Table S1 from HPV Integration in HNSCC Correlates with Survival Outcomes, Immune Response Signatures, and Candidate Drivers

List of the human and HPV genomic locations for the 320 identified integration events.</p

Table S2 from HPV Integration in HNSCC Correlates with Survival Outcomes, Immune Response Signatures, and Candidate Drivers

HPV gene expression levels in the 84 HNSCC tumors.</p

Table S3 from HPV Integration in HNSCC Correlates with Survival Outcomes, Immune Response Signatures, and Candidate Drivers

Network statistics for network constructed from 89 genes with/near integration events.</p

Supplemental Materials and Methods; Supplementary Tables 5-14; Supplementary Figures 1-3. from HPV Integration in HNSCC Correlates with Survival Outcomes, Immune Response Signatures, and Candidate Drivers

Supplemental Methods, Tables S5-S14, and Figures S1-S3</p

Table S4 from HPV Integration in HNSCC Correlates with Survival Outcomes, Immune Response Signatures, and Candidate Drivers

GO terms and KEGG pathways enriched for genes differentially expressed between integration-positive and integration-negative HNC tumors.</p

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

Supplementary methods and figures. from Subtypes of HPV-Positive Head and Neck Cancers Are Associated with HPV Characteristics, Copy Number Alterations, PIK3CA Mutation, and Pathway Signature

Table S5. from Subtypes of HPV-Positive Head and Neck Cancers Are Associated with HPV Characteristics, Copy Number Alterations, PIK3CA Mutation, and Pathway Signatures

The list of genes displayed in Figure 1D. </p

Supplemental Figure 2 from Genomic Integration of High-Risk HPV Alters Gene Expression in Oropharyngeal Squamous Cell Carcinoma

Differential mRNA expression of genes with copy number alterations. The relative mRNA expression of amplified genes was assessed across the all publically available next generation sequencing data where matched genome or exome-sequencing and transcriptome sequencing were available using the Oncomine database. Three plots were generated for each gene with copy number alterations, the respective gene is indicated on top of the plot. RNA expression was not evaluable for TCGA-CN-A49A, which harbored a SMOC1 amplification. DNA copy number calculated from exome or whole genome sequencing data is shown along the x-axis and absolute fragments per kilobase million are shown along the y-axis (Values are presented as Log base 2). Samples within the plots have either do not have genomic alterations or have mutations, gene fusions or copy number alterations as indicated in the inset legend. Blue dashed line indicates the limit for calling genomic deletions and the pink line for genomic amplifications. The black line indicates best fit for correlation between DNA copy number and gene expression.</p

Supplemental Table 4 from Genomic Integration of High-Risk HPV Alters Gene Expression in Oropharyngeal Squamous Cell Carcinoma

Number of viral-cellular amplicons generated and sequenced from responsive and recurrent tumors.</p

Table S4. from Subtypes of HPV-Positive Head and Neck Cancers Are Associated with HPV Characteristics, Copy Number Alterations, PIK3CA Mutation, and Pathway Signatures

Neoplasm-associated genes on chr3q and chr16q (identified by gene2Mesh). - The 'logFC', 'p-value' and 'q-value' columns are from testing the expression difference between HPV-KRT and HPV-IMU tumors (UM and TCGA combined). </p