26399 Cell-Free DNA KRAS 12, 13, 61, 146, Blood (KRASD)

​CRC, Colorectal cancer, EGFR, Epidermal growth factor receptor, Cell free DNA, cfDNA, cell-free DNA, circulating tumor DNA, liquid biopsy, KRAS WT, KRAS codon 12, KRAS codon 13, KRAS codon 61, KRAS codon 146, Circulating tumor cells, KRAS, RAS

An alternative to invasive tissue biopsies for the determination of KRAS 12, 13, 61,146 (G12A, G12C, G12D, G12R, G12S, G12V, G13D, Q61K, Q61L, Q61R, Q61H, and A146T) mutation status

Detecting molecular markers associated with response or resistance to specific therapy

This test is not intended as a screening test to identify cancer.  

This test is not a prenatal screening test.

GENETICS TEST INFORMATION:

This test evaluates cell-free DNA (cfDNA) in the peripheral blood for the presence of KRAS mutations at codons 12, 13, 61, and 146 (G12A, G12C, G12D, G12R, G12S, G12V, G13D, Q61K, Q61L, Q61R, Q61H, and A146T) in patients with colorectal cancer and can be used to assess eligibility for targeted therapies.
This test is not validated for serial monitoring of patients with cancer. This test is also not intended as a screening test to identify cancer.

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HIGHLIGHTS:

This test provides rapid detection of KRAS mutations in colorectal cancer patients as an alternative for KRAS analysis of tissue.

Current data suggests that the efficacy of epidermal growth factor receptor (EGFR)-targeted therapy in colorectal cancer patients is limited to patients whose tumors do not harbor mutations in the KRAS gene.

Only blood collected in Streck Cell-Free DNA BCT tubes will be accepted for analysis. Whole blood will be processed to produce platelet-poor plasma before cfDNA isolation.

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SHIPPING INSTRUCTIONS:

1. Samples should be transported at ambient temperature or refrigerated (4 degrees C).

2. Samples are viable for 7 days in the Streck Black/Tan Top Tube Kit (T715).

Patients with a negative test result may still harbor a KRAS mutation. Mutation testing of a tissue specimen for KRAS mutations should be considered for patients with who have a negative result with this test.

The limit of detection of this assay for the detection of KRAS mutations is influenced by the amount of cell-free DNA (cfDNA) in the blood. This is a biological variable that cannot be controlled.

This assay was designed to detect mutations in KRAS codons 12, 13, 61, and 146 (G12A, G12C, G12D, G12R, G12S, G12V, G13D, Q61K, Q61L, Q61R, Q61H, and A146T).

This test has not been clinically validated for use as a tool to monitor response to therapy or for early detection of tumors.

This test cannot differentiate between somatic and germline alterations.  Additional testing may be necessary to clarify the significance of results if there is a potential hereditary risk. 

Targeted cancer therapies are defined as antibody or small molecule drugs that block the growth and spread of cancer by interfering with specific cell molecules involved in tumor growth and progression. Multiple targeted therapies have been approved by the US Food and Drug Administration for treatment of solid tumor malignancies. Molecular genetic profiling is often needed to identify targets amenable to targeted therapies and to minimize treatment costs and therapy-associated risks.

One of the most common somatic alterations in colorectal cancer (CRC) and non-small cell lung cancer (NSCLC) is the presence of activating variants in the protooncogene KRAS. KRAS is recruited by ligand-bound (active) epidermal growth factor receptor (EGFR) to initiate the signaling cascade induced by the RAS/MAPK pathway. Because altered KRAS constitutively activates the RAS/MAPK pathway downstream of EGFR, agents such as cetuximab and panitumumab, which prevent ligand-binding to EGFR, do not appear to have any meaningful inhibitor activity on cell proliferation in the presence of altered KRAS. Current data suggest that the efficacy of EGFR-targeted therapies in CRC and NSCLC is confined to patients with tumors lacking KRAS mutations. An exception is the KRAS G12C variant that is targetable with variant-specific inhibitors.

 This test uses DNA extracted from tumor tissue to evaluate for the presence of KRAS (G12A, G12C, G12D, G12R, G12S, G12V, G13D, Q61K, Q61L, Q61R, Q61H, and A146T) variants. A positive result indicates the presence of an activating KRAS mutation and can be useful for guiding the treatment of patients with CRC and NSCLC.

​An interpretive report will be provided.

The interpretation of molecular biomarker analysis includes an overview of the results and the associated diagnostic, prognostic, and therapeutic implications