Recent recommendations listed 2 sets of tests: a set of essential tests (EGFR, ALK, ROS1) that can be used to direct therapy and an optional set (
BRAF, RET, MET, HER2, KRAS) that can be used to direct patients toward clinical trials.
On multivariable analysis, V600E, but not non-V600E,
BRAF mutation was correlated with worse overall survival and disease-free survival (hazard ratios, 2.76 and 2.04, respectively).
Here, we report on the results of a large-scale translational melanoma study with the primary aim of investigating the practicality of ctDNA analysis and its viability to serve as an alternative to tissue-based testing to assess
BRAF mutation status.
Similar to
BRAF status and PD1 expression, there is conflicting evidence regarding survival benefit based on LDH level in patient treated with checkpoint inhibitors [8, 9, 11, 12].
Ideas for new treatment options for BRAF-mutated CRCs concentrate on targeting the
BRAF mutation because this mutation is blamed for the bad prognosis.
Mutations in the KRAS (exons 2, 3, and 4), NRAS (exons 2, 3, and 4), HRAS (exon 2), and
BRAF (exon 15) of each tumor specimen were examined.
RET/PTC rearrangements and
BRAF mutations in thyroid tumorigenesis.
Our attempt was to study the frequency of
BRAF mutation in various thyroid diseases.
G12D) and
BRAF mutation exon 15 codon 600 at V600E (GAG), V600D (GAT), or V600K (AAG).
The data collection used consisted of n = 291 samples for which both histopathology whole-slide images and clinical data (including
BRAF and KRAS mutation status) were available, along with gene expression necessary for computing the
BRAF score [8].
The B-type Raf proto-oncogene (
BRAF) encodes an enzyme that takes part in intracellular signaling and cell growth, and
BRAF mutation has been frequently observed in CRC, supporting its role in tumorigenesis [4,17].