“…Notably, an increasing incidence of HNSCC has been observed in young to middle-aged men with oropharyngeal SCC (OPSCC) (3) and has been associated with HPV infection (4,5). HNSCC can also affect the oral cavity of non-smoker non-drinker (NSND) patients, especially in young and elderly women with oral tongue SCC (OTSCC) and gingival SCC respectively (6)(7)(8). Indeed, although some epidemiological studies may provide inconsistent data on the incidence of OSCC worldwide, a previous study using data from 22 international cancer registries showed that the increasing incidence of oral tongue SCC was reported among subjects <45 years old in some countries (9).…”
In some western countries, an increasing incidence of oral squamous cell carcinoma (OSCC) has been observed in non-smoker non-drinker patients (NSND), mostly in women with HPV-negative OSCC. In the context of the unknown etiology and mechanisms of tumorigenesis of OSCC in NSND, we discuss data supporting the hypothesis of a viral origin not related to HPV. OSCC from NSND are characterized by an antiviral DNA methylation and gene expression signature. Based on the similar increasing incidence of oral tongue SCC (OTSCC) and oropharyngeal SCC (OPSCC) in young women and men respectively, we hypothesize that changes in sexual behaviors may lead to an increasing incidence of herpesvirus in the oral cavity, especially HSV-2, similarly to what has already been described in HPV-positive OPSCC. Because viral genome integration has not been detected in OSCC from NSND, a "hit and run" viral mechanism involving epigenome deregulation could therefore play a key role at early steps of oral carcinogenesis in this population of patients. In conclusion, epidemiological, clinical and molecular data supports a "hit and run" viral origin of OSCC from NSND.
“…Notably, an increasing incidence of HNSCC has been observed in young to middle-aged men with oropharyngeal SCC (OPSCC) (3) and has been associated with HPV infection (4,5). HNSCC can also affect the oral cavity of non-smoker non-drinker (NSND) patients, especially in young and elderly women with oral tongue SCC (OTSCC) and gingival SCC respectively (6)(7)(8). Indeed, although some epidemiological studies may provide inconsistent data on the incidence of OSCC worldwide, a previous study using data from 22 international cancer registries showed that the increasing incidence of oral tongue SCC was reported among subjects <45 years old in some countries (9).…”
In some western countries, an increasing incidence of oral squamous cell carcinoma (OSCC) has been observed in non-smoker non-drinker patients (NSND), mostly in women with HPV-negative OSCC. In the context of the unknown etiology and mechanisms of tumorigenesis of OSCC in NSND, we discuss data supporting the hypothesis of a viral origin not related to HPV. OSCC from NSND are characterized by an antiviral DNA methylation and gene expression signature. Based on the similar increasing incidence of oral tongue SCC (OTSCC) and oropharyngeal SCC (OPSCC) in young women and men respectively, we hypothesize that changes in sexual behaviors may lead to an increasing incidence of herpesvirus in the oral cavity, especially HSV-2, similarly to what has already been described in HPV-positive OPSCC. Because viral genome integration has not been detected in OSCC from NSND, a "hit and run" viral mechanism involving epigenome deregulation could therefore play a key role at early steps of oral carcinogenesis in this population of patients. In conclusion, epidemiological, clinical and molecular data supports a "hit and run" viral origin of OSCC from NSND.
“…Indeed, other OSCC series that included non-smokers also reported similar data. 34 Moreover, some studies that discussed differences in the genetic profile of OSCC of smoker and nonsmokers have been reported elsewhere with divergent results, and the etiopathogenesis of OSCC in the nonsmoking population remains unknown. 34 While in some studies smoking history did not play a differential role in carcinogenesis, 34 most studies have reported that smokers are more affected by genetic instability.…”
Section: Discussionmentioning
confidence: 99%
“…34 Moreover, some studies that discussed differences in the genetic profile of OSCC of smoker and nonsmokers have been reported elsewhere with divergent results, and the etiopathogenesis of OSCC in the nonsmoking population remains unknown. 34 While in some studies smoking history did not play a differential role in carcinogenesis, 34 most studies have reported that smokers are more affected by genetic instability. Although tobacco can cause epigenetic changes in oral epithelial cells, inhibit multiple systemic immune functions of the host, and induce oxidative stress in tissues through its toxic metabolites leading to OSCC, there is no specific mutation signature associating smoking with OSCC.…”
Tobacco smoking involves a high risk of human malignancies, including oral cancer, because it contains multiple carcinogens that cause genetic instability. Thus, a worse prognosis would be expected for cancer patients who are smokers. The aim of this study was to assess the DNA damage response through the expression of checkpoint kinase 2 (CHK2), H2A histone family member X (H2AX), and P53 among smokers and non-smokers with oral squamous cell carcinoma (OSCC). Associations between immunoexpression of proteins and clinicopathological data and histopathological grading were also analyzed. A total of 35 individuals (18 non-smokers and 17 smokers) with OSCC of the tongue and/or floor of the mouth were included. Immunohistochemistry for H2AX was conducted for the identification of double-strand breaks, CHK2, and P53 to evaluate the expression of this protein in cell cycle regulation. The sample consisted of 22 males and 13 females, with a mean age of 63.9±11.8 years. OSCC of non-smokers were well-differentiated tumors in 50% of the cases, and those of smokers were equally distributed into moderately differentiated and poorly differentiated tumors (35.3% each). Overall, 31 (88.6%) cases were CHK2-positive, 27 (77.1%) were H2AX-positive, and 23 (65.7%) were P53-positive, with no difference between smokers and non-smokers (p > 0.05). No association was found between proteins and clinicopathologic data (p > 0.05). Similarities in CHK2, H2AX, and P53 immunohistochemical staining patterns were observed between smokers and non-smokers, and immunoexpression was not associated with clinicopathological parameters. However, the findings indicated consistent expression of these proteins in OSCC.
“…Although non-signi cant, the patients that smoked cigarettes and drank alcohol tend to have higher risks of lymph node ENE. [19] It could be related with the mechanisms of tumorigenesis. Those oral cancers related with smoking and BQ could harbour more genetic alterations from the environment carcinogens exposure and can be easier to metastasize or have ENE.…”
Objectives: Oral cavity squamous cell carcinoma (OSCC) is a leading cause of death in Taiwan, and most of the patients are male. Little is known about the differences in risk factors, cancer characteristics and treatment outcomes in female patients. The study aim is to investigate the clinicopathological and outcome differences between gender in patients affected by oral cancer in Taiwan.Methods: This is a retrospective study based on data obtained between 1995 and 2019. A total of 2,046 patients were recruited for analysis. Cancer characteristics, risk factors and treatment outcomes in patients with oral cancer between genders were collected. Results: Female patients represented the 6.7% of the entire cohort of study. Females were diagnosed at an older age and at an earlier local stage compared to male patients (p < 0.001). The female patients were less exposed to cigarette, alcohol, and betel-nut (BQ) (all p-values < 0.001). Tongue (55.1%) was the most frequent subsite involved in the female group, while buccal (38.4%) and tongue (35.3%) were more likely (p < 0.001) to be associated with male gender. In tongue cancer subgroup, female patients presented less frequently extra-nodal extension compared with male patients (p = 0.040). During the follow-up period, there was no significant difference in recurrence and overall deaths between genders.Conclusion:In Taiwan, the male to female ratio in OSCC is 14:1. The tumor subsite distribution, environment exposure and stage distribution are different between females and male. There are no differences in term of survival between female and male OSCC patients.
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