Sebaceous Carcinoma of the Suprapubic Area in a Liver Transplant Recipient

Abstract

Sebaceous carcinoma is a very rare and potentially aggressive carcinoma originating from the epithelial lining of the sebaceous gland. More than 70% of all cases are in the head and neck region, especially the periorbita; therefore, they are classified into ocular and extraocular sebaceous carcinoma. The reported risk factors are advanced age, male sex, previous irradiation, and genetic predisposition for Muir-Torre syndrome. The current case is of sebaceous carcinoma found in the suprapubic area of a 67-year-old male patient who had received liver transplantation 6 years before, and had been receiving oral tacrolimus. Examination of the gastrointestinal system did not reveal any other malignancies. Although nonmelanoma skin cancers may occur as a complication after liver transplantation, there have been no previous reports of sebaceous carcinoma after liver transplantation. Furthermore, the sebaceous carcinoma in this case occurred in an uncommon location. We report this case along with a review of the literature.

Management Considerations in Extraocular Sebaceous Carcinoma

“…More recently, external beam radiation therapy (XRT) has been used successfully as adjuvant therapy after surgical excision in extraocular SC with lymph node involvement, extensive local invasion, or for recurrent disease. 19,35,36,[47][48][49][50][51][52][53] Of note, the majority of reported cases lack crucial information, including margin status after excision and location of radiation site. See Table 1 for a summary of 15 reported extraocular SC cases using XRT.…”

Sebaceous adenoma in the setting of immunosuppression for kidney transplantation

“…Furthermore, the lesion occurred in the suprapubic or lower abdominal region; this is uncharacteristic for sebaceous adenomas, which typically arise in the head and neck region. Interestingly, a previous report identified a sebaceous neoplasm after solid-organ transplantation in the same suprapubic location 11 …”

“…Reports of sebaceous neoplasms with mixed adenoma and carcinoma features arising in transplant recipients suggest the possibility of a sebaceous adenoma–sebaceous carcinoma neoplastic sequence 11, 12. Histopathologic analysis of these lesions identified focal regions of infiltrative growth and cellular atypia within an otherwise mostly well-differentiated collection of sebaceous gland-forming sebocytes 11, 12. Although histopathologic analysis of our individual's lesion showed no evidence of sebaceous carcinoma, treatment with complete excision and close follow-up for recurrence is reasonable because the potential for malignant growth exists.…”

Role of microsatellite instability, immunohistochemistry and mismatch repair germline aberrations in immunosuppressed transplant patients: a phenocopy dilemma in Muir-Torre syndrome

“…Regarding the iatrogenic factors, azathioprine has been postulated to contribute to the selection of cells bearing DNA MMR deficits, evading its cytotoxic effects [35]: in fact, there is evidence suggesting that immunosuppressive drugs, most plausibly azathioprine, could determine the selection of a mutator phenotype predisposing to the development of sebaceous neoplasms [21]. Cyclosporine and tacrolimus are calcineurin inhibitors and have been hypothesised to increase tumour growth through the increase of transforming growth factor (TGF)-β and interleukin-6 [24,36]. Maluccio et al found that tacrolimus has a dose-dependent effect on tumour progression and TGF-β1 expression in mice [37].…”

“…Along the same lines, it is also known that the occurrence of sebaceous tumours is modulated by specific type of immunosuppressive drugs [19,20], and some primary and secondary immunodepressive conditions are associated to an increased incidence of rare sebaceous tumours [21], showing MSI and IHC aberrations. In this regard, beyond the direct pathogenic effect of oncogenic viruses [13], a role for immunosuppressive therapies [18,[22][23][24], genetic aberrations [22,25] and MLH1 hypermethylation [26] have been hypothesised. Regarding this latter phenomenon, it is known that some MSI-high cancers are due to aberrant MLH1 gene promoter methylation, a somatic event leading to LS/MTS phenocopies [26,27].…”