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Report discordant BRAF mutation status between matched primary cutaneous and metastatic melanoma samples.
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Somatic NRAS mutation in patient with generalized lymphatic anomaly
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This study found "rare mutations" in RAS genes in nearly 14% of colorectal cancer (CRC) -i.e., in almost a quarter (24.0%) of KRAS exon 2 wild type CRCs, including 2.3% in KRAS exon 3, 8.2% in KRAS exon 4 and 3.4% in NRAS. Stage I-III patients with PIK3CA or NRAS mutations developed more distant metastases (3-year risk in PIK3CA mutated and wild type patients: 23.3% vs 11.5%, P = 0.03.
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In a Slovenian population with melanoma, our analysis detected higher rate of BRAF mutation, lower rate of NRAS and c-KIT mutation compared to previously published studies in Europe and North America.
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High NRAS isoform 5 expression is associated with malignant melanoma.
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BRAF and NRAS mutations in Langerhans cell histiocytosis (LCH) suggest a possibility of the disease being driven by the activation of the MAPK/ERK pathway. These oncogenic mutations provide new opportunities in understanding LCH pathogenesis and may be a potential target of therapy
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Two patients harbored KRAS with codon 12 mutations; one harbored the gly12val mutation with a variation of leu597val in the BRAF exon 15 codon, the other harbored mutation in the BRAF exon 15 codon. One patient harbored a codon 117 mutation with a BRAF V600E mutation. The last patient harbored a NRAS exon 2 mutation with the GGT/GAT, V600G mutation in the BRAF exon 15 codon
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The study shows a high concordance of KRAS, NRAS, BRAF and PIK3CA gene mutations in plasma against mutation status in tumor tissue.
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FLT3-ITD was the most common mutated gene (16.2%, 42/259), followed by CEBPA (15.1%, 39/259), NRAS (14.7%, 38/259), and NPM1 (13.5%, 35/259). The results showed certain rules in the mutation profiling and concurrence of acute myeloid leukemia (AML) patients, which was related to the function classification of genes.
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No mutation was found in the NRAS gene in our patients
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NRAS found to be overexpressed in hepatocellular carcinoma (HCC) cell lines, preclinical HCC models, and human HCC tissues. NRAS overexpression correlated with poor survival and proliferation in vivo. NRAS expression was elevated in sorafenib-resistant compared to nonresistant HCC cells, and NRAS knockdown enhanced sorafenib efficacy in resistant cells.
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NRAS mutation c.181C>A (p.Gln61Lys) is associated with congenital nevus syndrome.
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The Q61R mutation of the NRAS gene is one of the most frequent driver mutations of thyroid cancer. The expression of NRAS(Q61R) in thyroid epithelial cells has a profound influence on groups of genes involved in the formation of intercellular contacts, as well as in processes of epithelial-mesenchymal transition and cell invasion.
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These findings highlight a novel mechanism for resistance to ER-stress through oncogenic activation of MEK/ERK signalling by RAC1 and NRAS.
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The primary aim of this study was to explore if patients with BRAF or NRAS mutant tumours compared to patients with wild-type tumours have an increased risk of developing disease recurrence following a negative sentinel lymph node biopsy (SLNB)
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Ectopic introduction of SPRY4 recapitulated the growth arrest phenotype of dual BRAF(V600E)/NRAS(Q61) expression while SPRY4 depletion led to a partial rescue from oncogenic antagonism.
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bFGF-mediated pluripotency maintenance in human induced pluripotent stem cells is associated with NRAS-MAPK signaling
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introducing a rapid and sensitive microarray-based assay for the multiplex detection of minority mutations of oncogenes (KRAS, NRAS and BRAF) with relevant diagnostics implications in tissue biopsies and plasma samples in metastatic colorectal cancer patients
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Gene mutations in BRAF, MSI-high status, and N-ras differ according to gender among patients with colorectal cancer
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The results suggest it is likely that all acquired naevi will be mutated for NRAS, thus supporting the role of the MAPK pathway in the development of benign melanocytic proliferations. These data confirm that additional genomic events besides somatic mutations in NRAS are required for melanoma development.