squamous epithelial-like eosinophilic cells that resemble the luminal cells lining eccrine sweat gland ducts); and in some cases c) clear cells (i.e. cells with small nuclei surrounded by pale cytoplasm). Poroma tumor tissues may appear highly vascularized and/or have areas of necrosis, i.e. dead or dying cells. Hidroacanthoma simplex variants are mainly composed of poroid cells, few cuticular cells, and no clear cells and are confined to the epidermis; dermal ductal variants are mostly confined to the superficial dermis and are composed of small solid and cystic nodular aggregates of poroid, cuticular, and clear cells; poroid hidradenoma variants have large aggregates of solid and cystic components and extend deeper into the dermis or even subcutis; and eccrine poroma variants are composed of all three cell types but are primarily located in the epidermis and superficial dermis. Poromas may have 2 or more of these variants in the same tumor tissue and the variants typically have histopathology findings that are not clearly distinguishable from each other. Immunohistochemistry
As detected by immunohistochemical analyses, the poroma tumor cells, regardless of variant type, test positive when probed with the AE1/AE3 antibody cocktail that detects various cytokeratin proteins. Tumor cells of the four variants also commonly express carcinoembryonic antigen (i.e. CEA) or MUC1 (also termed EMA) and, except for the hidroacanthoma simplex variant, the carcinoembryonic antigen and MUC1 protein. Gene abnormalities
The four poroma variants contain at least one of two YAP1 fusion genes, i.e.
abnormal genes caused by a mutation which merges a part of the YAP1 gene fused to part of either the Nuclear protein in testis gene (also termed the NUTM1 gene) or the MAML2 gene to form the YAP1::NUTM1 and YAP::MAML2 fusion genes, respectively. Rarely, they may also contain a WWTR1::NUTM1 fusion gene. The YAP1::MAML2 fusion gene is detected in ~63% of poromas, the YAP1::NUTM1 fusion in 20.2% to 66% of poromas, and the WWTR1::NUTM1 fusion gene in 1% of poromas. YAP1  and WNTR1 fusion genes have been implicated in the initiation, aggressiveness, metastasis, and/or therapy resistance of various neoplasms. Studies are needed to determine if they play a role in the development and/or progression of poromas. Diagnosis
The great diversity, rarity, and complex terminology of poromas make their diagnosis challenging. They have been misdiagnosed as other types of skin tumors including porocarcinomas, basal cell carcinomas, pyogenic granulomas, skin tags, plantar warts (i.e. warts on the palms or soles), fibromas, hemangiomas, pigmented moles, seborrheic keratosis, trichilemmomas, melanomas, Kaposi sarcomas, and other adnexal tumors. Poromas are typically diagnosed based on their clinical presentation; microscopic histopathology showing tumor tissues consisting of poroid, cuticular, and/or clear cells; and, in unclear cases, the presence of tumor cells that express a YAP1::NUTM1, YAP::MAML2, and/or WWTR1::NUTM1 fusion gene. However, these fusion genes also occur in porocarcinomas and cannot be used to differentiate poromas from their malignant counterpart. Poromas and porocarcinomas are distinguished based on their clinical findings and histopathology, e.g.