DOI: 10.1097/PAS.0b013e3181839aad
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PMID: 18971780
Issn Print: 0147-5185
Publication Date: 2009/01/01
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Excerpt
We read with great interest the recent article by Robson et al5 entitled “primary cutaneous apocrine carcinoma: a clinico-pathologic analysis of 24 cases.” This excellent article discusses a large series of these tumors and separates them into different patterns, examines the value of grading, and the impact of steroid receptor expression. Our comments are with respect to the final paragraph, which reads “Despite the close relationship between the breast and cutaneous sweat apparatus, in situ neoplasia of the skin sweat gland has not been reported.”
The published literature on in situ apocrine sweat lesions is scarce; however, there have been isolated case reports of pure in situ carcinoma.1,2,4 Other invasive apocrine carcinomas of the skin that have contained an in situ component have also been previously described.7,8 There have been a total of 9 cases of in situ sweat gland carcinoma, all of which were either high grade with comedonecrosis or with no specified grade mentioned.1,2,4,7,8 Of the cases that have specified a site of origin, all have occurred in the axilla; (the most common site of invasive apocrine carcinoma), or in the anogenital region where the so-called mammary-like glands (MLG) are found.1,2,4,8
We have also recently seen 2 in situ apocrine lesions of the scalp; a previously unreported finding. Both had the appearance of apocrine atypical ductal hyperplasia (ADH) or ductal carcinoma in situ (DCIS) of the breast. One was low grade in histology and the other showed a transition from low grade to high grade. There was 1 male (case 1) and 1 female (case 2) patient with ages of 62 to 76 years and they each presented with a short history of a scalp lesion <1.0 cm. One patient (case 2) had a remote history of ductal carcinoma of the breast 13 years prior (case 2); otherwise, there were no significant medical histories. Follow-up was available for case 1 and in 12 months here has been no evidence of recurrence. Case 2 has only been recently excised.
The cases showed similar features histologically. Case 1, excised from the right temple, consisted of a large area of acanthotic squamous epithelium, prominent sebaceous units, and abundant dilated and irregular apocrine glands, in keeping with a preexisting nevus sebaceous. The lesion also contained a dense area of small-angulated apocrine glands in a fibrotic stroma resembling apocrine sclerosing adenosis of the breast. The center of the lesion consisted of a lobular growth of large cystic ducts and smaller ducts with a cribriform architecture. These displayed a combination of micropapillae, “Roman bridge” type architecture and multilayering of apocrine type cells, identical to apocrine ADH and low-grade apocrine DCIS of the breast (Fig. 1). The intervening stroma was unremarkable. The lumina showed apical snouts and decapitation secretions as well as granular eosinophilic debris. The individual cells had voluminous granular eosinophilic cytoplasm and the nuclei contained eosinophilic nucleoli. In addition, there was a focus of epidermotropism by numerous single and duct forming apocrine cells and extension into neighboring normal apocrine sweat ducts in case 1 (Fig. 1 inset). In contrast to the pure low-grade ADH and DCIS-like lesion seen in case 1, case 2 demonstrated a transition to a high-grade apocrine in situ carcinoma with nuclei 3-4×normal, mitotic figures and central comedo-type necrosis (Fig. 2). The intervening stroma demonstrated focal sclerosis and chronic inflammation but there was no evidence of microinvasion or pagetoid involvement of the overlying skin. Case 1 was stained with low molecular weight keratin, cytokeratin 7, BRST-2, and androgen receptors and was strongly positive.
