Modaplex KNB Assays

KRAS (V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog) is an oncogene encoding for a GTPase transductor protein. It is involved in signal transduction (by converting GTP to GDP) and belongs to the RAS/MAPK pathway regulating cell proliferation, cell differentiation, cellular migration, and apoptosis[1].

NRAS is an oncogene encoding for the N-Ras protein. It is involved in regulating cell division (by converting GTP to GDP) and belongs to the RAS/MAPK pathway regulating cell proliferation, cell differentiation, cellular migration, and apoptosis [2].

BRAF is a proto-oncogene encoding for a serine/threonine protein kinase B-Raf. It is involved in signal transduction and belongs to the RAS/MAPK pathway regulating cell proliferation, cell differentiation, cellular migration, and apoptosis[3].

When either KRAS, NRAS, or BRAF is mutated, the cellular signaling is altered, leading to several abnormalities including cancer.

The Modaplex portfolio has been expanded with the Modaplex KRAS, NRAS and BRAF Mutation Analysis Kits for research use only. In one Modaplex run, 30 mutations in KRAS, NRAS, and BRAF genes can be detected and differentiated in three wells simultaneously.

 

The Modaplex KNB Analysis Kits are:

  • Developed under ISO 9001:2015 and the FDA’s Design Control Guidance for medical device manufacturers
  • Standardized kits with a comprehensive control concept
  • Ready-to-use assays with a simple and efficient workflow

 

For more details, please download our Modaplex KNB Brochure.

 


References:

[1] Kim et al, “The impact of KRAS mutations on prognosis in surgically resected colorectal cancer patients with liver and lung metastases: a retrospective analysis”, BMC Cancer, vol. 16, no:120, 2016.
[2] N. Irahara et al, “NRAS Mutations Are Rare in Colorectal Cancer”, Diagn Mol Patho, vol. 19, no. 3, pp: 157–163, 2010.
[3] W.Q. Li et al, “ BRAF mutations are associated with distinctive clinical, pathological and molecular features of colorectal cancer independently of microsatellite instability status”, Molecular Cancer, vol. 5 no. 2, 2006.