Histopathologic characteristics of 42 pituitary adenomas

Supplementary Legends - PDF file 122K, Legends for all Supplementary information

A key mutational process in cancer is structural variation, in which rearrangements delete, amplify or reorder genomic segments that range in size from kilobases to whole chromosomes 1 – 7 . Here we develop methods to group, classify and describe somatic structural variants, using data from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA), which aggregated whole-genome sequencing data from 2,658 cancers across 38 tumour types 8 . Sixteen signatures of structural variation emerged. Deletions have a multimodal size distribution, assort unevenly across tumour types and patients, are enriched in late-replicating regions and correlate with inversions. Tandem duplications also have a multimodal size distribution, but are enriched in early-replicating regions—as are unbalanced translocations. Replication-based mechanisms of rearrangement generate varied chromosomal structures with low-level copy-number gains and frequent inverted rearrangements. One prominent structure consists of 2–7 templates copied from distinct regions of the genome strung together within one locus. Such cycles of templated insertions correlate with tandem duplications, and—in liver cancer—frequently activate the telomerase gene TERT . A wide variety of rearrangement processes are active in cancer, which generate complex configurations of the genome upon which selection can act.

Supplementary Table S7 - XLSX file 61K, List of shRNAs used in this study

Table S4 includes immune signature and iCluster results.

PDF file - 386K, A, Cell viability relative to day 0 is shown following the indicated treatments in the indicated cell lines. Error bars represent the mean plus-minus SD of three replicates per condition. B, qPCR assessment of MYC mRNA expression in three MYC-amplified patient derived medulloblastoma cell lines treated with JQ1R or JQ1S at doses shown. Values represent mean plus-minus SD of six replicate measurements.

PDF file - 291K, Densitometry quantification of Western Immunoblots shown in Figures 4 and 5.

Table S7 contains microbe screening results.

Table S1 contains cohort description, Master Patient Table and MutSigCV results.

Supplementary Figure 2 - PDF file 17K, SKIL induces Matrigel invasion

All nonsynonymous mutations detected in WES samples

PDF file - 66K, A, Primers used for qPCR assays B, MYC gene sets in GSEA.

Supplementary Table S8 - XLSX file 51K, Primers used for quantitative real time PCR in this study

<p>File contains list of GISTIC Defined Recurrent SCNA genes that overlap between Humans and Dogs.</p>

PDF file - 72K, Nanostring CNV of MB002 and MB004.

Imputed copy-number profiles from expression data

PDF file - 63K, MYC gene sets enriched in medulloblastoma samples with high expression of MYC isoforms.