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BIOMARKER:

BRAF T1799A

i
Other names: BRAF, B-raf proto-oncogene, B-raf proto-oncogene, Serine/threonine kinase, V-Raf murine sarcoma viral oncogene homolog B, Serine/threonine-protein kinase B-Raf, Proto-oncogene B-Raf, BRAF1, RAFB1, B-raf proto-oncogene Serine/threonine-protein kinase, Murine sarcoma viral (V-Raf) oncogene homolog B1, B-raf serine/threonine-protein, 94 KDa B-raf protein, B-RAF1
Entrez ID:
2years
Transposon Mutagenesis Reveals RBMS3 Silencing as a Promoter of Malignant Progression of BRAFV600E-Driven Lung Tumorigenesis. (PubMed, Cancer Res)
Although RBMS3 silencing rendered BRAFV600E-driven lung tumors resistant to the effects of dabrafenib plus trametinib, the tumors were sensitive to inhibition of porcupine, an acyltransferase of WNT ligands necessary for their secretion. Analysis of TCGA patient samples revealed that chromosome 3P24, which harbors RBMS3, is frequently lost in NSCLC and correlates with poor prognosis. Collectively, these data reveal the role of RBMS3 as a lung cancer suppressor and suggest RBMS3 silencing may contribute to malignant progression.
Journal
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BRAF (B-raf proto-oncogene) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • CCND1 (Cyclin D1) • RBMS3 (RNA Binding Motif Single Stranded Interacting Protein 3)
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BRAF V600E • BRAF V600 • EGFR L858R • MYC expression • CCND1 expression • BRAF T1799A • CTNNB1 expression
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Mekinist (trametinib) • Tafinlar (dabrafenib)
2years
PERSONALISED CIRCULATING TUMOUR DNA ANALYSIS IN DIFFERENTIATED THYROID CANCER USING NEXT GENERATION SEQUENCING PANELS (ATA 2022)
The findings of this exciting pilot study support the use of personalised sequencing panels for ctDNA detection in AJCC stage II DTC and above. Further multi‐centre long term (> 5 year) clinical prospective trials are recommended to validate these findings and determine if detection of ctDNA predicts disease free survival or overall survival.
Next-generation sequencing • Circulating tumor DNA
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BRAF (B-raf proto-oncogene)
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BRAF V600E • BRAF V600 • BRAF T1799A
over2years
BRAF V600E protect from cell death via inhibition of the mitochondrial permeability transition in papillary and anaplastic thyroid cancers. (PubMed, J Cell Mol Med)
In the mitochondria of BRAF V600E mutant cells, there was an interaction between ERK1/2 and GSKa/ß, while upon BRAF V600E knockdown, interaction of GSKa/ß to ERK was decreased significantly. These results show that in thyroid cancer, BRAF V600E regulates the mitochondrial permeability transition through the pERK-pGSK-CypD pathway to resist death, providing new intervention targets for BRAF V600E mutant tumours.
Journal
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BRAF (B-raf proto-oncogene)
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BRAF V600E • BRAF V600 • BRAF T1799A