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HPV16 E7 Genetic Conservation Is Critical to Carcinogenesis.

  1. Author:
    Mirabello, Lisa
    Yeager, Meredith
    Yu, Kai
    Clifford, Gary M
    Xiao, Yanzi
    Zhu, Bin
    Cullen, Michael
    Boland, Joseph F
    Wentzensen, Nicolas
    Nelson, Chase W
    Raine-Bennett, Tina
    Chen, Zigui
    Bass, Sara
    Song, Lei
    Yang, Qi
    Steinberg, Mia
    Burdett, Laurie
    Dean, Michael
    Roberson, David
    Mitchell, Jason
    Lorey, Thomas
    Franceschi, Silvia
    Castle, Philip E
    Walker, Joan
    Zuna, Rosemary
    Kreimer, Aimée R
    Beachler, Daniel C
    Hildesheim, Allan
    Gonzalez, Paula
    Porras, Carolina
    Burk, Robert D
    Schiffman, Mark

  2. Author Address

    Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA. Electronic address: mirabellol@mail.nih.gov., Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA; Cancer Genomics Research Laboratory, Leidos Biomedical Research, Inc., Frederick, MD, USA., Infections and Cancer Epidemiology Group, International Agency for Research on Cancer 150, Cours Albert Thomas, 69372 Lyon Cedex 08, France., Sackler Institute for Comparative Genomics, American Museum of Natural History, New York City, NY, USA., Women 39;s Health Research Institute, Division of Research, Kaiser Permanente Northern California, Oakland, CA, USA., Department of Microbiology, The Chinese University of Hong Kong, Shatin, Hong Kong., Regional Laboratory, Kaiser Permanente Northern California, Oakland, CA, USA., Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY, USA., University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA., Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA; HealthCore Inc., Safety and Epidemiology, Wilmington, DE, USA., Agencia Costarricense de Investigaciones Biom 233;dicas (ACIB), former Proyecto Epidemiol 243;gico Guanacaste, Fundaci 243;n INCIENSA, Guanacaste, Costa Rica., Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY, USA; Departments of Pediatrics, Microbiology and Immunology, and Obstetrics & Gynecology and Women 39;s Health, Albert Einstein College of Medicine, Bronx, NY, USA.,
    1. Year: 2017
    2. Date: Sep 07
  2. Journal: Cell
    1. 170
    2. 6
    3. Pages: 1164-1174.e6
  4. Type of Article: Article
  5. ISSN: 0092-8674
  1. Abstract:

    Although most cervical human papillomavirus type 16 (HPV16) infections become undetectable within 1-2 years, persistent HPV16 causes half of all cervical cancers. We used a novel HPV whole-genome sequencing technique to evaluate an exceptionally large collection of 5,570 HPV16-infected case-control samples to determine whether viral genetic variation influences risk of cervical precancer and cancer. We observed thousands of unique HPV16 genomes; very few women shared the identical HPV16 sequence, which should stimulate a careful re-evaluation of the clinical implications of HPV mutation rates, transmission, clearance, and persistence. In case-control analyses, HPV16 in the controls had significantly more amino acid changing variants throughout the genome. Strikingly, E7 was devoid of variants in precancers/cancers compared to higher levels in the controls; we confirmed this in cancers from around the world. Strict conservation of the 98 amino acids of E7, which disrupts Rb function, is critical for HPV16 carcinogenesis, presenting a highly specific target for etiologic and therapeutic research. Published by Elsevier Inc.

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External Sources

  1. View Full Text
  2. DOI: 10.1016/j.cell.2017.08.001
  3. PMID: 28886384
  4. View record in Web of Science®
  5. WOS: 000409536000013

Library Notes

  1. Fiscal Year: FY2016-2017
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