Skin Tumors With Matrical Differentiation: Lessons From Hair Keratins, Beta-Catenin and PHLDA1 Expression

The study investigated matrical tumors other than pilomatricoma, focusing on cortical differentiation, the beta-catenin pathway, and PHLDA1 expression. In 36 tumors, including 18 purely matrical and 18 focally matrical tumors, researchers found sequential expression of K35, HOXC13, and K31, indicating cortical differentiation. Germinative matrix cells consistently showed nuclear beta-catenin accumulation and expressed LEF1 and PHLDA1. The findings suggested that nuclear beta-catenin and LEF1 expression were highly conserved across matrical tumors, indicating a common tumorigenesis mechanism driven by Wnt pathway activation. PHLDA1 expression was also consistent in these tumors and areas of matrical differentiation.