Comprehensive Data of P53 R282 Gene Mutation with Human Papillomaviruses (HPV)-Associated Oral Squamous Cell Carcinoma (OSCC)

Ekalaksananan, Tipaya; Wongjampa, Weerayut; Phusingha, Pensiri; Chuerduangphui, Jureeporn; Vatanasapt, Patravoot; Promthet, Supannee; Patarapadungkit, Natcha; Pientong, Chamsai

doi:10.1007/s12253-019-00673-6

Cited by 2 publications

(2 citation statements)

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“…Accordingly, in a whole‐exome sequencing study with OSCC samples, the most frequent mutations were in the TP53 and CDKN2A genes, but no association of specific mutations with HPV (Zammit et al., 2018). In other study investigating TP53 exon 8 mutation, the frequency of mutation was significantly higher in OSCC than in controls, however, with no significant relationship between HPV infection and mutation, which may indicate that HPV infection may not strongly affect the frequency of TP53 codon 282 mutation in OSCC (Ekalaksananan et al., 2020).…”

Section: Discussionmentioning

confidence: 86%

“…Oral squamous cell carcinomas (OSCC) account for more than 90% of the cancers at this location. Several risk factors are implicated in oral cancers; however, the main ones include smoking, alcohol consumption and infection by high‐risk genotypes of human papillomavirus (HR‐HPV) (Allameh et al., 2019; Chuerduangphui et al., 2016; Ekalaksananan et al., 2020; Jitani et al., 2015; Nwanze et al., 2015).…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of HPV and EBV in OSCC and the expression of p53, p16, E‐cadherin, COX‐2, MYC, and MLH1

et al. 2021

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Objective This study aimed to evaluate the presence of human papillomavirus (HPV) and Epstein–Barr virus (EBV) and the expression of p53, p16, E‐cadherin, COX‐2, MLH1, and MYC in oral squamous cell carcinoma (OSCC). Materials and Methods One hundred OSCC specimens were submitted to in situ hybridization for HPV and EBV, and immunohistochemistry for detection of the human proteins. Results Thirty‐one cases showed HPV in tumor tissue. EBV was not detected in any case investigated. The HPV(+) group demonstrated an increase of staining scores for nuclear p16 (p = .047), cytoplasmic MYC (p = .002), while a decrease for nuclear MLH1 (p = .048), suggesting that HPV may upregulate the expression of the first two proteins and down‐regulate the latter. Conclusion Our findings reinforce the hypothesis of the HPV‐related oral carcinogenesis involving the expression of p16 and MYC, and MLH1 suppression. Exclusively cytoplasmic stainings for p16, MLH1, and MYC were also associated with more advanced tumors. Finally, in view of the lack of studies correlating the HPV or EBV infection to the expression of oncoproteins, more researches assessing a broader panel of markers and employing different approaches are still necessary in order to understand the role of these viruses as well as the molecular mechanisms involved in the development and progression of oral carcinomas.

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Section: Discussionmentioning

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Evaluation of HPV and EBV in OSCC and the expression of p53, p16, E‐cadherin, COX‐2, MYC, and MLH1

et al. 2021

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Genetic Mutations Associated with Inflammatory Response Caused by HPV Integration in Oropharyngeal Squamous Cell Carcinoma

Atique,

Muniz,

Farshadi

et al. 2023

Biomedicines

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(1) Background: Head and neck cancer (HNC) ranks as the sixth most prevalent cancer in the world. In addition to the traditional risk factors such as alcohol and tobacco consumption, the implication of the human papillomavirus (HPV) is becoming increasingly significant, particularly in oropharyngeal cancer (OPC). (2) Methods: This study is based on a review analysis of different articles and repositories investigating the mutation profile of HPV-related OPC and its impact on patient outcomes. (3) Results: By compiling data from 38 datasets involving 8311 patients from 12 countries, we identified 330 genes that were further analyzed. These genes were enriched for regulation of the inflammatory response (RB1, JAK2, FANCA, CYLD, SYK, ABCC1, SYK, BCL6, CEBPA, SRC, BAP1, FOXP1, FGR, BCR, LRRK2, RICTOR, IGF1, and ATM), among other biological processes. Hierarchical cluster analysis showed the most relevant biological processes were linked with the regulation of mast cell cytokine production, neutrophil activation and degranulation, and leukocyte activation (FDR < 0.001; p-value < 0.05), suggesting that neutrophils may be involved in the development and progression of HPV-related OPC. (4) Conclusions: The neutrophil infiltration and HPV status emerge as a potential prognostic factor for OPC. HPV-infected HNC cells could potentially lead to a decrease in neutrophil infiltration. By gaining a better molecular understanding of HPV-mediated neutrophil immunosuppression activity, it is possible to identify a meaningful target to boost antitumor immune response in HNC and hence to improve the survival of patients with HNC.

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Comprehensive Data of P53 R282 Gene Mutation with Human Papillomaviruses (HPV)-Associated Oral Squamous Cell Carcinoma (OSCC)

Cited by 2 publications

References 42 publications

Evaluation of HPV and EBV in OSCC and the expression of p53, p16, E‐cadherin, COX‐2, MYC, and MLH1

Evaluation of HPV and EBV in OSCC and the expression of p53, p16, E‐cadherin, COX‐2, MYC, and MLH1

Genetic Mutations Associated with Inflammatory Response Caused by HPV Integration in Oropharyngeal Squamous Cell Carcinoma

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