The CleanPlex™ BRCA1 & BRCA2 Panel contains 218 pairs of PCR primers targeting the full exon of the BRCA1 and BRCA2 genes. The panel kit contains primers, multiplex PCR reagent, digestion reagent and other reagent components necessary for constructing amplicon libraries for Next-Generation Sequencing on Illumina Sequencers.
- 100% coverage of BRCA1 and BRCA2 with superior uniformity
The panel covers 100% of the coding regions and 10 bases beyond the exon–intron boundaries of the BRCA1 and BRCA2 genes. The observed uniformity of this panel (at ≥ 0.2x mean coverage) is over 99%.
The entire library preparation workflow can be finished in 2.5 hours with only 30-minute hands-on time from sample DNA to sequencing-ready libraries. No need of ligation, end repair, DNA fragmentation, overnight hybridization, or microfluidic devices!
- Take on difficult samples with limited DNA input
With an average amplicon size of 158 bp, this panel is compatible with degraded samples such as formalin-fixed, paraffin-embedded (FFPE) tissue DNA and circulating cell-free DNA (cfDNA). You can obtain high quality sequencing data for germline genotype calling even with just 200 pg of input DNA.
About BRCA1 and BRCA2
BRCA1 and BRCA2 are human genes that produce tumor suppressor proteins that help repair damaged DNA and ensure the stability of the cell’s genetic material. When either of these genes is mutated, DNA damage might not be properly repaired. As a result, cells are more likely to develop additional genetic alterations that can lead to cancer.
Specific inherited mutations in BRCA1 and BRCA2 increase the risk of female breast and ovarian cancers, and they have been associated with increased risks of several additional types of cancer. Together, BRCA1 and BRCA2 mutations account for about 20 to 25 percent of hereditary breast cancers and about 5 to 10 percent of all breast cancers. In addition, mutations in BRCA1 and BRCA2 account for around 15 percent of ovarian cancers overall. Breast and ovarian cancers associated with BRCA1 and BRCA2 mutations tend to develop at younger ages than their nonhereditary counterparts.