Dark homogeneous streak dermoscopic pattern correlating with specific KIT mutations in melanoma

Margaret I. Sanchez, Harold S. Rabinovitz, Margaret C. Oliviero, George W. Elgart, Carmen Perez, Susana Puig, Josep Malvehy, James M. Grichnik

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


Importance Mutations driving melanoma growth have diagnostic, prognostic, and therapeutic implications. Traditional classification systems do not correlate optimally with underlying melanoma growth-promoting mutations. Our objective was to determine whether unique dermoscopic growth patterns directly correlate with driving mutations. Observations We evaluated common driving mutations in 4 different dermoscopic patterns (rhomboidal, negative pigmented network, polygonal, and dark homogeneous streaks) of primary cutaneous melanomas; 3 melanomas per pattern were tested. Three of the 4 patterns lacked common mutations in BRAF, NRAS, KIT, GNAQ, and HRAS. One pattern, the dark homogeneous streaks pattern, had unique KIT mutations in the second catalytic domain of KIT in exon 17 for all 3 samples tested. Two tumors with the dark homogeneous streaks pattern turned out to be different primary melanomas from the same patient and had different sequence mutations but had an impact on the same KIT domain. Conclusions And Relevance While future study is required, these results have multiple implications. (1) The underlying melanoma-driving mutations may give rise to specific dermoscopic growth patterns, (2) BRAF/NRAS mutations in early melanomas may not be as common as previously thought, and (3) patients may be predisposed to developing specific driving mutations giving rise to melanomas or nevi of similar growth patterns.

Original languageEnglish (US)
Pages (from-to)633-639
Number of pages7
JournalJAMA Dermatology
Issue number6
StatePublished - Jun 2014
Externally publishedYes

ASJC Scopus subject areas

  • Dermatology


Dive into the research topics of 'Dark homogeneous streak dermoscopic pattern correlating with specific KIT mutations in melanoma'. Together they form a unique fingerprint.

Cite this