Melan-A is a useful addition to antibody panels as it is apparently specific for melanocytic lesions and is more sensitive than HMB-45; however, it has less value than S100 in the detection of spindle cell and desmoplastic melanomas.

Five hundred and sixty-three primary cutaneous melanomas were assessed for the presence of histological regression in relation to the thickness of the lesion and features such as sex, anatomical location and clinical outcome. Regression was more common in thin lesions, being seen in 46% of thin (less than 1.5 mm) lesions, 32% of intermediate (1.5-3.0 mm) lesions and 9% of thick (greater than 3.0 mm) lesions. However, severe regression was only identified in 6.5% of thin lesions, 5.2% of intermediate lesions and 1.5% of thick melanomas. Regression was more common in superficial spreading melanomas and in lesions from the trunk and lower limb. Moderate and severe regression were seen slightly more often in men. Clinical follow-up, although not of statistical significance, suggests that regression in thin lesions is a sinister histological feature.

From the files of the Scottish Melanoma Group, we have identified 100 cases of subungual malignant melanoma (melanoma arising in the nailbed), and this represents 2.8% of the total melanomas registered during the period 1979-1989. Almost equal numbers arose on the foot as on the hand, with the thumb and big toe as the commonest digit affected. More than 80% were greater than 1.5 mm, with the mean Breslow depth 4.7 mm, and 70% were Clark level IV or V. Approximately half of the cases were of acral lentiginous type. At 5-year follow-up (54 cases), 26 have died of melanoma, six have died of an unrelated disease, four are alive with recurrence and 18 are alive and well. Features related to clinical outcome at 3 years were Breslow depth, mitotic count and the presence of vascular invasion.

Aims-Compelling evidence from cell culture studies implicates cadherins in the neoplastic progression of melanocytic tumours but few reports describe the expression of cadherins and the related transmembrane proteins, catenins, in a full range of benign and malignant excised melanocytic tumours. Methods-Using immunohistochemistry and western blotting after tissue fractionation, the pattern of expression of cadherins/ catenins was studied in a range of surgically excised melanocytic tumours, from dysplastic naevi to stage III cutaneous metastatic malignant melanoma. Results-Appropriate membranous expression of E-cadherins and P-cadherins is seen in dysplastic naevocytes with an epithelioid phenotype and is largely maintained with malignant transformation to radial growth phase melanoma and primary vertical growth phase malignant melanoma.Loss of membranous E-cadherin is seen in a small number of vertical growth phase melanomas only when metastasis has occurred. However, there is a concomitant dramatic loss of membranous P-cadherin expression in all melanomas at the same stage. A minority of metastatic melanomas show de novo membranous N-cadherin expression in comparison with dysplastic naevi and primary melanoma. Membranous expression of the desmosomal cadherin, desmoglein, was not seen in any tumour studied. Frequently, catenin is aberrantly produced in the cytoplasm of cells in dysplastic naevi and metastatic malignant melanoma, with an implied compromise to adhesive function. Furthermore, membranous catenin expression was not seen in any of the 70 melanocytic tumours studied, implying obligatory transmembrane binding of cadherins to catenin for maintenance of adhesive function. Conclusions-The most important alterations in membranous cadherin and catenin expression are seen late in the biological progression of melanocytic tumours at the stage of "in transit" or regional lymph node metastasis, with implications for tumour growth, invasion, and dissemination. (J Clin Pathol: Mol Pathol 1999;52:151-157)

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