NRAS Mutation Analysis with Interpretation
6004 BT GH
Formalin Fixed, Paraffin Embedded Tissue
10 unstained 5-10 μM section glass slides at 20-25°C
and an H&E slide or the tissue block.
Tumor cells more than 50% of the total tissue and greater than
10mm2 in surface area on the block.
Specimens fixed in B5 fixative or that have been decalcified will not
be accepted. Tumor specimens containing less than 50% tumor cells or
are less than 10mm2 in area may be unacceptable.
7-10 working days
Negative for mutations (normal).
The presence of an oncogenic mutation in codons 12, 13, or 61 of
NRAS is indicative of a tumor that may respond to drugs
targeted at genes downstream of NRAS in the mitogen
activating protein kinase (MAPK) signaling cascade, as in malignant
melanoma cases. In contrast, mutations in NRAS can inhibit
therapeutic response to EGFR-targeted therapies in patients with
metastatic colorectal cancer.
NRAS mutations are found in the more aggressive variant of
chronic myelogenous leukemia (CMML) and may predict response to
farnesyl transferase inhibitors therapy in acute myeloid leukemia
The tissue should be reviewed by a pathologist prior to testing to
identify that it contains at least 50% tumor.
This assay detects mutations in codons 12, 13 and 61 (20 mutations in
Mutations in other locations within the NRAS gene or in any
other gene will not be detected.
Absence of NRAS mutations does not guarantee a positive
response to anti-EGFR therapies in metastatic colorectal cancer.
The presence of mutations in codons 12, 13, or 61 does not guarantee a
positive response to therapies in melanoma.
Massively parallel Next Generation DNA sequencing by synthesis,
semiconductor technology, Ion Personal Genomics Machine.