Potentially confused with chondrodermatitis nodularis chronica helicis and SCC, this auricular benign cystic degenerative inammatory disease is best left untreated. In most cases, the lesions do not involve both simultaneously and can be quite large (up to 4cm) and recurrent. A representative sample of auricular cartilage is required for diagnosis. Chondrodermatitis nodularis chronica helicis is the primary differen­tial diagnosis [11].

Adenoma NOS (ceruminous adenoma), pleomorphic adenoma, and syringocystoma papilliferum are the fth edition histologic categories for benign tumors of the ceru­minous glands. These tumors share some histologic features with the tumor in ques­tion. However, they also show signs of ceruminous differentiation, such as decapitation secretion and yellow ceroid pigment, which are absent in the described tumor. Most of the tumors are glandular in shape and may occasionally develop cysts. As a result of interglandular brosis, lesional cells invade the surrounding stroma. The architec­ture may be solid with features such as papillary or back-to-back glands. Immunostaining, hematoxylin and eosin-stained sections, and luminal epithelial cells are occasionally seen along with outer basal and myoepithelial cells [13]. Tumors have mild nuclear pleomorphism and low-to-moderate cellularity. With small nucleoli and ne granular chromatin, nuclei may be either round or oval. Columnar to cuboidal luminal cells typically have apical caps and decapitate secretions, rich eosinophilic cytoplasm, and well-dened cell borders. Cytoplasmic granules of ceroid pigment, a golden yellow or brownish color, are seen in most tumor cells [11].

This group includes cancers that develop in the ceruminous glands of the external ear. Adenocarcinoma NOS (“ceruminous adenocarcinoma”), “ceruminous adenoid cystic carcinoma”, and “ceruminous mucoepidermoid carcinoma” are the three separate histologic forms included. The histology of “adenoid cystic carcinoma and mucoepidermoid carcinoma” is identical to that of salivary gland carcinoma [11].

The middle ear and mastoid cavity are the only sites where adenoid cystic car­cinoma has been reported [22]. A preponderance of tubular and cribriform mor­phology characterizes low-grade tumors. In contrast, high-grade tumors are dened as those with solid morphology in at least 30% of the tumor area. In addition to morphology, other factors inuence prognosis. Surgery may not be able to cure low-grade tumors that have spread to inaccessible areas, such as the temporal bone. Adenoid cystic carcinoma is associated with fusions between the “MYB, MYBL1, and NF1B genes,” which are also present in metastases [23]. “MYB-NF1B gene fusion,” which upregulates MYB, is found to be specic to adenoid cystic carci­noma only. Immunohistochemistry has shown cases of MYB overexpression, but the specicity of these cases has been inconsistent [24]. In addition to HPV­associated sinonasal carcinoma [25], other tumor types have been found to express MYB by immunohistochemistry, including “basaloid squamous cell carcinoma, basal cell adenocarcinoma, and myoepithelial epithelial carcinoma” [26]. According to a recent study, a negative immunostaining result for MYB could indicate that the tumor would have a poorer prognosis. According to the same study, cytoplasmic beta-catenin positivity may increase tumor-associated mortality risk [27].