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BRAF
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BRAF Clinical Significance
BRAF is a downstream molecule from KRAS in a signaling pathway involved in cell cycling. Both KRAS and BRAF are prone to mutations in sporadic colorectal carcinomas (CRC). Several studies have demonstrated that mutations in KRAS lead to constitutive activation of this pathway, which may lead to cancer progression. This activation results in a failure to respond to anti-EGFR therapy. KRAS mutations are found in 30-40% of patients who fail to respond to Erbitux® (cetuximab) and Vectibix™ (panitumumab). Data presented at this year’s 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapies demonstrate that BRAF mutations are responsible for an additional 12-15% of patients who fail to respond to anti-EGFR treatment. This finding suggests that testing for the BRAF V600E mutation compliments KRAS mutation analysis and may be as important as KRAS testing for treatment decisions. Clarient now offers testing for both KRAS and BRAF mutations.
Methodology
Real-time PCR
Specimen Requirements
Formalin-fixed, paraffin-embedded block, unstained slides
CPT Codes
83907, 83891, 83898, 83896(x2), 88381, 83914, 83912-26
BRAF Facts
- BRAF mutations account for approximately 12-15% of colorectal cancer patients.
- BRAF mutations are biomarkers of non-response to anti-EGFR therapies.
- BRAF mutations have been shown in a number of clinical studies as a highly predictive factor of non-response to therapy with Erbitux® (cetuximab) or Vectibix® (panitumumab), in combination with chemotherapy, as well as in monotherapy.
Indications for Use
The BRAF (V600E) mutation analysis is predictive for anti-EGFR therapies (i.e., cetuximab and panitumumab).
BRAF Clinical Indications
Any tumor types that have indications or are candidates for anti-EGFR therapy — Colon, Lung, Pancreas, Ovary, Cervix, Breast, Endometrium, Biliary Tract, Liver Cancers
Turnaround Time
5-7 days
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