EGFR inhibitor, Colorectal cancer, NSCLC;
Tyrosine kinase inhibitors (TKI): Erbitux® (cetuximab), Vectibix™ (panitumumab)
Next Generation Sequencing Targeted HotSpots
QIAGEN® Human Tumor Actionable Mutations Panel (GeneRead™ DNAseq Targeted Panels V2) for targeted enrichment
Formalin Fixed Paraffin Embedded tissue block
3 slides (3-5 uM) per marker on adhesion glass
NOTE: Include a surgical pathology report with the sample if sending a block and/or slides
5.0 mL (min. 3.0 mL) whole blood EDTA, Sodium Heparin or ACD
3.0 mL (min. 1.0 mL) bone marrow EDTA, Sodium Heparin or ACD
Indefinite at ambient temperature (18-25°C) Whole blood and Bone Marrow stable at 18-25°C for 72 hours or 4°C for up to 7 days
Storage & Handling
Ship ambient. Protect from extreme temperature with an ice pack. Separate ice pack from specimen
Causes for Rejection
Improper specimen labeling; Insufficient sample volume; Clotted specimen; Specimen older than 7 days
Utilized as an independent predictor of colorectal cancer (CRC) and patient responsiveness to EGFR (TKI) inhibitor therapy.
- Sepulveda et al. (2017) Molecular Biomarkers for the Evaluation of Colorectal Cancer: Guideline From the American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology, and the American Society of Clinical Oncology. J Clin Oncol. 2017 Feb 6:JCO2016719807
- Neumann J et al. Epub 2009 Frequency and type of KRAS mutations in routine diagnostic analysis of metastatic colorectal cancer. Pathol. Res.Pract. 205(12), 858.
- Siena S et al (2009). Biomarkers Predicting Clinical Outcome of Epidermal Growth Factor Receptor - Targeted Therapy in Metastatic Colorectal Cancer. JNCI. 101: 1308-1324
- Allegra C J et al. (2009). ASCO Provisional Clinical Opinion: Testing for KRAS Gene Mutations in Patients with Metastatic Colorectal Carcinoma to Predict Response to Anti-Epidermal Growth Factor Receptor Monoclonal Antibody Therapy. JCO. 27: 2091-2096
- V. Shankaran et al. (2009). Economic implications of Kras testing in metastatic colorectal cancer (mCRC). Gastrointestinal Cancers Symposium. Abstratct No. 298.
- 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. http://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.
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