Nevocytes in melanoma-draining lymph nodes can be mistaken for melanoma metastases and may possibly transform to melanoma. During the development of a new technique for managing high-risk primary melanomas, selective lymph node dissection, we examined 4,821 nodes from 208 melanoma patients by light microscopy and immunohistochemistry. Nodal nevi were identified in 49 of 226 lymphadenectomy specimens (22%), a frequency considerably higher than previously recorded (5-6%). Nevi occurred in 57 of 4,821 nodes (1.2%), in 84% of patients in one node, in 13% of patients in two nodes, and in 3% of patients in three nodes. Nevocytes were detected in hematoxylin and eosin-stained sections in 38 of 49 cases (78%) and exclusively by immunocytochemistry with an antibody to S-100 protein in 11 of 49 (22%). Nevi were in the peripheral capsule in 93% of cases and in internal trabecula in the remaining 7%. Nevocytes surrounded a small vessel in 33% of cases. Nevi were more frequent in axillary (37 of 140, 26%) and cervical nodes (seven of 40, 18%) than in inguinal nodes (five of 46, 11%). Nevi were more frequent in sentinel nodes, the first nodes on the lymphatics draining a primary melanoma (11 of 284, 3.9%), than in nonsentinel nodes (46 of 4,537, 1.01%; p < 0.0008). One of 1,071 nodes from 50 patients with breast cancer (0.1%) and none of 521 nodes from 50 patients with pelvic cancer contained nevocytes. That nodal nevi are selectively present in melanoma patients raises the possibility of their origin from nodal melanocytes influenced by tumor products. Alternatively, the association may indicate that the nevocytes of cutaneous nevi can be disrupted and displaced by the growth of an adjacent melanoma.

Apart from the rare malignant melanomas occurring in blue nevi, primary cutaneous malignant melanoma arises in 1 of 3 ways, regardless of the presence or absence of a pre‐existing nevus. These three types have been designated: 1. Malignant melanoma, invasive, with adjacent intra‐epidermal component of Hutchinson's melanotic freckle type; 2. Malignant melanoma, invasive, with adjacent intra‐epidermal component of superficial spreading type; and 3. Malignant melanoma, invasive, without adjacent intra‐epidermal component. Occasionally, both clinically and histologically, there may be difficulty in deciding whether a malignant melanoma belongs to category 1 or 2, but, in the majority of cases, these 2 types can be quite readily distinguished. In addition to recording the histogenetic mode of development of a malignant melanoma, a histologic system of reporting is recommended which includes mitotic activity, levels of invasion, and vascular involvement. There are other parameters such as the cell type, pigmentation, lymphocytic infiltrates, evidence of spontaneous regression, associated nevi, and solar changes in the dermis, all of which are of unknown significance. The recording of these features, which are clearly of interest for research purposes, is left to individual discretion. It is emphasized that all the usual macroscopic descriptions and measurements should continue to be recorded.

Desmoplastic small round cell tumors (DSRCTs) present a reciprocal chromosomal translocation, t(11;22)(p13;q12), that results in fusion of Ewing's sarcoma and Wilms' tumor (WT1) genes. The authors evaluated 15 DSRCTs and 71 other tumors often considered in the differential diagnosis for immunoreactivity using a polyclonal antibody directed against the WT1 part of the chimeric protein resulting from this translocation. WT1 immunostaining was performed on paraffin material using the WT(C-19) antibody after heat-antigen retrieval. All the DSRCTs (15 of 15, 100%) demonstrated strong WT1 nuclear immunoreactivity. Ten of 14 nephroblastomas (71%) disclosed WT1-positive nuclei in accordance with the staining reported by others, and rare and focal nuclear positivity was detected in two of 17 rhabdomyosarcomas. WT1 immunoreactivity was not observed in Ewing's sarcoma/primitive neuroectodermal tumors (zero of 21, 0%), neuroblastomas (zero of 17, 0%), or rhabdoid tumors of the kidney (zero of two, 0%). In nephroblastoma, differential diagnosis with DSRCT was not difficult: Clinical and morphologic data are not similar for these two entities. The current study validates WT1 immunoreactivity as a useful marker to separate DSRCT from other small round cell tumors.