qBiomarker Somatic Mutation PCR Array: Human Pancreatic Cancer The Human Pancreatic Cancer qBiomarker Somatic Mutation PCR Array is a translational research tool that allows rapid, accurate, and comprehensive profiling of the somatic mutations in human pancreatic cancer samples in the following key genes: APC, BRAF, CDKN2A, CTNNB1, KRAS, NRAS, PIK3CA, SMAD4, and P53. These mutations warrant extensive investigation to enhance the understanding of carcinogenesis and identify potential drug targets. Numerous research studies have demonstrated the utility of individual and multiple somatic mutation status information in identifying key signaling transduction disruptions. For example, the mutation status of the EGFR and KRAS genes can predict the physiological response to certain drugs targeting these molecules. The Human Pancreatic Cancer qBiomarker Somatic Mutation PCR Array, with its comprehensive content coverage, is designed for studying mutations in the context of pancreatic cancer and has the potential for discovery and development of effective biomarkers for this cancer type and other cancer types in which these mutations were identified. This array includes 38 DNA sequence mutation assays designed to detect the most frequent, functionally verified, and biologically significant mutations in human pancreatic cancer. These mutations were chosen from curated, comprehensive somatic mutation databases and peer-reviewed scientific literature, and represent the most frequently recurring somatic mutations compiled from over 3800 pancreatic cancer samples. Each 96-well array allows profiling mutation status of 2 samples, while each 384-well format array allows mutation profiling of 8 samples. The simplicity of the product format and operating procedure enables routine somatic mutation profiling in any research laboratory with access to real-time PCR instruments.    

APC: 1 Assay
The most commonly detected APC inactivation mutations are mainly composed of truncation mutations (due to nonsense mutations and frameshift mutations) and point mutations between codons 1250 and 1578.
BRAF: 1 Assay
The most important BRAF mutation in pancreatic cancer leads to increased kinase activity, the p. V600E mutation.
CDKN2A: 3 Assays
The top CDKN2A loss-of-function mutations occur in the consensus ankyrin domain, which leads to inability to form stable complexes with its targets.
CTNNB1: 9 Assays
The most frequently detected CTNNB1/beta-catenin mutations result in abnormal signaling in the WNT signaling pathway. The mutated codons are mainly several serine/threonine residues targeted for phosphorylation by GSK-3beta.
KRAS: 10 Assays
The mutation assays include the most frequently occurring mutations in KRAS codons 12, 13, and 61. Mutations at these positions result in reduced intrinsic GTPase activity and/or cause KRAS to become unresponsive to RasGAP.
NRAS: 2 Assays
The most important NRAS mutations in pancreatic cancer occur at codon 61.
PIK3CA: 3 Assays
The most frequently occurring PIK3CA mutations mainly belong to two classes: gain-of-function kinase domain activating mutations and helical domain mutations that mimic activation by growth factors.
SMAD4: 1 Assay
SMAD4 encodes a member of the Smad family of signal transduction proteins. Mutations or deletions in this gene have been shown to result in pancreatic cancer, juvenile polyposis syndrome, and hereditary hemorrhagic telangiectasia syndrome.
TP53: 8 Assays
The most frequently detected somatic mutations in TP53 are largely composed of DNA-binding domain mutations which disrupt either DNA binding or protein structure.