Sylvester Study Provides New Insights on Melanomas

A new Miller School study led by James Grichnik, M.D., Ph.D., professor of dermatology and cutaneous surgery, provides new insights into the genetic mutations that can lead to melanomas.

“Mutations driving melanoma growth have diagnostic, prognostic and therapeutic implications,” said Grichnik, Chief of the Frankel Family Division of Melanocytic Tumors, and Director of the Anna Fund Melanoma Program in the Sylvester Comprehensive Cancer Center. “Our study showed an association with the growth patterns of early melanomas, and the mutations that caused that tumor – a finding that may help clinicians identify specific types of melanoma and identify patients predisposed to developing certain types of mutations.”

The study, “Dark Homogeneous Streak Dermoscopic Pattern Correlating with Specific KIT Mutations in Melanoma,” was published April 2 in JAMA Dermatology, an online publication of the Journal of the American Medical Association.

In their clinical practice, the dermatologists at UHealth-University of Miami Health System use surface microscopes called dermoscopes to examine the surface patterns of melanomas. However, the traditional melanoma classification system, which is based on clinical and pathologic findings, does not correlate well with the growth-promoting mutations, according to Grichnik. “Our hope is that this preliminary study will lead to a better understanding of the underlying molecular processes that lead to melanoma,” he added, “and allow us to develop a more coherent mutation-based classification system.”

For the study, the Miller School researchers examined 182 dermoscopic images of melanomas and evaluated the mutations associated with four different skin melanoma patterns – rhomboidal, negative pigmented network, polygonal and dark homogeneous streaks. Three melanomas per pattern were tested. Three of the four lacked any of the common melanoma growth-promoting mutations, and the fourth – showing dark streaks – had unique KIT mutations.

Grichnik noted that cancer researchers have identified common genetic mutations in thick melanomas, primarily mutations in BRAF (V-raf murine sarcoma viral oncogene homolog B1) and NRAS (neuroblastoma RAS viral oncogene homolog). “To our surprise, all of the patterns tested did not show BRAF or NRAS mutations,” he said. “This suggests that these genetic mutations may not be as common as previously thought in thin melanomas.”

Miller School co-authors were Margaret I. Sanchez, M.D., research associate; Harold S. Rabinovitz, M.D., voluntary professor of dermatology and cutaneous surgery; Margaret C. Oliviero, RNP; George W. Elgart, M.D., professor of dermatology and cutaneous surgery and member of the Melanoma Site Disease Group at Sylvester, and Carmen Perez, clinical research coordinator at Sylvester. Other authors were Susana Puig, M.D., and Josep Malvehy, M.D., from the Instituto de Salud Carlos III in Barcelona, Spain.

Melanoma has been on the rise in the United States for the past 30 years, according to the American Cancer Society, which estimates that 76,100 new melanomas will be diagnosed this year and about 9,710 people are expected to die of melanoma. The large majority of melanomas are thin, rather than thick.

“Learning more about the genetic mutations driving melanomas may help us identify which lesions are more likely to be lethal, and could lead to more directed genetic testing for risk factors,” Grichnik said. “As our therapies improve, we may be able to affect the molecular processes that lead to melanoma and halt or prevent the progression of this deadly disease.”

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