Focus on HPV Infection and the Molecular Mechanisms of Oral Carcinogenesis - PubMed (original) (raw)

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Focus on HPV Infection and the Molecular Mechanisms of Oral Carcinogenesis

Luigi Santacroce et al. Viruses. 2021.

Abstract

This study is focused on the epidemiological characteristics and biomolecular mechanisms that lead to the development of precancerous and cancerous conditions of oral lesions related to Human Papilloma Virus (HPV) infections. Current evidence from the literature demonstrates the role of HPV in potentially malignant oral disorders. Therefore, the underlying biomolecular processes can give arise, or contribute to, benign lesions as well as to oral carcinogenesis.

Keywords: HPV; maxillary-facial surgery; oral cancer; oral carcinogenesis; oral infections; oral microbiota.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1

Figure 1

Precursor conditions: infections, chronic mouth’s irritation, immune suppression and immune disorders (i.e., transplanted patients, due to the chronic inflammatory state associated with graft-versus-host disease (GVHD), lifestyle and environmental factors (e.g., alcohol abuse, tobacco smoking/chewing, betel quid or guṭkha chewing, marijuana, poor oral hygiene), low socio-economic status (poor or no access to oral health care facilities), dietary factors, radiation exposure, and genetic polymorphisms. (Adapted from [1]).

Figure 2

Figure 2

This table relates the HPVs with the different degrees of risk for developing precancerous lesions or cancer (From WHO/IARC Agents Classified by the IARC Monographs, IARC Monographs on the identification of carcinogenic hazards to humans, until 2019).

Figure 3

Figure 3

The oncogenic pathways of the HPV due to the activity of the viral oncoproteins E6 and E7 (Bak: Bcl-2 homologous antagonist/killer, FADD: Fas-associated protein with death domain, FLICE: procaspase 8, IAP-2: Interferon regulatory factor 3,CBP/300: CREB binding protein, TADA3: Transcriptional adaptor 3, Tyk2: tyrosine kinase 2).

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