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. 2023 Jun 26;11(7):1838.
doi: 10.3390/biomedicines11071838.

The TP53 Codon 72 Arginine Polymorphism Is Found with Increased TP53 Somatic Mutations in HPV(-) and in an Increased Percentage among HPV(+) Norwegian HNSCC Patients

Affiliations

The TP53 Codon 72 Arginine Polymorphism Is Found with Increased TP53 Somatic Mutations in HPV(-) and in an Increased Percentage among HPV(+) Norwegian HNSCC Patients

Svein Erik Moe et al. Biomedicines. .

Abstract

Background: Somatic TP53 mutations are frequent in head and neck squamous cell carcinoma (HNSCC) and are important pathogenic factors.

Objective: To study TP53 mutations relative to the presence of human papillomavirus (HPV) in tumors in HNSCC patients.

Methods: Using a custom-made next-generation sequencing (NGS) panel on formalin-fixed, paraffin-embedded tumor tissue, we analyzed somatic TP53 mutations and the TP53 single-nucleotide polymorphism (SNP) codon 72 (P72R; rs1042522) (proline → arginine) from 104 patients with HNSCC.

Results: Only 2 of 44 patients with HPV-positive (HPV(+)) HNSCC had a TP53 somatic mutation, as opposed to 42/60 HPV-negative (HPV(-)) HNSCC patients (p < 0.001). Forty-five different TP53 somatic mutations were detected. Furthermore, in HPV(-) patients, we determined an 80% prevalence of somatic TP53 mutations in the TP53 R72 polymorphism cohort versus 40% in the TP53 P72 cohort (p = 0.001). A higher percentage of patients with oral cavity SCC had TP53 mutations than HPV(-) oropharyngeal (OP) SCC patients (p = 0.012). Furthermore, 39/44 HPV(+) tumor patients harbored the TP53 R72 polymorphism in contrast to 42/60 patients in the HPV(-) group (p = 0.024).

Conclusions: Our observations show that TP53 R72 polymorphism is associated with a tumor being HPV(+). We also report a higher percentage of somatic TP53 mutations with R72 than P72 in HPV(-) HNSCC patients.

Keywords: HPV; TP53; head and neck cancer; singe-nucleotide polymorphism; somatic mutation.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
TP53 R72 SNPs influence the risk of head and neck squamous cell carcinoma depending on the HPV status of the tumor. Red arrows indicate the SNPs dual pathway with regards to HPV-tumor status. Black arrows indicate that persistent HPV-infection and TP53 mutations, respectively, further influence the risk of HNSCC development.

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