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BRAF (gene) BRAF is a human gene that encodes a protein called B-Raf. The gene is also referred to as proto-oncogene B-Raf and v-Raf murine sarcoma viral oncogene homolog B, while the protein is more formally known as serine/threonine-protein kinase B-Raf. [5][6]
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 ...
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 ...
Melanoma is the most dangerous type of skin cancer; it develops from the melanin -producing cells known as melanocytes. [1] It typically occurs in the skin, but may rarely occur in the mouth, intestines, or eye (uveal melanoma). [1][2] In women, melanomas most commonly occur on the legs; while in men, on the back. [2]
Sorafenib is a protein kinase inhibitor with activity against many protein kinases, including VEGFR, PDGFR and RAF kinases. [4][5] Of the RAF kinases, sorafenib is more selective for c-Raf than B-RAF. [6] (. See BRAF (gene)#Sorafenib for details the drug's interaction with B-Raf.) Sorafenib treatment induces autophagy, [7] which may suppress ...
BRAF V600E gene and SMO gene mutations have been found in ameloblastomas. V600E mutation is also seen in other malignant and benign neoplasms, which activate the MAP kinase pathway required for cell division and differentiation but is the most commonly seen mutation in ameloblastoma. [8] [7] 72% of BRAF mutations are found in the mandible. [7]
75-year-old patient with BRAF mutant metastatic cutaneous melanoma who had previously received pembrolizumab (best response of Progressive Disease within 5 months) followed by dabrafenib plus trametinib (discontinued trametinib after 1 month due to toxicity and achieved Stable Disease before progressing after seven years on dabrafenib).
Human c-Raf is a member of a larger family of related protein kinases. Two further members - found in most vertebrates - belong to the same family: B-Raf and A-Raf. Apart from the different length of their non-conserved N- and C-terminal ends, they all share the same domain architecture, structure and regulation.