2020
DOI: 10.1016/j.archoralbio.2020.104738
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High p16INK4a immunoexpression is not HPV dependent in oral leukoplakia

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Cited by 12 publications
(6 citation statements)
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“…Immunohistochemistry for p16 with a threshold of 70% positive cell staining correlates well with the diagnosis, but p16 is often dysregulated in non-HPV dysplasia (Tomo et al, 2020). Consequently, p16 immunohistochemistry alone is not a reliable surrogate for HPVassociated dysplasia (Hendawi et al, 2020) and direct detection of high-risk HPV DNA or E6/E7 RNA by in situ hybridisation is advised (Mes et al, 2020).…”
Section: Hpv-a Ssociated Dys Pl a S Iamentioning
confidence: 99%
“…Immunohistochemistry for p16 with a threshold of 70% positive cell staining correlates well with the diagnosis, but p16 is often dysregulated in non-HPV dysplasia (Tomo et al, 2020). Consequently, p16 immunohistochemistry alone is not a reliable surrogate for HPVassociated dysplasia (Hendawi et al, 2020) and direct detection of high-risk HPV DNA or E6/E7 RNA by in situ hybridisation is advised (Mes et al, 2020).…”
Section: Hpv-a Ssociated Dys Pl a S Iamentioning
confidence: 99%
“…Pooled estimates of HPV prevalence in OLK (20.2%) and PVL (24.7%) were no different to other potentially malignant conditions, such as oral lichen planus (23.0%) and oral submucous fibrosis (28.6%), and were independent of OED (de la Cour, Sperling, Belmonte, Syrjänen, & Kjaer, 2020). HPV has not been found to be a driver of oncogenesis or a contributor to MT of OLK, although overexpression of p16INK4A in dysplastic epithelium has been noted (Wu et al, 2019), but found not to be HPV‐dependent (Tomo et al, 2020). Furthermore, p16 is not a reliable biomarker for HPV infection in patients with OLK or OSCC (Sundberg et al, 2019; Sundberg et al, 2020).…”
Section: Clinical and Histopathological Determinants Of Malignant Tramentioning
confidence: 99%
“…demonstrated that p16 levels may be high even in the absence of HPV infection. 64 Moreover, presence of HPV DNA fails to accurately represent a transcriptionally active viral process in OCSCC. 14 , 65 Taken together, while evidence suggests that HPV may play a significant etiological role in NSND for OPSCC, HPV does not appear to be a main driver of OCSCC.…”
Section: Resultsmentioning
confidence: 99%
“…13 Mirghani et al further supported the notion that p16 immunohistochemistry is an unreliable surrogate marker for HPV oncogenesis in OCSCC, given its low specificity, 12 whereas Tomo et al demonstrated that p16 levels may be high even in the absence of HPV infection. 64 Moreover, presence of HPV DNA fails to accurately represent a transcriptionally active viral process in OCSCC. 14,65 Taken together, while evidence suggests that HPV may play a significant etiological role in NSND for OPSCC, HPV does not appear to be a main driver of OCSCC.…”
Section: Infectious Factorsmentioning
confidence: 99%