High frequency of BRAF mutations in nevi

By P. Pollock, U. Harper, Katherine S. Hansen, Laura M. Yudt, M. Stark, C. Robbins, T. Moses, G. Hostetter, U. Wagner, J. Kakareka and 8 more. Nature Genetics, 2003

1,713 citations recorded by the source corpus.

Subfields: Computational Theory and Mathematics, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/927d305566046939b6a8884a50fbba376295360a

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Citations in the corpus

Oncogenic BRAF induces senescence and apoptosis through pathways mediated by the secreted protein IGFBP7. (2008, positive): “Activating BRAF mutations are also present in up to 82% of melanocytic nevi (Pollock et al., 2003), which are benign skin lesions that rarely progress to melanoma (Bennett, 2003; Chin et al.”
Senescence-messaging secretome: SMS-ing cellular stress (2009, background): “In human melanocytic naevus cells (which often express BRAF E600 (Ref”
Genomic Classification of Cutaneous Melanoma (2015, result): “As in previous reports (Pollock et al., 2003), both BRAF V600 and K601 Cell 161, 1681–1696, June 18, 2015 ª2015 Elsevier Inc. 1683 Prominent mechanisms of pathway alterations in BRAF, RAS, NF1 and Triple Wild-Type (WT) subtypes with potential predictive genetic alterations indicated (1, 2, 3, 4, 5,…”
Early dissemination seeds metastasis in breast cancer (2016, positive): “Strongly oncogenic mutations characterize benign tumours that do not metastasize 36–38 ; indeed, strong activation of oncogenic pathways represses metastasis while increasing proliferation 39,40 .”
The essence of senescence. (2010, background): “At least as remarkable was the finding that the same mutation is present in the large majority of nevi (Pollock et al. 2003).”
The signals and pathways activating cellular senescence. (2005, background): “T than i ayer t itt for i a it is e gress tion p ctiv t s to t as a w to d ribuepresent a general case of in vivo oncogene-ind enescence (Bennett, 2003; Pollock et al., 2003).”
BRAF mutation in thyroid cancer. (2005, background): “…initial discovery, BRAF mutations have now been reported in numerous types of human cancer with various frequencies (Garnett & Marais 2004), being most prevalent in melanomas and nevi, present in 66 and 82% of these dermatologic lesion types, respectively (Davies et al. 2002, Pollock et al. 2003).”
BRAF mutation is associated with DNA methylation in serrated polyps and cancers of the colorectum (2004, background): “11 13 In extraintestinal tumours, BRAF mutations also appear to occur early in tumorigenesis, for example in naevi, 49 and in specific subgroups, for example serous borderline tumours which are precursors of low grade ovarian serous carcinomas.”
MAP kinase signalling pathways in cancer (2007, background): “The existence of suppressors of mutant B-Raf is suggested by the finding that >80% of benign naevi contain oncogenic B-Raf mutations without ever progressing to melanoma (Pollock et al., 2003).”