Mutations of the BRAF gene in human cancer

By Helen R. Davies, G. Bignell, Charles Cox, P. Stephens, S. Edkins, S. Clegg, J. Teague, H. Woffendin, Mathew J. Garnett, W. Bottomley and 42 more. Nature, 2002

10,701 citations recorded by the source corpus.

Subfields: Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/7febffe8fcc986e4e0aeaf8beceb5ec75d9e9446

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In Molecular Biology

1. R. Roskoski
2. Dan Pinkel
3. Donna Albertson
4. Marcos Malumbres
5. K. Polyak
6. Walter Kolch
7. C. Der
8. P. Roberts

In Pathology and Forensic Medicine

1. R. Roskoski
2. A. Bardelli
3. C. Der
4. P. Roberts
5. L. Diaz
6. Joe W. Gray
7. Allan Balmain
8. Bruce A. J. Ponder

Citations in the corpus

• Chromosome aberrations in solid tumors (2003, background): “High-throughput mutation detection strategies are now sufficiently advanced that it is possible to screen for gene mutations and polymorphisms in entire tumor genome”
• BRAF mutations and RET/PTC rearrangements are alternative events in the etiopathogenesis of PTC (2003, methodology): “BRAF is the first cancer-causing gene identified from the Cancer Genome Project, and in an extensive screen of 530 cancer cell lines, 43 harbored BRAF mutations (Davies et al., 2002).”
• Determinants of BRAF mutations in primary melanomas. (2003, background): “Twenty-four (75%) of these mutations were the single base-pair substitution T1796A, and eight (25%) were tandem mutations either GT3 AG (six [18.8%] of the eight mutations) and GT3 AA (two [6.2%] of the eight mutations), as previously described ( 6 ).”
• Phosphatase‐mediated crosstalk between MAPK signaling pathways in the regulation of cell survival (2008, background): “In addition, mutations of B-Raf, which increase the activity of the MEK1,2ERK1,2 pathway, were found in several malignancies and expression of such mutants in NIH3T3 cells lead to transformation (11, 20).”
• The genetics and genomics of cancer (2003, background): “Recently, the potential of high-throughput screening for detecting mutations in potential cancer genes has become apparen”
• Non-small cell lung cancer: current treatment and future advances. (2016, background): “BRAF somatic mutations have been found in 1–4% of all NSCLC, most commonly in patients with adenocarcinomas (54,66-70).”
• Melanoma biology and new targeted therapy (2007, background): “NRAS is mutated in between 15p and 30p of melanomas, the most common substitution being leucine for glutamine at position 61 (Q61L”
• KIT as a therapeutic target in metastatic melanoma. (2011, neutral): “Mucosal Ex 9 N463S No 1:1 NA Mucosal Ex 11 L576Pa Yes (>10) 1:1 Mixed Mucosal Ex 11 L576Pa Yes (5-10) 1:1 Mixed”
• Phase II trial of sorafenib in advanced thyroid cancer. (2008, background): “The B-type Raf kinase (BRAF) in the mitogenactivated protein kinase signaling pathway is known to play a key role in thyroid cancer,(13) and an acidic substitution at a single amino acid residue, V600E, occurs frequently.(14) BRAF is associated with substantially higher basal kinase activity compare”
• Oncogenic BRAF induces senescence and apoptosis through pathways mediated by the secreted protein IGFBP7. (2008, neutral): “This mutation substantially increases protein kinase activity, resulting in constitutive BRAFMEK-ERK signaling (Davies et al., 2002).”
• Mutations in BRAF and KRAS characterize the development of low-grade ovarian serous carcinoma. (2003, methodology): “One of the three RAF members, BRAF, has been recently reported to be activated by somatic mutation in many human cancers, with mutations in BRAF occurring at a particularly high rate in cutaneous melanoma and papillary carcinoma of the thyroid ( 2 ,3).”
• Lessons from the cancer genome. (2013, neutral): “The studies quickly hit pay dirt, with the finding of mutations in BRAF in 50% of melanomas, PIK3CA in 25%–30% of breast and colorectal cancers, EFGR in 10%–15% of non-small cell lung cancers, FGFR2 in 15%–20% of endometrial cancers, and JAK2 in myeloproliferative diseases (Davies et al., 2002; Dutt”
• Association Between BRAF V600E Mutation and Mortality in Patients With Papillary Thyroid Cancer (2013, background): “This mutation causes a valine– to–glutamic acid change in codon 600 of the BRAF protein, resulting in BRAF V600E, which possesses elevated serine/ threonine protein kinase activities and constitutively activates the mitogenactivated protein kinase signaling pathway in human cancer.(13) Many studies ”