An Atypical Fibroxanthoma and Intradermal Nevus Collision Tumor-Potential for Misdiagnosis.

Atypical fibroxanthomas (AFX) are rare cutaneous tumors, which typically present as a solitary ulcerated papule or nodule on sun-damaged skin. Despite malignant-appearing features on histology, AFX typically pursue a benign clinical course. In rare instances, AFX can form collision tumors with other lesions. However, to the best of our knowledge, AFX in collision with a nevus has never been previously reported. In this study, we describe such a lesion for its novelty and challenge in diagnosis, as this case was originally considered to be melanoma arising in a nevus. On histologic examination, there were 2 distinct populations of cells; one composed of markedly atypical and pleomorphic epithelioid and oval to spindled cells, consistent with AFX, and the other, a bland-appearing intradermal nevus with congenital features. The AFX population stained positive with smooth muscle actin, CD10, and CD68 and was negative for S100, SOX10, Melan-A, desmin, pancytokeratin, CK5/6, and p63. Deep to this was a second population of small, bland-appearing melanocytes in a broad, band-like distribution. This unusual collision tumor between AFX and an intradermal nevus highlights the important role immunohistochemistry plays in avoiding the misdiagnosis and potential overtreatment of benign or low-grade lesions, and in identifying potential mimickers.

Immunohistochemical expression of retinoblastoma protein in cutaneous melanomas.

Retinoblastoma protein (pRB) is the product of a tumour-suppressor gene (rb) mapped to chromosome 13q14. pRB acts as a control checkpoint at the G1 phase of the cell cycle, preventing cells from entering into the S phase. Mutational inactivation of both normal alleles leads to loss of pRB expression and the development of malignant neoplasms. Absence of pRB occurs in retinoblastomas, sarcomas and several other types of tumours. The potential role of pRB in the pathogenesis of cutaneous melanoma is unknown, and was the subject of this investigation. Formalin-fixed, paraffin-embedded sections of four cutaneous melanoma metastases, 17 primary invasive melanomas and 10 predominantly intradermal melanocytic naevi were studied. Monoclonal antibodies directed against pRB and Ki-67 antigen were used after microwave heating of sections to restore antigenicity. pRB was not detected in morphologically normal epidermal melanocytes. In five naevi, only scattered cells (1%) expressed pRB, whereas in the other five naevi, pRB expression was undetectable. In contrast, pRB was detected in all primary and metastatic melanomas (5-70% of cells). Expression was always localized to nuclei. Ki-67 expression was detected only in the melanomas, with both cellular staining and regional localization similar to that shown by pRB in 13 of the 20 melanomas studied with both antibodies. pRB appears to be expressed at higher levels in melanomas than in benign naevi. It therefore seems unlikely that loss of rb expression is an important factor in the pathogenesis of melanoma.

Utility of a proliferation marker in distinguishing between benign naevocellular naevi and naevocellular naevus-like lesions with malignant properties.

In the present study we have investigated the utility of the proliferation marker MIB 1 in distinguishing between benign naevocellular naevi and naevocellular naevus-like lesions with malignant potential. Percentages of MIB 1 immunoreactivity in the intradermal portion of the lesions were determined. In benign congenital and acquired naevi, as well as in dysplastic naevi, there was no or only a slight intradermal melanocytic proliferation (0-2%), whereas vertical growth phase melanomas exhibited a substantial proliferative activity (11-48%). In five cases of naevus-lke lesions, which had all relapsed as unmistakable malignant melanomas (locally or metastatically) after primary surgery, there was also clear proliferative activity (9-67%). Our findings suggest that MIB 1 may be a useful tool in the routine histopathological examination of problematic naevocellular lesions.

Malignant melanoma within an intradermal nevus.

We describe a case of malignant "dermal" melanoma that arose within a preexisting intradermal nevus. Clinically, the lesion had recently enlarged. Histologically, two patterns were noted. One was an intradermal nevus in the upper portion of the dermis; the other was a deeper nodule composed of malignant neoplastic cells that extended into the reticular dermis. No melanocytic epidermal junctional activity was noted. Despite careful clinical investigation, no alternative primary source was found. Neoplastic transformation of the intradermal nevus without junctional activity is our proposed interpretation of the lesion's histology. Immunohistochemical stains demonstrated that the deeper dermal neoplastic cells were positive for both HMB-45 and PCNA, whereas the superficial nevoid-appearing cells were negative; these findings support our postulate that this melanoma arose within an intradermal nevus. It is important to distinguish this neoplasm from other diagnostic possibilities, including a metastatic lesion originating from another site.

Mucinous naevocellular naevi.

We report 4 cases of a naevocellular naevus variant containing abundant amounts of mucinous matrix. The mucinous matrix was Alcian blue (pH 2.5) and Halle's colloidal iron positive and mucicarmine and PAS negative. When the blocks of tumours were cut down, regions typical of common intradermal naevi were found in all 4 cases. The differential diagnosis with mucinous carcinoma of the skin and myxoid malignant melanoma is discussed.