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B-Raf is a 766-amino acid, regulated signal transduction serine/threonine-specific protein kinase.Broadly speaking, it is composed of three conserved domains characteristic of the Raf kinase family: conserved region 1 (CR1), a Ras-GTP-binding [11] self-regulatory domain, conserved region 2 (CR2), a serine-rich hinge region, and conserved region 3 (CR3), a catalytic protein kinase domain that ...
V600E is a mutation of the BRAF gene in which valine (V) is substituted by glutamic acid (E) at amino acid 600. [1] [2] It is a driver mutation in a proportion of certain diagnoses, including melanoma, [3] [4] hairy cell leukemia, [5] [6] papillary thyroid carcinoma, [7] [8] colorectal cancer, [9] non-small-cell lung cancer, [10] [11] Langerhans cell histiocytosis, [12] Erdheim–Chester ...
Also, for noninvasive applications from peripheral blood or urine, the DNA test must be specific enough to detect mutations at variant allele frequencies of less than 0.1%. [ 22 ] Currently, by optimizing the traditional PCR, there's a new invention, amplification-refractory mutation system (ARMS) is a method for detecting DNA sequence variants ...
After performing a multivariate analysis, it was found that the absence of tumor capsule was the only parameter associated (P=0.0005) with BRAF V600E mutation. [5] According to recent studies, papillary cancers carrying the common V600E mutation tend to have a more aggressive long-term course.
High Resolution Melt (HRM) analysis is a powerful technique in molecular biology for the detection of mutations, polymorphisms and epigenetic differences in double-stranded DNA samples. It was discovered and developed by Idaho Technology and the University of Utah. [1] It has advantages over other genotyping technologies, namely:
In 2012, a study established 27 colorectal PDX models that did not diverge from their respective human tumors in histology, gene expression, or KRAS/BRAF mutation status. [22] Due to their stability, the 27 colorectal PDX models may be able to serve as pre-clinical models in future drug studies.
Vemurafenib only works in melanoma patients whose cancer has a V600E BRAF mutation (that is, at amino acid position number 600 on the B-Raf protein, the normal valine is replaced by glutamic acid). [4] About 60% of melanomas have this mutation. It also has efficacy against the rarer V600K BRAF (the normal valine is replaced by lysine) mutation ...
The BRAF gene is a proto-oncogene that, when mutated, is associated with many cancers. Normally, the amount of BRAF protein is kept under control in cells through the action of miRNA. In normal situations, the amount of RNA from BRAF and the pseudogene BRAFP1 compete for miRNA, but the balance of the 2 RNAs is such that cells grow normally.
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