Differential expression of PHLDA1 (TDAG51) in basal cell carcinoma and trichoepithelioma

Departments of Dermatology and Pathology, University of California, San Francisco, CA, U.S.A.
British Journal of Dermatology (Impact Factor: 4.28). 09/2012; 167(5). DOI: 10.1111/j.1365-2133.2012.11165.x
Source: PubMed


Background A recent small series demonstrated perfect sensitivity and specificity utilizing immunostaining for PHLDA1, a marker of follicular stem cells, in the distinction of desmoplastic trichoepithelioma and morphoeiform basal cell carcinoma (BCC) in small biopsy specimens.
Objectives To assess this result more broadly.
Methods We performed immunoperoxidase staining of BCCs (superficial n = 16, nodular n = 15, micronodular n = 15, infiltrative n = 17, morphoeiform n = 16, infundibulocystic n = 14) and trichoepitheliomas (conventional n = 19, desmoplastic n = 16) with PHLDA1.
Results Morphoeiform BCCs typically lacked PHLDA1 staining (88% demonstrated no staining and 12% of cases had staining in < 25% of the tumour), while in contrast 74% of classical and 88% of desmoplastic trichoepitheliomas demonstrated strong PHLDA1 staining in over half of the tumour. However, micronodular BCCs demonstrated focal to diffuse positive staining in a third of the cases.
Conclusions Based upon our staining results, we discuss the biological significance of PHLDA1 expression and the limits in its diagnostic utility.

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    ABSTRACT: Until the 1990s, basal cell carcinoma (BCC) was viewed as the most common epithelial neoplasm developing in association with nevus sebaceus (NS). Currently, trichoblastoma is thought of as the most prevalent basaloid neoplasm in NS. The follicular stem cell marker pleckstrin homology-like domain, family A, member 1 (PHLDA1) also known as T-cell death-associated gene 51 (TDAG51) labels trichoepithelioma (TE) but not BCC. Therefore, we explored its usefulness in basaloid neoplasms developing in NS. We studied immunohistochemically PHLDA1 in 10 nodular BCCs, 11 TEs, 11 trichoblastomas and 25 NS with basaloid tumors. Additionally, we examined the expression of BCC marker BerEP4 and the distribution of Merkel cells that function as surrogate markers for benign follicular neoplasms. Nineteen of the 25 basaloid tumors in NS were PHLDA1-negative comparable to BCC arising de novo and six tumors were PHLDA1-positive comparable to solitary trichoblastomas and TEs. Fewer Merkel cells were seen in BCCs associated with NS when compared with trichoblastoma. BerEP4 did not discriminate between the neoplasms. We raise concern that the unquestioned assessment that basaloid tumors developing in association with NS represent mostly trichoblastomas and not BCC may not be true. This influences clinical care, as it is paramount in the decision of whether to excise these lesions or not.
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