Tongue cancer causes
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]
Overview
Causes
The causes of tongue cancer includes the following:
- Tobacco
- Cancer of the tongue is correlated the closest with the use of tobacco products.
- Approximately 90% of patients with oral cavity cancers use tobacco products and that the relative risk of oral cavity cancers increases with the amount smoked and the duration of the smoking.
- In persons who smoke the incidence of oral cavity cancers is approximately six times that of those who do not smoke.
- Tobacco exposure causes progressive sequential histological changes to the oral mucosa. Prolonged period of exposure eventually leads to neoplastic transformation, in particular changes in the expression of p53 mutations. If the tobacco exposure is discontinued, these changes may be reversible.
- There is compelling evidence supporting the benefit for head and neck cancer patients to cease smoking after treatment for their cancer. Approximately 40% of patients who continued to smoke after definitive treatment for an oral cavity malignancy developed recurrence or developed a second head and neck malignancy. In patients who stopped smoking after treatment, approximately 6% went on to develop a recurrence.
- There has been recent increase in the incidence of oral cavity cancer in young adults in the recent years. The explosive use of smokeless tobacco, or snuff, in certain regions of the United States has lead to increased numbers of mandibular alveolus, buccal mucosa, and tongue cancers.
- Alcohol
- The correlation between alcohol consumption, particularly hard liquor, and oral cavity cancer is significant, especially in patients taking more than four consumptions per day.
- Approximately 75% of patients who develop oral cavity cancers consume alcohol, and the cancer occurs six times more often in persons who drink than in those who do not drink. The role of alcohol consumption in the development of tongue cancer appears to be independent of smoking.
- The use of alcohol has a synergistic effect on the risk of carcinogenesis rather than cumulative effect. The risk for a person who drinks alcohol and smokes tobacco is fifteen times that of an individual with neither of these habits.
- Other factors
- A number of other factors have been associated with an increased incidence of tongue cancer such as the use of the product of the Areca catechu tree, the betel nuts or quid as well as the use of slaked lime. This mixture is highly irritating to the oral mucosa, and as well as carcinogenic.
- The mutations in tumor suppressor genes has been reported in patients with cancers of the oral cavity. The most abundant carcinogens in tobacco constitute nitrosamines. Nitrosamines can damage DNA, leading to point mutations. These point mutations lead to deregulation of tumor suppressor genes (TP53), which is located on chromosome 17. The other oncogenes associated with oral squamous cell cancers of tongue include c-myc and erb -b1.
- The human papillomavirus, an epitheliotropic DNA virus, is another etiologic agent for carcinogenesis, transforming cells to a malignant phenotype. Human papillomavirus (HPV) has been detected in various amounts in persons with oral dysplasia, leukoplakia, and malignancy. In the subset of patients without other risk factors, HPV should be considered as an etiologic factor, and proper handling of biopsy specimens be sent for analysis. See also Human Papillomavirus.
- Plummer-Vinson syndrome (Fe deficiency anemia; achlorhydria; and mucosal atrophy of the mouth, pharynx, and esophagus) has been associated with an increased risk of cancer of the tongue. Increasing amounts of data suggest that vitamins A and C, along with the carotenoids, may be protective against epithelial cancers. Riboflavin and iron deficiencies are known to produce dysplastic changes to the oral mucosa. This may partly explain its relationship to alcoholism, which may result in riboflavin deficiency and oral cancer.
The role of occupational and environmental exposures in the development of cancer is an expanding field of study and may eventually be more important once the underlying molecular biology of cancer is better understood.