ACE Extended Cancer Panel

for DNA and RNA

The most complete and accurate solution for tumor profiling and informatics

ACE Extended Cancer Panel for DNA and RNA 2017-02-07T10:47:12+00:00

Augmented Cancer Panel for Cancer Research and Clinical Trials

Key Features

  • Over 1,400+ cancer genes plus 200+ miRNA genes
  • Augmented for accuracy with ACE technology
  • Comprehensive coverage of key cancer pathway genes
  • > 500x mean coverage over the extended footprint (DNA)
  • Sensitivity for both known and novel fusion events (RNA)
  • Complete informatics analysis
    • Alterations reported include SNVs, LOH, CNVs, gene fusions and low-level variant expression
    • Most accurate and extensive variant annotation with > 40 public and proprietary databases including COSMIC,The Cancer Genome Atlas, Cancer Gene Census and PharmGKB™

ACE Extended Cancer Panel for DNA Analysis

The most advanced of its kind, the ACE Extended Cancer Panel includes a core set of clinically actionable* genes, all genes in the Cancer Gene Census, genes from TCGA reports, those within canonical cancer pathways proposed by Vogelstein et. al., (Science, Mar 29 2013) and other leading academic groups, as well as an additional 200 cancer related microRNA genes and important pharmacogenomic genes*.

The ACE Extended Cancer Panel has been designed to support both discovery research and clinical trials. It provides more coverage of gene pathways and functions known to be involved in cancer biology than any other panel commercially available (TABLE 1). Up until now discovery researchers have had to make a choice between the breadth of sequencing used to find novel variants in cancer-related genes, and the depth of sequencing needed to identify variants present at low allelic fraction. The Personalis Extended Cancer Panel is the first service to combine the breadth of coverage for novel variant discovery across key cancer pathway genes, with the sequencing depth needed to detect variants present at low allelic fraction.

The accuracy of our ACE Cancer Panel has also been enhanced over standard NGS panel approaches by augmenting and repairing coverage gaps, especially in targeted regions with high-GC content. This is accomplished by performing separate targeted capture under optimized sample prep conditions and combining data from these separate targeted preps into a single high quality sequencing dataset. This results in genes with more complete coverage.
* Genes referred to here as being clinically actionable reflects the fact that the efficacy of cancer drugs, FDA approved or in clinical trials, are thought to be modulated by variants in these genes. This does not imply that this panel is for clinical use – it is a Research Use Only service.

TABLE 1: Example of the number of genes included in commercially available panels.

Pathways Panel 1 Panel 2 Panel 3 ACE Extended Cancer Panel Difference ≥
Notch 5 9 9 15 +67%
P13K-Akt 67 67 103 125 +21%
P53 18 19 24 31 +30%
TGF-beta 11 12 20 30 +50%
MAPK 37 46 58 90 +55%
JAK-STAT 26 33 36 52 +45%
Apoptosis 17 18 22 37 +68%
Cell cycle 28 31 42 55 +31%
Transcriptional misregulation 30 35 48 99 +106%
miRNA 51 53 69 185 +168%

ACE Extended Cancer Panel for RNA Analysis

Personalis’ ACE Extended Cancer Panel for RNA analysis allows for an unparalleled detection of unique variant types not identifiable by DNA sequencing analysis alone. Our panel is the first of its kind and targets the coding RNA of the over 1,400+ cancer panel genes, providing detection of important cancer associated features. For example, due to the breadth of our ACE Cancer Panel RNA sequencing, we are able to identify SNVs, Indels, gene expression levels, and gene fusion events in a very wide array of cancer-associated genes. Personalis’ ACE Extended Cancer Panel for RNA allows for extensive gene fusion discovery of both clinically actionable* fusions involving critical genes such as ALK, ROS1 and RET and novel fusions involving other targeted genes that might otherwise be missed.

Personalis’ targeted approach to RNA sequencing benefits researchers in two ways, when compared with conventional (untargeted) RNAseq. First, it focuses sequencing on the genes actually involved in cancer biology, allowing deeper sequencing coverage of this RNA. Secondly, it largely excludes intronic RNA from unspliced transcripts. This eliminates a major source of background, again allowing deeper interrogation of the actual mRNA. For FFPE samples where the RNA may be degraded, targeted RNA sequencing has a third benefit: it can capture the RNA of exons distal to the poly-A tail, even if few transcript molecules remain intact connecting the two.