rockville, MD 20850, USA
Mark Schiffman
Division of Cancer Epidemiology and Genetics (DCEG), National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA
Robert D. Burk
Departments of Pediatrics, Microbiology and Immunology, Epidemiology and Population Health, and Obstetrics & Gynecology and Women’s Health, Albert Einstein College of Medicine, Bronx, NY 10461, USA
Of the ~60 human papillomavirus (HPV) genotypes that infect the cervicovaginal epithelium, only 12–13 “high-risk” types are well-established as causing cervical cancer, with HPV16 accounting for over half of all cases worldwide. While HPV16 is the most important carcinogenic type, variants of HPV16 can differ in their carcinogenicity by 10-fold or more in epidemiologic studies. Strong genotype-phenotype associations embedded in the small 8-kb HPV16 genome motivate molecular studies to understand the underlying molecular mechanisms. Understanding the mechanisms of HPV genomic findings is complicated by the linkage of HPV genome variants. A panel of experts in various disciplines gathered on 21 November 2016 to discuss the interdisciplinary science of HPV oncogenesis. Here, we summarize the discussion of the complexity of the viral–host interaction and highlight important next steps for selected applied basic laboratory studies guided by epidemiological genomic findings.
