The American Journal of dermatopathology · 2025
Comparison of the IHC Expression of p16, p53, and MIB-1 in Extragenital Skin Bowenoid Lesions With High- and Low- Chronic Sun Damage.
СтатьяСравнительное исследованиеНазвание и аннотация: Перевод в очереди
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Gil-Pallares Pedro, Gil-Pallares Maria E, Navarro-Bielsa Alba, Figueroa-Silva Olalla, Taboada-Paz Laura, Suárez-Peñaranda José M
Аннотация
BACKGROUND: Bowen disease and bowenoid actinic keratosis are difficult to distinguish due to overlapping histopathology. This study evaluates the role of p16, p53, and MIB-1 staining patterns in differentiating high-chronic sun damage (H-CSD) and low-chronic sun damage bowenoid lesions.
METHODS: Sixty extragenital in situ squamous cell carcinomas were included. Lesions with elastosis were considered H-CSD. P16, p53, and MIB-1 staining patterns were classified as block, gradient, or focal.
RESULTS: Seventy-two percent of lesions were H-CSD. Full-thickness dysplasia was observed in all lesions, and basal layer involvement in 97%. P16 staining was positive in 80%, matching areas of higher atypia, with block pattern more frequent in H-CSD (58% vs. 47%, P = 0.047). P53 was positive in 47%, with block pattern more common in H-CSD (40% vs. 18%, P = 0.02). MIB-1 was positive in all cases. P16 and MIB-1 patterns coincided in 75%, independently of sun exposure.
CONCLUSIONS: P16 and p53 expression may be less frequent in bowenoid lesions than previously described. Histopathological features like basal layer and adnexal or follicular involvement may not differentiate H-CSD from low-chronic sun damage lesions or Bowen disease from bowenoid actinic keratosis. Variations in p16, p53, and MIB-1 staining could indicate different dysplasia pathways, although further studies are needed to clarify their prognostic significance.
METHODS: Sixty extragenital in situ squamous cell carcinomas were included. Lesions with elastosis were considered H-CSD. P16, p53, and MIB-1 staining patterns were classified as block, gradient, or focal.
RESULTS: Seventy-two percent of lesions were H-CSD. Full-thickness dysplasia was observed in all lesions, and basal layer involvement in 97%. P16 staining was positive in 80%, matching areas of higher atypia, with block pattern more frequent in H-CSD (58% vs. 47%, P = 0.047). P53 was positive in 47%, with block pattern more common in H-CSD (40% vs. 18%, P = 0.02). MIB-1 was positive in all cases. P16 and MIB-1 patterns coincided in 75%, independently of sun exposure.
CONCLUSIONS: P16 and p53 expression may be less frequent in bowenoid lesions than previously described. Histopathological features like basal layer and adnexal or follicular involvement may not differentiate H-CSD from low-chronic sun damage lesions or Bowen disease from bowenoid actinic keratosis. Variations in p16, p53, and MIB-1 staining could indicate different dysplasia pathways, although further studies are needed to clarify their prognostic significance.