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Tricholemmoma and tricholemmal carcinoma and Cowden syndrome
Published in Longo Caterina, Diagnosing the Less Common Skin Tumors, 2019
Eugenia Veronica Di Brizzi, Simonetta Piana, Giuseppe Argenziano, Elvira Moscarella
Tricholemmoma is a benign tumor with differentiation toward pilosebaceous follicular epithelium. Tricholemmal carcinoma is the malignant form of tricholemmoma with outer root sheath differentiation. Both tumors were described first by Headington and French in 1962.1
Skin and soft tissue
Published in Tor Wo Chiu, Stone’s Plastic Surgery Facts, 2018
A tricholemmoma is a hair-follicle tumour often misdiagnosed clinically as BCC; it is relatively common, though the true incidence is difficult to determine. The cells of origin come from the outer root sheath, and histologically there are plaques of squamous cells containing glycogen.
Skin
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Zbigniew W. Wojcinski, Lydia Andrews-Jones, Daher Ibrahim Aibo, Rie Kikkawa, Robert Dunstan
Tricholemmoma is usually clinically described as a single nodule or plaque (rarely multiple). It is believed that this tumor arises from the external root sheath epithelium. Two main histological presentations have been recognized (Tellechia 2015). The first histological type is characterized by closely packed nests of epithelial cells surrounded by a relatively thick eosinophilic hyaline basement membrane. The peripheral cells in these nests take a palisading arrangement and have abundant pale eosinophilic cytoplasm with small vacuoles while the central cells are smaller with a small central nucleus and lesser amount of eosinophilic cytoplasm. This histological type is thought to derive from the inferior segment of the hair follicle or bulbar part of the external root sheath. The second histological subtype usually touches or is associated with a thickened overlying epidermis and is constituted by neoplastic trabeculae and islands lined by epithelial cells with a moderately abundant pale eosinophilic cytoplasm. These islands and trabeculae contain central trichilemmal keratin (no trichohyaline granules formation). The stroma is more abundant in this subtype compared to the bulbar type and made of fine collagenous fibrils with sometimes small amounts of mucin. This second presentation is called the isthmic type due to similarities with the isthmic epithelium of the normal hair follicle. This tumor has been reported in dog (Walsh and Corapi 1986) and seems to occur very rarely in rodents (Mecklenber et al. 2013). A desmoplastic version has also been recently described in dog (Kok et al. 2017).
Multiple secondary neoplasms in nevus sebaceus excision
Published in Baylor University Medical Center Proceedings, 2022
Travis S. Dowdle, David A. Mehegran, Dylan Maldonado, Cort D. McCaughey
Nevus sebaceus is of particular clinical interest because of its association with the development of secondary neoplasms of varying rarity. Secondary tumors are typically benign, but malignant neoplasms have also been observed. The most common benign neoplasms include trichoblastoma and syringocystadenoma papilliferum. Additional benign neoplasms such as apocrine/eccrine adenoma, trichilemmoma, and sebaceoma have been observed.3 It has been estimated that approximately 40% of syringocystadenoma papilliferum lesions are associated with nevus sebaceus.4
Basal cell carcinoma within nevus sebaceous of the trunk
Published in Baylor University Medical Center Proceedings, 2019
Ian T. Watson, Andrew DeCrescenzo, So Yeon Paek
Trichoblastoma (34.7%), syringocystadenoma papilliferum (24.7%), apocrine adenoma (10%), and trichilemmoma (5.3%) are the most common secondary neoplasms found within NS.2 The incidence of BCC in NS is about 1%, making it the most common secondary malignancy.2 In one report of 65 NS tissue samples, 95% of lesions displayed HRAS gene mutations and 5% had a KRAS mutation. These oncogenic mutations may explain a predisposition to the development of secondary tumors because additional genetic “hits” occur later in life.3