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The Torre-Muir syndrome includes multiple sebaceous neoplasms and keratoacanthomas, as well as multiple internal malignancies. We describe three cases of this unusual association which has not previously been reported in the German-speaking literature. The Torre-Muir syndrome appears to have a close connection to the cancer family syndrome [17, 34].
Primary sebaceous tumors of salivary glands are extremely rare, although sebaceous glands are commonly present in parotid and submandibular glands. A review of the files of the Armed Forces Institute of Pathology yielded 21 cases of primary salivary gland sebaceous tumors. Five were sebaceous adenomas, 9 sebaceous lymphadenomas, 5 sebaceous carcinomas and 2 sebaceous lymphadenocarcinomas. Seventeen tumors were located in the parotid gland and one each in the submandibular gland, the minor salivary glands of buccal mucosa and in ectopic salivary gland tissue in a periparotid lymph node. Thirteen tumors occurred in males and six in females. The peak incidence for all the sebaceous tumors, occurred in the sixth and seventh decades. The influence of age, sex, race, clinical symptoms, and pathology on survival is reviewed for each tumor group. Our histopathologic observations strongly suggest that sebaceous lymphadenoma and sebaceous lymphadenocarcinoma arise from sebaceous glandular rests in a lymph node in a fashion similar to that of a Warthin tumor.
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Surprisingly little is understood about the physiologic and pathologic processes that involve intraoral sebaceous glands. Neoplasms are rare. Hyperplasia of these glands is undoubtedly more common, but criteria for the diagnosis of intraoral sebaceous hyperplasia have not been established. These lesions are too often misdiagnosed as large "Fordyce granules" or, when very large, as sebaceous adenomas. On the basis of a series of 31 nonneoplastic sebaceous lesions and on published data, the following definition is proposed: intraoral sebaceous hyperplasia occurs when a lesion, judged clinically to be a distinct abnormality that requires biopsy for diagnosis or confirmation of clinical impression, has histologic features of one or more well-differentiated sebaceous glands that exhibit no fewer than 15 lobules per gland. Sebaceous glands with fewer than 15 lobules that form an apparently distinct clinical lesion on the buccal mucosa are considered normal, whereas similar lesions of other intraoral sites are considered ectopic sebaceous glands. Sebaceous adenomas are less differentiated than sebaceous hyperplasia.
Primary sebaceous neoplasms of the salivary glands are extremely rare occurrences; furthermore, sebaceous lymphadenocarcinoma has only been reported in three patients. We report a case of sebaceous lymphadenocarcinoma arising in a lymphadenoma of the parotid gland. The patient was a 55-year-old man who presented with a parotid mass of 3 years' duration. Histologically, the lesion consisted of a sebaceous lymphadenoma with transition to a sebaceous carcinoma. The cytologic touch-preparation at the time of frozen section showed clusters of benign sebaceous cells in a rich lymphocytic background together with tridimensional clusters of malignant epithelial cells, strongly raising the suspicion of a malignant neoplasm arising in a benign sebaceous lesion. Malignant transformation of the sebaceous lymphadenoma, although rare, should be considered in enlarging, locally invasive parotid lesions, considering that clinical behavior and prognosis will be determined by the nature of the malignant component.
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Androgen receptors (AR) are present in normal skin being localized to the basal and differentiating cells of the sebaceous gland, and as such, sebaceous glands are androgen sensitive tissue. Androgen receptor expression was examined in 43 sebaceous neoplasms including 8 sebaceous carcinomas, 22 sebaceous adenomas, 12 specimens showing sebaceous hyperplasia, and 1 sebaceous epithelioma, as well as in 14 squamous cell carcinomas, 2 clear cell acanthomas, and 35 basal cell carcinomas. Epithelial membrane antigen (EMA) expression was also examined in all of the sebaceous neoplasms. All specimens were fixed in formalin and embedded in paraffin. Diffuse positive nuclear androgen receptor antibody immunohistochemical staining was observed in all samples of sebaceous neoplasms, whereas approximately 60% of basal cell carcinomas showed only focal positivity for nuclear androgen receptor immunoreactivity. Clear cell acanthomas and squamous cell carcinomas were uniformly negative. Whereas all sebaceous neoplasms exhibited immunoreactivity for androgen receptors, the staining pattern was more marked in the nuclei of seboblasts and differentiating sebocytes in the adenomatous, hyperplastic, and epitheliomatous lesions than in the nuclei of the less differentiated sebaceous carcinoma cells. All the sebaceous neoplasms except for sebaceous carcinomas exhibited immunoreactivity for EMA. In the sebaceous carcinomas, EMA staining was absent in the most poorly differentiated specimen, but with increasing differentiation, the carcinomas became immunoreactive to EMA. We have shown that the nuclei of sebaceous neoplasms, including sebaceous gland carcinomas, show immunoreactivity for androgen receptors (AR), that immunohistochemical staining for the presence of AR may be a reliable marker of sebaceous differentiation, and that the AR may be a better marker of sebaceous differentiation than EMA, particularly in poorly differentiated sebaceous carcinomas.
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