Whole-exome sequencing reveals somatic mutations in HRAS and KRAS, which cause nevus sebaceus

  • Levinsohn J
  • Tian L
  • Boyden L
 et al. 
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Abstract

TO THE EDITOR Epidermal genetic mosaicism is evident as stripes of affected skin which typically appear in S or V-shaped whorled, streaked, and linear patterns called lines of Blaschko (Blaschko, 1901). These patterns represent dorsoventral migratory pathways of neuroectoderm during embryogenesis (Moss et al., 1993). Mosaic lesions result from somatic mutation during development, with timing of such events determining the extent and distribution of skin involvement. Epidermal nevi (EN) are common cutaneous mosaic disorders seen in 0.1– 0.3% of births, and fall into two classes: keratinocytic epidermal nevi (KEN) and organoid epidermal nevi, which includes nevus sebaceus (NS) and follicular nevi (Solomon and Esterly, 1975). NS comprises approximately half of EN, and typically appears on the scalp as a yellowish-orange linear plaque with hyperkeratosis, acanthosis, a markedly increased number of sebaceous lobules and abortive hair follicles with resulting alopecia (Figure 1a– d). In contrast to KEN, in which neoplasia is rare, tumors develop in nearly 14% of all NS cases, and in more than 23% of affected adults (Cribier et al., 2000), suggesting that the

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Authors

  • Jonathan L. Levinsohn

  • Li C. Tian

  • Lynn M. Boyden

  • Jennifer M. McNiff

  • Deepak Narayan

  • Erin S. Loring

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