KRAS Mutation, EGFR Inhibitor Response Featured
Test Code
KRAS
Associations
Colorectal cancer
Methodology
Primer-extension PCR utilizing shifted termination assay (STA) technology followed by capillary electrophoresis (CE)
CPT Codes
83890 x2 – Isolation or extraction (DNA isolation)
83892 x2 – Enzymatic digestion (enzyme treatment)
83898 – PCR amplification
83900 – Amplification, target, multiplex, first 2 (PCR amplification)
83901 x11 – Amplification, target, multiplex, each additional (PCR amplification)
83907 – Cell lysis
83909 x2 – Separation and identification
83914 x2 – Mutation identification
838912-26 – Interpretation and report
88305-T – Surgical pathology examination
83892 x2 – Enzymatic digestion (enzyme treatment)
83898 – PCR amplification
83900 – Amplification, target, multiplex, first 2 (PCR amplification)
83901 x11 – Amplification, target, multiplex, each additional (PCR amplification)
83907 – Cell lysis
83909 x2 – Separation and identification
83914 x2 – Mutation identification
838912-26 – Interpretation and report
88305-T – Surgical pathology examination
Turnaround Time
8-10 business days
Specimen Requirements
10% neutral buffered formalin fixed paraffin embedded tissue (Notify MPLN when other fixatives are used.)
NOTE: Include a surgical pathology report with the sample.
NOTE: Include a surgical pathology report with the sample.
Specimen Stability
Stable at 18-25°C indefinitely
Storage & Handling
Ship ambient
Causes for Rejection
Improper specimen labeling; Insufficient sample; Inadequate fixation and/or processing
Reference Range
The assay detects 12 mutations found in codon 12 and 13 of the KRAS oncogene
Codon 12
Codon 13
Codon 12
- Gly12Ser (GGT>AGT)
- Gly12Arg (GGT>CGT)
- Gly12Cys (GGT>TGT)
- Gly12Asp (GGT>GAT)
- Gly12Ala (GGT>GCT)
- Gly12Val (GGT>GTT)
Codon 13
- Gly13Ser (GGC>AGC)
- Gly13Arg (GGC>CGC)
- Gly13Cys (GGC>TGC)
- Gly13Asp (GGC>GAC)
- Gly13Ala (GGC>GCC)
- Gly13Val (GGC>GTC)
Related Content
BRAF; CellSearch; I MSI
Description
Utilized as an independent predictor of colorectal cancer (CRC) patient responsiveness to EGFR inhibitor therapy
References
- Tol J. (2009). Chemotherapy, bevacizumab and cetuximab in metastatic colorectal cancer. N Engl J Med. 360:563-72.
- De Roock W et al. (2008). KRAS wild-type state predicts survival and is associated to early radiological response in metastatic colorectal cancer treated with cetuximab. Ann Oncol. 19:508-515.
- Karapetis CS et al. (2008). K-ras Mutations and benefit from cetuximab in advanced colorectal cancer. NEJM. 359:1757-1765.
- Lievre A et al (2008). KRAS mutations as an independent prognostic factor in patients with advanced colorectal cancer treated with cetuximab. J Clin Oncol. 26:374-379.
- NCCN Practice Guidelines v.3.2008. www.nccn.org.
- Di Fiore F et al. (2007). Clinical relevance of KRAS mutation detection in metastatic colorectal cancer treated by Cetuximab plus chemotherapy. Br J Cancer. 96:1166-1169.
- Lievre A et al. (2007). KRAS mutation status is predictive of response to cetuximab therapy in colorectal cancer. Cancer Res. 66:3992-3995.
