NRAS encodes a membrane protein GTPase that is a central mediator of downstream growth factor receptor signaling, critical for cell proliferation and survival. Mutations in codons 12, 13, and 61 of NRAS have been reported in 7-22% of acute myeloid leukemia, 12% of chronic myelomonocytic leukemia, 20% of blastic plasmacytoid dendritic cell neoplasm, 16% of juvenile myelomonocytic leukemia, 4-10% of myelodysplastic syndromes, and 5% of primary myelofibrosis. In addition, NRAS mutations have been described in approximately 15% of cases of B-ALL and, interestingly, some cases of ALL may show more than one abnormality in the RAS pathway. NRAS mutations are associated with an unfavorable prognosis in chronic myelomonocytic leukemia and primary myelofibrosis. NRAS mutations are also associated with an unfavorable prognosis in myelodysplastic syndrome, particularly in patients predicted to have lower-risk myelodysplastic syndrome (NCCN Guidelines for Myelodysplastic Syndromes). NRAS mutations do not seem to have significant prognostic impact in AML.

NRAS mutations occur in approximately 1--6% of colorectal cancers. Several studies have shown that patients with NRAS-mutated tumors are less likely to respond to cetuximab or panitumumab, but this may not have an effect on PFS or overall survival.

Somatic mutations in NRAS have been found in approximately 13-25% of all malignant melanomas. The result of these mutations is constitutive activation of NRAS signaling pathways. NRAS mutations are found in all melanoma subtypes, but may be slightly more common in melanomas derived from chronic sun-damaged (CSD) skin . Currently, there are no direct anti-NRAS therapies available.

RAS mutations (HRAS, NRAS and KRAS) are found in all epithelial thyroid malignancies. The frequency of HRAS mutations in thyroid carcinomas is 4%. RAS mutations are identified in 10-20% of papillary carcinomas, 40-50% of follicular carcinomas and 20-40% of poorly differentiated and anaplastic carcinomas .

NRAS gene belongs to the family of RAS genes. It encodes a G protein that is important in the transmission of growth-promoting signals from the cell surface receptors to the nucleus through RAS-RAF- mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)-AKT cell signaling pathways. NRAS mutations are the most common type of RAS mutations in thyroid nodules. Activating point mutations in NRAS gene have been associated with follicular-patterned neoplasms including follicular adenoma, follicular carcinoma and follicular variant papillary thyroid carcinoma cases. NRAS mutations have been also detected in a subset of poorly differentiated carcinoma and anaplastic carcinoma. NRAS mutations concentrate in codon 61, while those in codons 12 or 13 are rare. According to some studies, there is a significant correlation between RAS mutations and distant bone metastases among follicular and papillary carcinomas. However, RAS mutations are also frequently found in encapsulated follicular variant of papillary carcinoma, a tumor with an indolent behavior. Clinical correlation is recommended.

RAS mutations have also been identified in benign Follicular Adenomas(FA); however, it is unclear whether RAS positive FA have a higher chance of progression to cancer. The prevalence of this mutation in benign thyroid nodules is between 20 and 40%. The low overall prevalence of RAS mutations in thyroid cancers and the relatively high mutation rate in benign nodules makes ras mutation analysis unsuitable as a standalone test to predict malignancy in indeterminate thyroid nodules.

NRAS is a member of the RAS family of oncogenes and activating mutations of NRAS have been reported in about 1% of NSCLCs and are mostly exclusive of other known driver mutations. The Q61 codon is most frequently affected. In preclinical studies, cell lines harboring NRAS mutation(s) showed variable sensitivities to pathway inhibitors.

NRAS is a member of the RAS family of oncogenes and activating mutations of NRAS have been reported in a wide variety of tumors including occasional cases of cholangiocarcinomas.

NRAS is a member of the RAS family of oncogenes and activating mutations of NRAS have been reported in a wide variety of tumors including occasional cases of bladder cancer. This finding may influence targeted therapy options.

NRAS is a member of the RAS family of oncogenes. Activating point mutations in NRAS gene have been reported in a wide variety of tumors and they mostly concentrate in codons 12, 13 and codon 61. Activating mutations in NRAS are rare in pancreatic ductal adenocarcinomas (PDAC). The predictive and prognostic significance of NRAS mutations in PDAC is unclear and needs to be further studied. Correlation with other clinical and laboratory findings is recommended.

This gene is a known cancer gene.

This gene is a known cancer gene.

NRAS gene belongs to the family of RAS genes. It encodes a G protein that is important in the transmission of growth-promoting signals from the cell surface receptors to the nucleus through RAS-RAF-mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)-AKT cell signaling pathways. NRAS mutations are rare in glial neoplasms and are found in about 1% of cases. The clinicopathologic significance of NRAS mutations in glial neoplasms remains to be further elucidated.

NRAS gene belongs to the family of RAS genes. It encodes a G protein that is important in the transmission of growth-promoting signals from the cell surface receptors to the nucleus through RAS-RAF- mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)-AKT cell signaling pathways. NRAS mutations are identified in multiple cancer types and tend in concentrate in codons 12, 13, and 61. NRAS mutations are rare in urothelial carcinomas of both the upper and lower urinary tract and are found in about 1% of cases. Currently, there are no direct anti-NRAS therapies available. The clinicopathologic significance of NRAS mutations in urothelial carcinoma remains to be further elucidated.