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Test ID: KRASC KRAS Mutation Analysis, 7 Mutation Panel, Colorectal

Useful For

Prognostic markers for cancer patients treated with epidermal growth factor receptor-targeted therapies

Additional Tests

Test ID Reporting Name Available Separately Always Performed
SLIRV Slide Review in MG No, (Bill Only) Yes

Testing Algorithm

When this test is ordered, slide review will always be performed at an additional charge.

Method Name

Polymerase Chain Reaction (PCR) Analysis

Reporting Name

KRAS Mutation Analysis, Colorectal

Specimen Type

Varies


Specimen Required


Pathology report must accompany specimen in order for testing to be performed.

 

Preferred:

Specimen Type: Tissue

Container/Tube: Tissue block

Collection Instructions: Submit a formalin-fixed, paraffin-embedded tissue block.

 

Acceptable:

Specimen Type: Tissue

Container/Tube: Slides

Specimen Volume: 1 stained and 5 unstained

Collection Instructions: Submit 1 slide stained with hematoxylin and eosin and 5 unstained, nonbaked slides with 5 micron-thick sections of the tumor tissue.


Specimen Minimum Volume

Formalin-fixed, paraffin-embedded (FFPE) tissue block (preferred) or 1 slide stained with hematoxylin-and-eosin and 5 unstained, nonbaked slides (5-microns thick sections) of the tumor tissue.

Specimen Stability Information

Specimen Type Temperature Time Special Container
Varies Ambient (preferred)
  Frozen 
  Refrigerated 

Clinical Information

Colorectal cancer is currently among the most common malignancies diagnosed each year. Strategies that focus on early detection and prevention effectively decrease the risk of mortality associated with the disease. In addition, an increase in survival rate for individuals with advanced stage colorectal cancer has been observed as a result of advancements in standard chemotherapeutic agents and the development of specialized targeted therapies. Monoclonal antibodies against epidermal growth factor receptor (EGFR), such as cetuximab and panitumumab, represent a new area of targeted therapy for such patients. However, studies have shown that not all individuals with colorectal cancer respond to EGFR-targeted molecules. Because the combination of targeted therapy and standard chemotherapy leads to an increase in toxicity and cost, strategies that help to identify the individuals most likely to benefit from such targeted therapies are desirable.

 

EGFR is a growth factor receptor that is activated by the binding of specific ligands (epiregulin and amphiregulin), resulting in activation of the RAS/MAPK pathway. Activation of this pathway induces a signaling cascade ultimately regulating a number of cellular processes including cell proliferation. Dysregulation of the RAS/MAPK pathway is a key factor in tumor progression. Targeted therapies directed to EGFR, which inhibit activation of the RAS/MAPK pathway, have demonstrated some success (increased progression-free and overall survival) in patients with colorectal cancer.

 

One of the most common somatic alterations in colon cancer is the presence of activating mutations in the proto-oncogene KRAS. KRAS is recruited by ligand-bound (active) EGFR to initiate the signaling cascade induced by the RAS/MAPK pathway. Because mutant 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 mutant KRAS. Current data suggest that the efficacy of EGFR-targeted therapies in colon cancer is confined to patients with tumors lacking KRAS mutations. As a result, the mutation status of KRAS can be a useful marker by which patients are selected for EGFR-targeted therapy.

 

At this time, this test is approved specifically for colorectal tumors and metastatic lesions from a colorectal primary. Refer to KRASO / KRAS Mutation Analysis, 7 Mutation Panel, Other (Non-Colorectal) for KRAS testing in noncolorectal tumors.

Reference Values

An interpretative report will be provided.

Interpretation

An interpretative report will be provided.

Clinical Reference

1. Khambata-Ford S, Garrett CR, Meropol NJ, et al: Expression of Epiregulin and Amphiregulin and K-ras mutation status predict disease control in metastatic colorectal cancer patients treated with Cetuximab. J Clin Oncol 2007;25:3230-3237

2. Lievre A, Bachet JB, Le Corre D, et al: KRAS mutation status is predictive of response to Cetuximab therapy in colorectal cancer. Cancer Res 2006;66(8):3992-3995

3. Spano JP, Milano G, Vignot S, Khayat D: Potential predictive markers of response to EGFR-targeted therapies in colorectal cancer. Crit Rev Oncol Hematol 2008;66:21-30

Day(s) and Time(s) Performed

Monday through Friday

Analytic Time

5 days

Test Classification

This test has been cleared, approved or is exempt by the U.S. Food and Drug Administration and is used per manufacturer's instructions. Performance characteristics were verified by Mayo Clinic in a manner consistent with CLIA requirements.

CPT Code Information

81275-KRAS (v-Ki-ras2 Kirsten rat sarcoma viral oncogene) (eg, carcinoma) gene analysis, variants in codons 12 and 13

 

Additional Test

88381-Microdissection, manual

LOINC Code Information

Test ID Test Order Name Order LOINC Value
KRASC KRAS Mutation Analysis, Colorectal 85509-8

 

Result ID Test Result Name Result LOINC Value
53273 Result Summary 50397-9
53274 Result 82939-0
53275 Interpretation 69047-9
53276 Specimen 31208-2
53277 Source 31208-2
54445 Tissue ID 80398-1
53278 Released By 18771-6

Forms

1. Molecular Genetics: Inherited Cancer Syndromes Patient Information (T519) in Special Instructions.

2. If not ordering electronically, complete, print, and send an Oncology Test Request (T729) with the specimen.

Mayo Clinic Laboratories | Gastroenterology Catalog Additional Information:

mml-gi-pathology