scholarly journals Concordance and Discordance Rates of V-Raf Murine Sarcoma Viral Oncogene Homolog B1 (BRAF) V600E Status in Metastatic against Primary Lesion of Melanoma: A Meta-analysis

JMA Journal ◽  
2020 ◽  
Vol 3 (3) ◽  
pp. 274-279
Keyword(s):  
Meta Analysis ◽  
Primary Lesion ◽  
Braf V600e ◽  
Viral Oncogene ◽  
Murine Sarcoma ◽  
Viral Oncogene Homolog

scholarly journals Treatment of NRAS-mutated advanced or metastatic melanoma: rationale, current trials and evidence to date

2017 ◽  
Vol 9 (7) ◽  
pp. 481-492 ◽  
Author(s):  
Amélie Boespflug ◽  
Julie Caramel ◽  
Stephane Dalle ◽  
Luc Thomas
Keyword(s):  
Metastatic Melanoma ◽  
Cytotoxic Chemotherapy ◽  
Disease Course ◽  
Line Treatment ◽  
First Line ◽  
Viral Oncogene ◽  
Melanoma Patients ◽  
Murine Sarcoma ◽  
Review Current ◽  
Viral Oncogene Homolog

The disease course of BRAF (v-raf murine sarcoma viral oncogene homolog B1)-mutant melanoma has been drastically improved by the arrival of targeted therapies. NRAS (neuroblastoma RAS viral oncogene homolog)-mutated melanoma represents 15–25% of all metastatic melanoma patients. It currently does not have an approved targeted therapy. Metastatic patients receive immune-based therapies as first-line treatments, then cytotoxic chemotherapy like carboplatin/paclitaxel (C/P), dacarbazine (DTIC) or temozolomide (TMZ) as a second-line treatment. We will review current preclinical and clinical developments in NRAS-mutated melanoma, and analyze ongoing clinical trials that are evaluating the benefit of different targeted and immune-based therapies, either tested as single agents or in combination, in NRAS-mutant melanoma.

scholarly journals V-raf murine sarcoma viral oncogene homolog B (BRAF) mutations in hairy cell leukaemia

2015 ◽  
Vol 58 (1) ◽  
pp. 62
Author(s):  
Neeraj Arora ◽  
Sheila Nair ◽  
Rekha Pai ◽  
Sukesh Nair ◽  
Auro Viswabandya ◽  
...  
Keyword(s):  
Hairy Cell Leukaemia ◽  
Cell Leukaemia ◽  
Hairy Cell ◽  
Braf Mutations ◽  
Viral Oncogene ◽  
Murine Sarcoma ◽  
Viral Oncogene Homolog

scholarly journals Ring Finger Protein 149 Is an E3 Ubiquitin Ligase Active on Wild-type v-Raf Murine Sarcoma Viral Oncogene Homolog B1 (BRAF)

2012 ◽  
Vol 287 (28) ◽  
pp. 24017-24025 ◽  
Author(s):  
Seung-Woo Hong ◽  
Dong-Hoon Jin ◽  
Jae-Sik Shin ◽  
Jai-Hee Moon ◽  
Young-Soon Na ◽  
...  
Keyword(s):  
Ubiquitin Ligase ◽  
E3 Ubiquitin Ligase ◽  
Ring Finger ◽  
Ring Finger Protein ◽  
Wild Type ◽  
Viral Oncogene ◽  
Finger Protein ◽  
Type V ◽  
Murine Sarcoma ◽  
Viral Oncogene Homolog

scholarly journals Atypical BRAF and NRAS Mutations in Mucosal Melanoma

Cancers ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1133 ◽  
Author(s):  
Nicolas Dumaz ◽  
Fanélie Jouenne ◽  
Julie Delyon ◽  
Samia Mourah ◽  
Armand Bensussan ◽  
...  
Keyword(s):  
Mapk Pathway ◽  
Mucosal Melanoma ◽  
Mitogen Activated Protein Kinase ◽  
Nras Mutation ◽  
Viral Oncogene ◽  
Mitogen Activated Protein ◽  
Murine Sarcoma ◽  
Worse Prognosis ◽  
Viral Oncogene Homolog

