SGc arises from the adnexal epithelium of<unk>  glands, most commonly the Meibomian glands or glands of Zeis. On histology, there are irregular lobules of different sizes with undifferentiated cells and distinct<unk>  cells with a foamy cytoplasm. The pathogenesis of SGc remains poorly understood. The majority of SGc are solitary and sporadic and believed to be associated with such factors as ultraviolet exposure, radiotherapy, and immunosuppression. Other SGc including those occurring outside of the head and neck region and the presentation of multiple at a time are believed to be associated with genetic defects including defects in mismatch repair genes, Muir–Torre syndrome (MTS), and familial retinoblastoma. The observation of extraocular SGc arising from Bowen disease or actinic keratosis and the predisposition of SGc to arise in sun-exposed areas suggest a role for ultraviolet exposure or intraepidermal neoplasia in the pathogenesis of some SGc in sun-exposed areas. While there are markedly increased rates of cutaneous neoplasms in solid organ transplant recipients, there is evidence to suggest that solid organ transplantation may increase the risk of SGc up to 90 times. Others have observed a significantly increased risk of SGc in patients with AIDS, suggesting some role for immunosuppression. Reports have also shown the onset of SGc within the field of irradiation for patients undergoing radiotherapy for retinoblastoma, eczema, or cosmetic epilation. There are cases reported of SGc arising from nevus<unk> . MTS is an autosomal dominant cancer syndrome characterized by multiple<unk>  and visceral neoplasms, the most common being colorectal adenocarcinoma. MTS results from defects in DNA mismatch repair genes, MLH1, MSH2, and MSH6, leading to a buildup of unstable microsatellite sequences and replication errors predisposing to various malignancies. Patients with MTS may present with numerous<unk>  tumors at a younger age (mean age of 53 years) and in atypical locations, including extraocular. The incidence of MTS in patients with<unk>  neoplasms as high as 14 to 50%. Besides mutations in mismatch repair genes, Wnt/beta-catenin signaling is known to be altered and play a significant role in the development of<unk>  tumors. Altered expression of beta-catenin, p21, sonic hedgehog signaling (Shh), and E-cadherin have been associated with invasion, metastasis, and poor clinical outcomes. More recently, mutations in tumor suppressor genes including p53 and Rb have been associated with the development of sporadic SGc as well as SGc in MTS patients with intact mismatch repair and subsets of younger patients presenting with SGc harboring trancriptionally active high-risk human papillomavirus (HPV).
Sebaceous carcinoma
Medulloepithelioma
Lymphoepithelioma
Bartholin gland carcinoma
Basal-cell carcinoma
Trichoepithelioma
Pyogenic granuloma
Angiokeratoma