Distinct phenotypic changes between the superficial and deep component of giant congenital melanocytic naevi: a rationale for curettage.
BACKGROUND
Giant congenital melanocytic naevi (GCMN) convey a 14-fold increased melanoma risk. In contrast, medium congenital melanocytic naevi (MCMN) are rarely associated with malignant transformation. Management of patients with GCMN is challenging and there is no consensus on the most appropriate strategy for treating these patients.


OBJECTIVE
To provide a rationale for performing curettage of GCMN in the neonatal period in order to reduce the risk of malignant transformation to melanoma.


METHODS
Twenty-six infants with GCMN who underwent biopsies before excisional surgery (n = 7) or curettage (n = 19) during the past 14 years (Academic Hospital, Vrije Universiteit Brussel) and 10 MCMN patients who underwent excision biopsies (Radboud University Nijmegen Medical Centre) were included in this study. Using these biopsies, we performed genetic and detailed immunohistochemical evaluations of changes that are associated with malignant transformation. Variables of interest included melanoma-associated BRAF mutations, proliferative activity, vascularity, cellular context and extracellular matrix architecture.


RESULTS
GCMN and MCMN did not show oncogenic BRAF mutation and displayed similar features with respect to the amount of nonmelanocytic cells within the naevus and matrix architecture. Naevus cells in the superficial component of the GCMN, however, were more proliferative, and this component was more vascular compared with its deep component and with MCMN. In this study, none of the 19 newborn patients who underwent curettage developed a melanoma within a mean follow-up time of 7 years.


CONCLUSIONS
The data presented here support the idea that curettage of GCMN in neonates has the potential for lowering the risk of developing cutaneous melanoma by not only obtaining an important numerical reduction of naevus cells but also removing the 'active' melanocytes.
De Raeve
L E
LE
Academisch Ziekenhuis, Vrije Universiteit Brussel, Department of Dermatology, Belgium.
Claes
A
A
Ruiter
D J
DJ
van Muijen
G N P
GN
Roseeuw
D
D
van Kempen
L C L T
LC
D001706:Biopsy; D049109:Cell Proliferation; D024042:Collagen Type I / Q000096:biosynthesis; D003475:Curettage; D018450:Disease Progression; D005109:Extracellular Matrix / Q000378:metabolism / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D008545:Melanoma / Q000517:prevention & control; D009154:Mutation; D009508:Nevus, Pigmented / Q000151:congenital* / Q000378:metabolism / Q000473:pathology / Q000601:surgery*; D010641:Phenotype; D048493:Proto-Oncogene Proteins B-raf / Q000235:genetics; D012878:Skin Neoplasms / Q000151:congenital* / Q000378:metabolism / Q000473:pathology / Q000601:surgery*
D024042:Collagen Type I; C482119:BRAF protein, human; D048493:Proto-Oncogene Proteins B-raf