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Product summary

  • Technology NGS
  • Application Solid tumour
  • Areas of interest Prostate cancer
  • Gene Targets 1 - 4+
  • Aberration Types SNV, indel
  • Product Code Various
  • Regulatory Status For Research Use Only; Not for Diagnostic Procedures.



Prostate cancer is now the second leading cause of cancer in men, with recent genome-wide studies helping to clarify the genetic basis of this common but complex disease1. Many of these studies have reinforced the importance of homologous end repair genes including: ATM, BRCA1, BRCA2 and PALB2, in the mechanism of prostate cancer development. Mutations in these genes result in cells having to repair lesions through other non-conservative mutagenic mechanisms.

Choose your ideal prostate cancer NGS panel from our range of fully optimised NGS panel content. Simply mix and match the genes or individual exons you require and get the most out of your sequencing runs. Use in conjunction with the SureSeq™ FFPE DNA Repair Mix* for improved NGS library yields, %OTR (on target rate) and mean target coverage from challenging FFPE derived samples.

Getting started with your SureSeq myPanel™ NGS Custom Panel could not be simpler, find out more in this video…

  • Hybridisation-based enrichment delivering unparalleled coverage uniformity — detect low frequency prostate cancer variants consistently with confidence
  • Panel content designed with experts and from current literature to target all relevant regions  — get the most comprehensive insight into disease-driving mutations
  • Complimentary Interpret NGS data analysis software — Easy-to-use analysis solution for accurate detection of all variants

Gene targets

Select a gene to view exon coverage examples:

* Exon examples not yet available

Want to customise these gene targets?

We have a regularly updated, expert-curated library of pre-optimised cancer panel content for you to select from. Simply mix and match the gene, exonic or intronic content you need to create a prostate cancer NGS cancer panel that meets your exact requirements.


Superior coverage uniformity

A number of genetic factors have been found that increase prostate cancer risk, including heritable mutations in the genes BRCA1 and BRCA2. BRCA1 is a key player in cellular control systems, having been linked to DNA damage response and repair, transcriptional regulation and chromatin modelling2, while BRCA2 function is linked to DNA recombination and repair processes, being of particular importance in the regulation of RAD51 activity. Figure 1 illustrates the superior uniformity of coverage of key exons of BRCA1 and BRCA2 from an FFPE sample.

PALB2 is a BRCA2 binding protein and the BRCA2-PALB2 interaction is essential for BRCA2-mediated DNA repair. Recently it has been shown that correct PALB2 function is necessary for the homologous recombination repair via interaction with BRCA1, revealing that PALB2 is actually a linker between BRCA1 and BRCA23. The ATM gene, located on chromosome 11q 22–23, includes 66 exons with a 9168 base NGS Custom Prostate Cancer panel 3 pair coding sequence, and encodes a PI3K-related protein kinase (PIKK) that helps maintain genomic integrity. The PI3K-AKT-mTOR oncogenic pathway is frequently enhanced in prostate cancer playing a vital role in development and maintenance4. Figures 2 and 3 illustrate the excellent uniformity of coverage of key exons of PALB2 and ATM, respectively.

SureSeq myPanel NGS Custom Prostate Cancer Panel workflow

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  • SureSeq myPanel NGS Custom Prostate Cancer Panel


  1. Thoma, C, (2015) The complex relationships of malignant cells in lethal metastatic castration-resistant disease, Nature Reviews Urology 12, 237
  2. Castro, E. et al, (2012) The role of BRCA1 and BRCA2 in prostate cancer. Asian Journal of Andrology, 14 (3):409-414.
  3. Pakkanen, S. et al, (2009) PALB2 variants in hereditary and unselected Finnish Prostate cancer cases. Journal of Negative Results in BioMedicine, 8 (1).
  4. Angèle, S. et al, (2004). ATM polymorphisms as risk factors for prostate cancer development. British Journal of Cancer, 91(4): 783–787.

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