Melanocytic "ball-in-mitts" and "microalveolar structures" and their role in the development of cellular blue nevi. Ann Diagn Pathol. 2007 Jun;11(3):160-75.

To test the hypothesis of whether cellular blue nevi (CBN) may originate from "ordinary" compound and dermal nevi, a total of 275 melanocytic nevi including 59 CBN, 34 ordinary blue nevi, 87 combined nevi (including 43 so-called clonal nevi), 35 deep penetrating nevi, and 60 ordinary compound and dermal nevi (30 of each) were studied for the presence of so-called ball-in-mitts and microalveolar structures. A ball-in-mitts structure was defined as a single centrally placed melanocyte with a round to oval nucleus (the "ball" cell) and a clear, dusty, or pigmented cytoplasm encircled by a single dendritic cell (the "mitt" cell) with an oval to spindle-shaped nucleus and slender bipolar processes containing melanin and surrounding at least one fourth of the ball's diameter. A microalveolar structure was defined as a group of 2 to 10 centrally placed melanocytes with round to oval nuclei and clear, dusty, or pigmented cytoplasm (balls) surrounded by one or more cells (mitts) with spindle-shaped nuclei and slender bipolar processes containing melanin. Microscopically, ball-in-mitt and microalveolar structures were detected in all types of nevi studied, with the highest incidence in combined nevi (82%), CBN (76%), and ordinary "nonblue" nevi (73%). In CBN, ball-in-mitts and microalveolar structures tended to be located in the deeper portion of the lesions, whereas in ordinary nonblue nevi, they were most often found superficially, just below the epidermis; in clonal nevi, these structures were often confined to the "clonal" parts. Immunohistochemically, ball-in-mitts and microalveolar structures were positive for HMB45. Ultrastructurally, the balls tended to have round to oval nuclei, whereas the mitts possessed oval, elongated to spindled nuclei. Melanosomes were found in various stages in the cells of both structures. The cytoplasm of the mitts typically formed elongated polar processes, sometimes with club-like widenings at the ends, completely or partially encircling the balls. In the microalveolar structures, the adjacent cells forming the mitts surrounded the ball cells like a chain. Our study suggests that some or even most cases of CBN may evolve from ordinary nonblue nevi. This process may involve several steps and is probably reflected by the appearances of combined nevi, deep penetrating nevi, and CBN. These nevi often show a morphological overlap, and ball-in-mitts and microalveolar structures found in various stages of their development seem to greatly account for this overlap.

Infiltrating giant cellular blue naevus. J Clin Pathol. 2007 Jan;60(1):82-4.

INTRODUCTION: Cellular blue naevi (CBN) measure 1-2 cm in diameter and affect the dermis, occasionally extending into the subcutaneous fat. The case of a 14-year-old boy with a giant CBN (GCBN) involving the right half of the face, the jugal mucosa and the lower eyelid with a tumour that had infiltrated the bone and the maxillary and ethmoidal sinuses is reported. METHODS: Biopsies were taken from the skin, jugal mucosa and maxillary sinus. The following markers were used in the immunohistochemical evaluation: CD34, CD56, HMB-45, anti-S100, A-103, Melan A and MIB-1. RESULTS: The biopsy specimens showed a biphasic pattern affecting the lower dermis, subcutaneous fat, skeletal muscle, bone, jugal mucosa and maxillary sinus, but there was no histological evidence of malignancy. The tumour cells were CD34-, CD56-, HMB45+, anti-S100+ and A-103+. Melan A was focally expressed. No positive MIB-1 cells were identified. Discussion: The present case shows that GCBN may infiltrate deeply, with no evidence of malignancy.

Genomic analysis of blue nevi and related dermal melanocytic proliferations.Am J Surg Pathol. 2005 Sep;29(9):1214-20.

Blue nevi are benign dermal melanocytic proliferations that can sometimes share overlapping microscopic features with melanoma. We used comparative genomic hybridization to analyze three groups of dermal melanocytic proliferations. Group 1 consisted of 10 cellular blue nevi and 1 deep penetrating nevus, none of which showed chromosomal aberrations. Group 2 consisted of 11 lesions that were histopathologically ambiguous. Three of these lesions demonstrated chromosomal aberrations (three or fewer per lesion). Group 3 consisted of seven histopathologically malignant lesions, each showing three or more chromosomal aberrations. Moderate to severe cytologic atypia and a mitotic rate of three or more mitoses per 10 high power fields were present in six of eight (75%) lesions that had at least three chromosomal aberrations but were absent in 15 of 20 (75%) lesions without chromosomal aberrations. Necrosis was present in four of the 29 (13%) lesions, with every lesion with necrosis demonstrating three or more genomic abnormalities. In conclusion, histopathologically unequivocally benign or malignant dermal melanocytic proliferations show nonoverlapping patterns of chromosomal aberrations. Ambiguous lesions can be separated into lesions with and without chromosomal aberrations. Future studies with clinical follow-up are necessary to determine which aberrations are most informative for classification of these lesions.