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We present two boys with Noonan syndrome and the identical de novo RAF1 missense variant c.1082G>C/p.(Gly361Ala) affecting the CR3, but located outside the kinase activation segment. The p.(Gly361Ala) mutation has been identified as a RAF1 allele conferring resistance to RAF inhibitors. This amino acid change favors a RAF1 conformation that allows for enhanced RAF dimerization and increased intrinsic kinase activity
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The functional assessment supported the pathogenicity of the RAF1 and RIT1 VUSs, while the significance of two variants of unknown significance in A2ML1 remained unclear.
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Our report presents the second familial case of Noonan syndrome due to a germline p.S427G substitution in RAF] with no occurrence of a malignant tumor. It may suggest that carrying a germline mutation in the RAF1 oncogene is not associated with an increased risk of tumor development. Since RAF1 mutations have been observed as a somatic event in many types of cancer.
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Data indicate that Raf-1 proto-oncogene, serine-threonine kinase (RAF1) is a negative regulator of hepatocarcinogenesis.
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we report a patient with an inherited RAF1-associated Noonan syndrome, presenting with an antenatally diagnosed abnormality of skull shape, bilateral subdural haematomas, of unknown cause, delayed myelination and polymicrogyria.
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Raf1 may serve as a novel prognostic factor and potential target for improving the longterm outcome of nonsmall cell lung cancer (NSCLC).
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Results provide evidence that RAF1 binding to SPRY4 is regulated by miR-1908 in glioma tumors.
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High RAF1 expression is associated with malignant melanoma.
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two premature neonates with progressive biventricular hypertrophy found to have RAF1 variants in the CR2 domain, are reported.
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Data indicate connector enhancer of kinase suppressor of Ras 1 protein (CNK1) as a molecular platform that controls c-raf protein (RAF) and c-akt protein (AKT) signalling and determines cell fate decisions in a cell type- and cell stage-dependent manner.
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CRAF is a bona fide alternative oncogene for BRAF/NRAS/GNAQ/GNA11 wild type melanomas
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Authors evaluated the expression of known targets of miR-125a and found that sirtuin-7, matrix metalloproteinase-11, and c-Raf were up-regulated in tumor tissue by 2.2-, 3-, and 1.7-fold, respectively. Overall, these data support a tumor suppressor role for miR-125a.
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Overexpression of ciRS-7 in HCT116 and HT29 cells led to the blocking of miR-7 and resulted in a more aggressive oncogenic phenotype, and ciRS-7 overexpression permitted the inhibition of miR-7 and subsequent activation of EGFR and RAF1 oncogenes
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miR-497 could serve as a tumor suppressor and a potential early diagnostic marker of gastric cancer by targeting Raf-1 proto-oncogene.
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RAF1 may have a role in survival in hepatocellular carcinoma, and indicate whether sorafenib should be used as a postoperative adjuvant
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Mutational activation of Kit-, Ras/Raf/Erk- and Akt- pathways indicate the biological importance of these pathways and their components as potential targets for therapy.
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Results indicate that des-gamma-carboxy prothrombin (DCP) antagonizes the inhibitory effects of Sorafenib on hepatocellular carcinoma (HCC) through activation of the Raf/MEK/ERK and PI3K/Akt/mTOR signaling pathways.
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DiRas3 binds to KSR1 independently of its interaction with activated Ras and RAF.
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RhoA/ROCK and Raf-1/CK2 pathway are responsible for TNF-alpha-mediated endothelial cytotoxicity via regulation of the vimentin cytoskeleton.
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Although Raf-1 gene is not mutated, an abnormality of Raf-1 kinase feedback regulation enhances its antiapoptotic function, and Raf-1 can still be a pharmaceutical target to increase chemotherapy or radiotherapy sensitivity in these cancer cells.