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Oropharyngeal squamous cell carcinoma: p16/p53 immunohistochemistry as a strong predictor of HPV tumour status
Author(s) -
Benzerdjeb Nazim,
Tantot Juliet,
Blanchet Christophe,
Philouze Pierre,
Mekki Yahia,
Lopez Jonathan,
DevouassouxShisheboran Mojgan
Publication year - 2021
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/his.14350
Subject(s) - immunohistochemistry , hpv infection , oncology , human papillomavirus , polymerase chain reaction , medicine , surrogate endpoint , staining , p53 expression , cancer research , pathological , biology , pathology , cancer , gene , cervical cancer , biochemistry
Aims Oropharyngeal squamous cell carcinomas (OPSCC) related to human papillomavirus (HPV) infection have a better prognosis than those without HPV infection. Although p16 INK4a overexpression is used as a surrogate marker for HPV infection, 5–20% of p16‐positive OPSCC are described as being unrelated to HPV infection, with worse overall survival compared to OPSCC‐related HPV. There is therefore a risk of undertreating a proportion of OPSCC patients falsely considered to be HPV‐driven because of p16 positivity. TP53 mutations are highly prevalent in OPSCC driven by mutagens in tobacco and alcohol. We describe herein a combined p16/p53 algorithm to predict HPV tumour status in OPSCC. Methods and results A total of 110 OPSCC were identified in the database of the pathology department and were studied using p16 and p53 immunohistochemistry. For p16‐positive or p16‐negative/wild‐type patterns‐p53 (WT‐p53) cases ( n = 63), DNA in‐situ hybridisation for high‐risk HPV was performed, and if negative the HPV status was controlled by HPV DNA polymerase chain reaction (PCR) ( n = 19). A significant association between TP53 mutation and pattern of p53 expression was found (WT‐p53, seven of 16, P < 0.001). The p16‐positive/WT‐p53 was significantly associated with HPV + tumour status (p16‐positive/WT‐p53, 50 of 110, P < 0.001). Interestingly, a subset of p16‐positive OPSCC was unrelated to HPV (13.5%, eight of 59), and showed mutant‐type staining of p53 expression. Conclusions The p16 protein immunopositivity in conjunction with the mutant‐type pattern of p53 staining helped to reclassify a subset of p16‐positive OPSCC as OPSCC‐unrelated HPV. This approach could be routinely applied by pathologists involved in the management of OPSCC, because of their potential therapeutic implications.