When mutated, HRAS can act as an oncogene, causing normal cells to become cancerous. Somatic HRAS mutations have been associated with some cases of bladder, thyroid and kidney cancers and in nevi. Based on clinical evidence in melanoma with the related family member NRAS, downstream pathway MEK inhibitors may be a feasible treatment strategy. The effectiveness of MEK inhibitors for HRAS-mutant thyroid and bladder cancer patients has not yet been investigated.

RAS is a family of small GTPases and acts as an oncogene. Point mutations in codons 12 and 13 of RAS gene increases its affinity for GTP and those in codon 61 inactivate its autocatalytic GTPase function, resulting in permanent RAS activation and stimulation of its downstream targets along the MAPK and PI3K/AKT signaling pathways. In thyroid, RAS (HRAS, NRAS and KRAS) mutations are identified in 10--20% of papillary carcinomas, 40--50% of follicular carcinomas, 10% of medullary carcinomas, and 20--40% of poorly differentiated and anaplastic carcinomas. The frequency of HRAS mutations in thyroid carcinomas is approximately 4%. HRAS mutations at codon 61 have been reported in a variety of thyroid lesions and are especially prevalent in the follicular variant of papillary thyroid carcinoma. However, the predictive or prognostic significance of HRAS mutation in thyroid carcinoma is not clear and correlation with other clinical and laboratory findings is necessary.

When mutated, HRAS can act as an oncogene. Somatic HRAS mutations have been associated with some cases of upper and lower urinary tract urothelial carcinoma, thyroid, and kidney cancers and in nevi. The frequency of HRAS mutations in upper and lower urinary tract urothelial carcinoma are about 10%. Interestingly, it has been shown that the HRAS mutation in lower urinary tract urothelial carcinoma may occur in tumors without FGFR3 mutations.

When mutated, HRAS can act as an oncogene, causing normal cells to become cancerous. Somatic HRAS mutations have been associated with some cases of bladder, thyroid and kidney cancers and in nevi. HRAS mutations are rarely found in the breast and the HRAS Q61R mutation has not been previously reported in this cancer. Inferring the clinical evidence seen in melanoma, downstream pathway MEK inhibitors may be a feasible treatment strategy. The effectiveness of MEK inhibitors for HRAS-mutant thyroid and bladder cancer patients has not yet been investigated.

RAS is a family of small GTPases and acts as an oncogene. Point mutations in codons 12 and 13 of RAS gene increases its affinity for GTP and those in codon 61 inactivate its autocatalytic GTPase function, resulting in permanent RAS activation and stimulation of its downstream targets along the MAPK and PI3K/AKT signaling pathways. HRAS mutation has been reported in up to 5% and 9% of head/neck and vulvar squamous cell carcinoma, respectively. The predictive and prognostic significance of HRAS mutations in squamous cell carcinoma is unclear and needs further elucidation.

This gene is a known cancer gene.

This gene is a known cancer gene.