@article {639,
	title = {Keratoacanthoma Shares Driver Mutations with Cutaneous Squamous Cell Carcinoma.},
	journal = {J Invest Dermatol},
	volume = {136},
	year = {2016},
	month = {2016 08},
	pages = {1737-1741},
	keywords = {Aged, Aged, 80 and over, Biomarkers, Tumor, Biopsy, Carcinoma, Squamous Cell, Cohort Studies, Diagnosis, Differential, Exome, Female, Humans, Keratoacanthoma, Loss of Heterozygosity, Male, Middle Aged, Mutation, Polymorphism, Single Nucleotide, Skin, Skin Neoplasms, Whole Exome Sequencing},
	issn = {1523-1747},
	doi = {10.1016/j.jid.2016.04.002},
	author = {Lim, Young H and Fisher, Jonathan M and Bosenberg, Marcus W and Choate, Keith A and Ko, Christine J}
}
@article {190,
	title = {Somatic Activating RAS Mutations Cause Vascular Tumors Including Pyogenic Granuloma.},
	journal = {J Invest Dermatol},
	volume = {135},
	year = {2015},
	month = {2015 Jun},
	pages = {1698-1700},
	keywords = {Adolescent, Cell Proliferation, Child, Child, Preschool, Female, Gene Expression Regulation, Neoplastic, Granuloma, Pyogenic, Humans, Infant, Infant, Newborn, Male, Mutation, ras Proteins, Vascular Neoplasms},
	issn = {1523-1747},
	doi = {10.1038/jid.2015.55},
	author = {Lim, Young H and Douglas, Stephanie R and Ko, Christine J and Antaya, Richard J and McNiff, Jennifer M and Zhou, Jing and Choate, Keith A and Narayan, Deepak}
}
@article {289,
	title = {Multilineage somatic activating mutations in HRAS and NRAS cause mosaic cutaneous and skeletal lesions, elevated FGF23 and hypophosphatemia.},
	journal = {Hum Mol Genet},
	volume = {23},
	year = {2014},
	month = {2014 Jan 15},
	pages = {397-407},
	abstract = {<p>Pathologically elevated serum levels of fibroblast growth factor-23 (FGF23), a bone-derived hormone that regulates phosphorus homeostasis, result in renal phosphate wasting and lead to rickets or osteomalacia. Rarely, elevated serum FGF23 levels are found in association with mosaic cutaneous disorders that affect large proportions of the skin and appear in patterns corresponding to the migration of ectodermal progenitors. The cause and source of elevated serum FGF23 is unknown. In those conditions, such as epidermal and large congenital melanocytic nevi, skin lesions are variably associated with other abnormalities in the eye, brain and vasculature. The wide distribution of involved tissues and the appearance of multiple segmental skin and bone lesions suggest that these conditions result from early embryonic somatic mutations. We report five such cases with elevated serum FGF23 and bone lesions, four with large epidermal nevi and one with a giant congenital melanocytic nevus. Exome sequencing of blood and affected skin tissue identified somatic activating mutations of HRAS or NRAS in each case without recurrent secondary mutation, and we further found that the same mutation is present in dysplastic bone. Our finding of somatic activating RAS mutation in bone, the endogenous source of FGF23, provides the first evidence that elevated serum FGF23 levels, hypophosphatemia and osteomalacia are associated with pathologic Ras activation and may provide insight in the heretofore limited understanding of the regulation of FGF23.</p>},
	keywords = {Adolescent, Child, Exome, Female, Fibroblast Growth Factors, Gene Expression Regulation, Developmental, GTP Phosphohydrolases, Humans, Hypophosphatemia, Male, Membrane Proteins, Mutation, Nevus, Nevus, Pigmented, Osteomalacia, Proto-Oncogene Proteins p21(ras), Sequence Analysis, DNA, Skin, Skin Neoplasms},
	issn = {1460-2083},
	doi = {10.1093/hmg/ddt429},
	author = {Lim, Young H and Ovejero, Diana and Sugarman, Jeffrey S and Deklotz, Cynthia M C and Maruri, Ann and Eichenfield, Lawrence F and Kelley, Patrick K and J{\"u}ppner, Harald and Gottschalk, Michael and Tifft, Cynthia J and Gafni, Rachel I and Boyce, Alison M and Cowen, Edward W and Bhattacharyya, Nisan and Guthrie, Lori C and Gahl, William A and Golas, Gretchen and Loring, Erin C and Overton, John D and Mane, Shrikant M and Lifton, Richard P and Levy, Moise L and Collins, Michael T and Choate, Keith A}
}
