Subtypes of HPV-Positive Head and Neck Cancers Are Associated with HPV Characteristics, Copy Number Alterations, PIK3CA Mutation, and Pathway Signatures

Clin Cancer Res. 2016 Sep 15;22(18):4735-45. doi: 10.1158/1078-0432.CCR-16-0323. Epub 2016 Apr 18.

Abstract

Purpose: There is substantial heterogeneity within human papillomavirus (HPV)-associated head and neck cancer (HNC) tumors that predispose them to different outcomes; however, the molecular heterogeneity in this subgroup is poorly characterized due to various historical reasons.

Experimental design: We performed unsupervised gene expression clustering on deeply annotated (transcriptome and genome) HPV(+) HNC samples from two cohorts (84 total primary tumors), including 18 HPV(-) HNC samples, to discover subtypes and characterize the differences between subgroups in terms of their HPV characteristics, pathway activity, whole-genome somatic copy number alterations, and mutation frequencies.

Results: We identified two distinct HPV(+) subtypes (namely HPV-KRT and HPV-IMU). HPV-KRT is characterized by elevated expression of genes in keratinocyte differentiation and oxidation-reduction process, whereas HPV-IMU has strong immune response and mesenchymal differentiation. The differences in expression are likely connected to the differences in HPV characteristics and genomic changes. HPV-KRT has more genic viral integration, lower E2/E4/E5 expression levels, and higher ratio of spliced to full-length HPV oncogene E6 than HPV-IMU; the subgroups also show differences in copy number alterations and mutations, in particular the loss of chr16q in HPV-IMU and gain of chr3q and PIK3CA mutation in HPV-KRT.

Conclusions: Our characterization of two subtypes of HPV(+) HNC tumors provides valuable molecular level information that point to two main carcinogenic paths. Together, these results shed light on stratifications of the HPV(+) HNCs and will help to guide personalized care for HPV(+) HNC patients. Clin Cancer Res; 22(18); 4735-45. ©2016 AACR.

MeSH terms

  • Class I Phosphatidylinositol 3-Kinases / genetics*
  • Cluster Analysis
  • DNA Copy Number Variations*
  • Gene Amplification
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic
  • Gene Expression Regulation, Viral
  • Head and Neck Neoplasms / etiology*
  • Head and Neck Neoplasms / metabolism
  • Humans
  • Mutation*
  • Papillomaviridae / genetics*
  • Papillomavirus Infections / complications*
  • Papillomavirus Infections / virology
  • Signal Transduction

Substances

  • Class I Phosphatidylinositol 3-Kinases
  • PIK3CA protein, human