Abstract
Human papillomavirus (HPV)-independent vulvar squamous cell carcinomas (VSCC) and its precursors frequently harbour TP53 mutations. Recently, six p53 immunohistochemical (IHC) patterns have been defined, which have shown strong correlation with TP53 mutation status. However, few studies have applied this new six-pattern framework and none of them exhaustively compared p53 IHC positivity and patterns between invasive VSCC and adjacent skin lesion. We performed p53 IHC in a series of 779 HPV-independent VSCC with adjacent skin and evaluated the IHC slides following the newly described classification. Some 74.1% invasive VSCC showed abnormal p53 IHC staining. A skin lesion was identified in 450 cases (57.8%), including 254 intraepithelial precursors and 196 inflammatory/reactive lesions. Two hundred and ten of 450 (47%) VSCC with associated skin lesions showed an abnormal p53 IHC stain, with an identical staining pattern between the VSCC and the adjacent skin lesion in 80% of the cases. A total of 144/450 (32%) VSCC showed wild-type p53 IHC both in the invasive VSCC and adjacent skin lesion. Finally, 96/450 (21%) VSCC showed p53 IHC abnormal staining in the invasive VSCC but a wild-type p53 staining in the skin lesion. Most of the discordant cases (70/96; 73%) showed adjacent inflammatory lesions. In conclusion, the p53 IHC staining and pattern are usually identical in the VSCC and the intraepithelial precursor.
Highlights
Vulvar squamous cell carcinomas (VSCC) may arise via human papillomavirus (HPV)-associated and -independent pathways [1,2]
They include differentiated vulvar intraepithelial neoplasia, the classical precursor of HPV-independent VSCC [3,4,5,6,7,8], and other new entities that have recently been added to the list of HPV-independent premalignant lesions: high-grade squamous intraepithelial lesion (HSIL)-like lesion [9], referred to as basaloid dVIN [10], vulvar acanthosis with altered differentiation (VAAD) [11], and the closely related differentiated exophytic vulvar intraepithelial lesion (DEVIL) [12]
Our study provides a representative picture of the distribution of the p53 IHC patterns in a large unselected sample of HPV-independent VSCC from a wide geographic origin
Summary
Vulvar squamous cell carcinomas (VSCC) may arise via human papillomavirus (HPV)-associated and -independent pathways [1,2]. The precursor of HPV-associated VSCC, i.e., high-grade squamous intraepithelial lesion (HSIL), is a well-characterized lesion with clear-cut morphological features. Several intraepithelial precursors have been described in association with HPV-independent VSCC They include differentiated vulvar intraepithelial neoplasia (dVIN), the classical precursor of HPV-independent VSCC [3,4,5,6,7,8], and other new entities that have recently been added to the list of HPV-independent premalignant lesions: HSIL-like lesion [9], referred to as basaloid dVIN [10], vulvar acanthosis with altered differentiation (VAAD) [11], and the closely related differentiated exophytic vulvar intraepithelial lesion (DEVIL) [12]. The morphologic features of dVIN are subtle [14] and not infrequently overlap with inflammatory lesions [13], vulvar HSIL [9], and VAAD/DEVIL [3]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
