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NRAS point mutation could be considered as evidence, consistent with a Pulmonary Langerhans' cell Histiocytosis diagnosis.
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Comparatively to BRAF mutation, results found that NRAS mutations are frequent in the follicular variant of papillary thyroid carcinoma.
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Studied NRAS and B-Raf proto-oncogene serine/threonine kinase (BRAF) mutations in Turkish cutaneous melanoma patients and their association with clinical stage of the melanomas.
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Tet2/Nras double-mutant leukemia showed preferential sensitivity to MAPK kinase (MEK) inhibition in both mouse model and patient samples
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Our study provided the first evidence that miR-29a suppressed lung cancer cell growth through inhibition of NRAS
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NRAS mutations harbor commonly in neurocutaneous melanosis.
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Ets-1 is induced by BRAF or MEK kinase inhibition, resulting in increased NRAS expression, which could be blocked by inactivation of Usp9x.
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we used hot-spot mutation sequencing to examine whether KRAS/NRAS mutations, a characteristic feature of mesonephric carcinoma,1 are also present in mesonephric hyperplasia. None of the mesonephric hyperplasia cases harboured a KRAS or NRAS mutation.
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BRAF mutations more frequently affected individuals younger than 61 with phototype II. In contrast, NRAS mutations were more frequent in phototype III cases. Mutations of both genes were more frequent in cases with satellitosis in the first melanoma, and in cases with ulceration in the subsequent lesions.
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Identification of KRAS/NRAS/BRAF mutation status is crucial to predict the therapeutic effect and determine individual therapeutic strategies for patients with colorectal cancer.
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common conjunctival melanocytic nevi have mutually exclusive mutations in BRAF and NRAS. The two conjunctival blue nevi harbored GNAQ mutations. This suggests the driver mutations of conjunctival nevi are similar to those of nevi of the skin. At the molecular level, conjunctival nevi appear more like cutaneous nevi than choroidal nevi
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the mutational status of BRAF, NRAS, and TERT promoter genes in 97 melanomas, was investigated.
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Deciphering KRAS and NRAS mutated clone dynamics in MLL-AF4 paediatric leukaemia by ultra deep sequencing analysis.
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N-Ras preferentially populated raft domains when bound to mant-GDP. It lost its preference for rafts when associated with a GTP mimic, mant-GppNHp. The isolated lipidated C-terminal peptide of N-Ras was outside of the liquid-ordered rafts, most likely in the bulk-disordered lipid. Substitution of the N-Ras N-terminal G domain with a homologous G domain of H-Ras disrupted the nucleotide-dependent lipid domain switch.
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We report herein for the first time that 30% of cutaneous NRAS mutant melanomas have a high M%NRAS. Chromosome instability, (chromosome 1 polysomy, intratumor copy number variation of chromosome1/NRAS) rather than the acquired copy neutral LOH seems to be responsible for most of the cases with high M%NRAS.
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NRAS status (exons 2-4) was analyzed by Pyrosequencing in a case series of 50 squamous cell anal carcinoma patients.
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NRAS-mutant tumors tended to behave more aggressively particularly in early stages of the disease in studied high-risk melanoma population.
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Data show that mutations in NRAS are associated with poor survival.
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In the title.
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Authors analyzed 421 samples from CLM patients for their all-RAS mutation status to compare the overall survival rate (OS), recurrence-free survival rate (RFS), and the pattern of recurrence between the patients with and without RAS mutations.