Primary mucosal melanomas represent a minority of melanomas, but have a significantly worse prognosis than cutaneous melanomas. A better characterization of the molecular pathogenesis of this melanoma subtype could help us understand the risk factors associated with the development of mucosal melanomas and highlight therapeutic targets. Because the Mitogen-Activated Protein Kinase (MAPK) pathway plays such a significant role in melanoma development, we explore v-raf murine sarcoma viral oncogene homolog B (BRAF) and neuroblastoma RAS viral oncogene homolog (NRAS) mutations in mucosal melanoma and compare them to the mutation profiles in cutaneous melanoma and other tumors with BRAF and NRAS mutations. We show that in addition to being less frequent, BRAF and NRAS mutations are different in mucosal melanoma compared to cutaneous melanomas. Strikingly, the BRAF and NRAS mutation profiles in mucosal melanoma are closer to those found in cancers such as lung cancer, suggesting that mutations in mucosal melanoma could be linked to some genotoxic agents that remain to be identified. We also show that the atypical BRAF and NRAS mutations found in mucosal melanomas have particular effects on protein activities, which could be essential for the transformation of mucosal melanocytes.

scholarly journals Necessity of Microdissecting Different Tumor Components in Pulmonary Tumor Pyrosequencing

2016 ◽  
Vol 2016 ◽  
pp. 1-5
Author(s):  
Dahui Qin ◽  
Zhong Zheng ◽  
Shanxiang Shen ◽  
Prudence Smith ◽  
Farah K. Khalil
Keyword(s):  
Gene Mutations ◽  
Molecular Testing ◽  
Tissue Sampling ◽  
Wild Type ◽  
Kras Mutations ◽  
Viral Oncogene ◽  
Pulmonary Tumor ◽  
New Challenges ◽  
Murine Sarcoma ◽  
Viral Oncogene Homolog

Microdissection is a useful method in tissue sampling prior to molecular testing. Tumor heterogeneity imposes new challenges for tissue sampling. Different microdissecting methods have been employed in face of such challenge. We improved our microdissection method by separately microdissecting the morphologically different tumor components. This improvement helped the pyrosequencing data analysis of two specimens. One specimen consisted of both adenocarcinoma and neuroendocrine components. When both tumor components were sequenced together for KRAS (Kirsten rat sarcoma viral oncogene homolog) gene mutations, the resulting pyrogram indicated that it was not a wild type, suggesting that it contained KRAS mutation. However, the pyrogram did not match any KRAS mutations and a conclusion could not be reached. After microdissecting and testing the adenocarcinoma and neuroendocrine components separately, it was found that the adenocarcinoma was positive for KRAS G12C mutation and the neuroendocrine component was positive for KRAS G12D mutation. The second specimen consisted of two morphologically different tumor nodules. When microdissected and sequenced separately, one nodule was positive for BRAF (v-raf murine sarcoma viral oncogene homolog B1) V600E and the other nodule was wild type at the BRAF codon 600. These examples demonstrate that it is necessary to microdissect morphologically different tumor components for pyrosequencing.

scholarly journals AXL Is a Novel Predictive Factor and Therapeutic Target for Radioactive Iodine Refractory Thyroid Cancer

Cancers ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 785 ◽  
Author(s):  
Francesca Collina ◽  
Lucia La Sala ◽  
Federica Liotti ◽  
Nella Prevete ◽  
Elvira La Mantia ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cell Lines ◽  
Therapeutic Target ◽  
Braf V600e ◽  
Specific Gene ◽  
Thyroid Cell ◽  
Thyroid Cells ◽  
Viral Oncogene ◽  
Rat Thyroid ◽  
Viral Oncogene Homolog

Papillary thyroid carcinomas (PTCs) have an excellent prognosis, but a fraction of them show aggressive behavior, becoming radioiodine (RAI)-resistant and/or metastatic. AXL (Anexelekto) is a tyrosine kinase receptor regulating viability, invasiveness and chemoresistance in various human cancers, including PTCs. Here, we analyze the role of AXL in PTC prognosis and as a marker of RAI refractoriness. Immunohistochemistry was used to assess AXL positivity in a cohort of human PTC samples. Normal and cancerous thyroid cell lines were used in vitro for signaling, survival and RAI uptake evaluations. 38.2% of human PTCs displayed high expression of AXL that positively correlated with RAI-refractoriness and disease persistence or recurrence, especially when combined with v-raf murine sarcoma viral oncogene homolog B(BRAF) V600E mutation. In human PTC samples, AXL expression correlated with V-akt murine thymoma viral oncogene homolog 1 (AKT1) and p65 nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) activation levels. Consistently, AXL stimulation with its ligand growth arrest-specific gene 6 (GAS6) increased AKT1- and p65 NF-kB-phosphorylation and promoted survival of thyroid cancer cell lines in culture. Enforced expression or activation of AXL in normal rat thyroid cells significantly reduced the expression of the sodium/iodide symporter (NIS) and the radioiodine uptake. These data indicate that AXL expression levels could be used as predictor of RAI refractoriness and as a possible novel therapeutic target of RAI resistant PTCs.

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