SS 09-02HPV16 Whole-Genome Sequencing of 2364 Cervical Cancers and Controls in the IARC International Studies

12. Genomics
G. Clifford 1, L. Mirabello 2, M. Schiffman 2, V. Tenet 1, N. Wentzensen 2, M. Cullen 3, J. Boland 3, X. Zhang 4, S. Franceschi 1, K. Yu 2, Q. Yang 4, R. Burk 5, M. Yeager 3.
1International Agency for Research on Cancer, Lyon, France (France), 2Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, U.S.A. (United States), 3Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, U.S.A.; Cancer Genomics Research Laboratory, Leidos Biomedical Research, Inc., Frederick, U.S.A. (United States), 4Cancer Genomics Research Laboratory, Leidos Biomedical Research, Inc., Frederick, U.S.A. (United States), 5Albert Einstein College of Medicine, USA (United States)

Background / Objectives

High-risk HPV types, as well as variant lineages of HPV16, differ considerably in carcinogenicity despite close evolutionary relatedness, but methods to assess the genetic basis of such variation have been lacking.  We seek to leverage the type of next-generation sequencing technologies and analyses that have been developed for human genomics, to study the viral genetic component of cervical cancer risk.


Methods

Using an Ampliseq and Ion Torrent-based method developed at NCI U.S.A., we are sequencing  DNA derived from FFPE, frozen biopsies or cervical cell samples  from 2364 HPV16-positive women: 1521 cervical cancer cases, 213 CIN2/3, and 630 controls. Cervical samples have been collected worldwide from 37 diverse populations by the International Agency for Research on Cancer (IARC). Using case-control comparisons, we are evaluating associations between viral genetic variation and cancer risk, including (1) comparison of viral lineages and sublineages, (2) individual SNPs, and (3) gene-level associations. We are also studying human genetic variation and ancestry in relationship to HPV16 genetic variation and cancer risk.


Results

At the time of abstract submission, whole viral genome sequences have been obtained and analyzed for 1,550 HPV16-positive samples (1,044 cervical cancer cases, 118 CIN2/3, and 388 controls). Variation in the HPV16 E1 and URR regions are strongly and significantly associated with cervical cancer risk. Completed findings for 2,364 HPV16-positive women in the IARC biobank will present the final results at the meeting. 


Conclusion

Based on preliminary data, the chance of this approach defining viral genetic determinants of cervical cancer risk appears high, and we are planning to apply it to other high-risk HPV types. This technology now permits much larger studies and more complete genotype-phenotype examinations of HPV genomes than previously possible.


References