High p16INK4a immunoexpression is not HPV dependent in oral leukoplakia

Tomo, Saygo; Biss, Stephanye Pinto; Crivelini, Marcelo Macedo; Oliveira, Sandra Helena Penha de; Biasoli, Éder Ricardo; Tjioe, Kellen Cristine; Bernabé, Daniel Galera; Villa, Luisa L.; Miyahara, Glauco Issamu

doi:10.1016/j.archoralbio.2020.104738

Cited by 13 publications

(10 citation statements)

References 47 publications

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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%

Oral epithelial dysplasia: Recognition, grading and clinical significance

et al. 2021

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The concept of epithelial dysplasia was introduced into oral pathology over 60 years ago, following the recognition that some oral lesions had the potential to progress to oral cancer, now recognised as oral potentially malignant disorders (OPMDs). Attempts to grade oral dysplasia systematically were introduced into the literature in 1969, using photographic standards as reference (Smith et al., 1969) and internationally agreed classifications were formulated later

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Section: Hpv-a Ssociated Dys Pl a S Iamentioning

confidence: 99%

Oral epithelial dysplasia: Recognition, grading and clinical significance

et al. 2021

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“…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%

Molecular, genomic and mutational landscape of oral leukoplakia

Farah

2020

Oral Diseases

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Oral leukoplakia (OLK) and its more aggressive clinical variant proliferative verrucous leukoplakia (PVL) remain enigmatic disorders clinically and histopathologically. Despite decades of research into both, there has been only incremental advancement in our understanding of their aetiology and pathogenesis and only minimal improvement in effective management strategies. Currently, no specific prognostic genetic or molecular marker has been reported for leukoplakia. There is, however, an emerging body of evidence characterising the genomic and transcriptomic profile of OLK. Regardless of the significance of cellular and architectural features of OLK and PVL, it is clear from studies reported in this review that new emerging evidence points to the presence of premalignant molecular subtypes of leukoplakia which require further investigation. This up‐to‐date review explores the contemporary genomic, transcriptomic and mutational landscape of leukoplakia broadly, discusses concepts that may not be widely recognised or accepted and purposefully highlights studies with juxtaposed findings in an effort to challenge dogma. It also highlights the urgent need for a concerted international effort of original collaborative research which will only occur by pooling collective efforts, resources and intellect to define the molecular fingerprint of this enigmatic disorder, in the hope it will better inform diagnosis, stratification and treatment.

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“…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%

Molecular drivers of oral cavity squamous cell carcinoma in non-smoking and non-drinking patients: what do we know so far?

et al. 2022

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Oral cavity squamous cell carcinoma (OCSCC) is one of the most common head and neck cancers worldwide. It is well known that risk factors for OCSCC include tobacco and excess alcohol consumption. However, in recent years, OCSCC incidence has been increasing in patients without these traditional risk factors. The cause of this increase is unclear and various genetic, environmental, and infectious factors have been hypothesized to play a role. Additionally, there are expert opinions that oral cancer in non-smoking, non-drinking (NSND) patients have a distinct phenotype resulting in more aggressive disease presentation and poorer prognosis. In this review, we summarize the current state of knowledge for oral cavity cancer in patients without traditional risk factors.

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High p16INK4a immunoexpression is not HPV dependent in oral leukoplakia

Cited by 13 publications

References 47 publications

Oral epithelial dysplasia: Recognition, grading and clinical significance

Oral epithelial dysplasia: Recognition, grading and clinical significance

Molecular, genomic and mutational landscape of oral leukoplakia

Molecular drivers of oral cavity squamous cell carcinoma in non-smoking and non-drinking patients: what do we know so far?

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