The epidemiology of tongue cancer: a review of global incidence

Moore, SR; Johnson, Newell W.; Pierce, AM; Df, Wilson

doi:10.1111/j.1601-0825.2000.tb00105.x

Cited by 135 publications

(128 citation statements)

References 49 publications

(77 reference statements)

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“…5,[9][10][11][12][13][14][15][16][17] Furthermore, increased oral cancer mortality rates reported between 1955 and 1989 in several European countries among young adults (<44 years) were also observed for other smoking-related cancers (eg, lung and esophagus). 18 Although incidence rates and trends over time varied substantially from country to country, 1,19,20 regional trends in oral cavity incidence were largely mirrored by similar trends for oropharynx cancers. 12 In addition to the strong effect of year of birth, incidence rates substantially increased with age 13 and were consistently higher in men when compared with women.…”

Section: Trends In Incidence Of Oral Cavity and Oropharyngeal Cancersmentioning

confidence: 99%

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Current topics in the epidemiology of oral cavity and oropharyngeal cancers

2007

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Oral cancer incidence rates rose dramatically during the twentieth century in the United States and Europe, especially among individuals under the age of 60 years. Although influenced by age, sex, and country of origin, incidence trends were most strongly affected by elevated risk among individuals born after approximately 1915. This cohort effect was indicative of strong behavioral influences on oral cancer risk. In this article, associations between oral cancer risk and established behavioral risk factors including alcohol and tobacco use are reviewed. Additionally, possible associations between oral cancer risk and oral hygiene, diet, nutritional status, and sexual behavior as well as the influence of genetic factors on oral cancer risk are considered. Special emphasis is placed on evaluating possible risk differences in individuals above and below the age of 45 and in users and nonusers of alcohol and tobacco. Oral squamous cell carcinomas arise from several anatomic sites within the oral cavity and oropharynx, but most commonly from the oral, mobile tongue.1 In the 1980s, 2 cancer centers in the United States (U.S.) reported an increase in the proportion of incident oral tongue cancers diagnosed in men younger 40 years.2,3 Although absolute numbers had increased, these reports provided no real evidence of rising incidence. Shortly thereafter, however, a significant 2-fold increase in oral tongue cancer mortality rates between 1950 and 1982 was reported in the U.S. for men younger than 30 years. 4 This finding was corroborated by a study in Scotland. 5 Further analysis of the Scottish data revealed that the increase in incidence was not restricted to those younger than 40 but extended to all age groups less than 65 years of age born after 1920-a strong ''cohort effect.'' The cohort effect was indicated by a strong effect of year of birth on oral cancer incidence rates. A flurry of research on global changes in oral cancer incidence was stimulated by these reports.

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Section: Trends In Incidence Of Oral Cavity and Oropharyngeal Cancersmentioning

confidence: 99%

“…1 In the 1980s, 2 cancer centers in the United States (U.S.) reported an increase in the proportion of incident oral tongue cancers diagnosed in men younger 40 years. 2,3 Although absolute numbers had increased, these reports provided no real evidence of rising incidence.…”

Section: Trends In Incidence Of Oral Cavity and Oropharyngeal Cancersmentioning

confidence: 99%

Current topics in the epidemiology of oral cavity and oropharyngeal cancers

2007

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“…The prognosis of oral cancer, the major site being the tongue, is equally dismal, with an increasing incidence worldwide, particularly in young adults. 2 Patients with oral cancer have a high mortality rate, because of field cancerization effects that result in second primary tumors, particularly in the esophagus. 3,4 Thus, new chemopreventive and therapeutic approaches are much needed to prevent and treat these deadly cancers.…”

mentioning

confidence: 99%

Prevention of upper aerodigestive tract cancer in zinc‐deficient rodents: Inefficacy of genetic or pharmacological disruption of COX‐2

Fong¹,

Jiang²,

Riley³

et al. 2007

Intl Journal of Cancer

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Zinc deficiency in humans is associated with an increased risk of upper aerodigestive tract (UADT) cancer. In rodents, zinc deficiency predisposes to carcinogenesis by causing proliferation and alterations in gene expression. We examined whether in zinc-deficient rodents, targeted disruption of the cyclooxygenase (COX)-2 pathway by the COX-2 selective inhibitor celecoxib or by genetic deletion prevent UADT carcinogenesis. Tongue cancer prevention studies were conducted in zinc-deficient rats previously exposed to a tongue carcinogen by celecoxib treatment with or without zinc replenishment, or by zinc replenishment alone. The ability of genetic COX-2 deletion to protect against chemically-induced forestomach tumorigenesis was examined in mice on zinc-deficient versus zinc-sufficient diet. The expression of 3 predictive biomarkers COX-2, nuclear factor (NF)-j B p65 and leukotriene A 4 hydrolase (LTA 4 H) was examined by immunohistochemistry. In zinc-deficient rats, celecoxib without zinc replenishment reduced lingual tumor multiplicity but not progression to malignancy. Celecoxib with zinc replenishment or zinc replenishment alone significantly lowered lingual squamous cell carcinoma incidence, as well as tumor multiplicity. Celecoxib alone reduced overexpression of the 3 biomarkers in tumors slightly, compared with intervention with zinc replenishment. Instead of being protected, zinc-deficient COX-2 null mice developed significantly greater tumor multiplicity and forestomach carcinoma incidence than wild-type controls. Additionally, zinc-deficient COX-22/2 forestomachs displayed strong LTA 4 H immunostaining, indicating activation of an alternative pathway under zinc deficiency when the COX-2 pathway is blocked. Thus, targeting only the COX-2 pathway in zinc-deficient animals did not prevent UADT carcinogenesis. Our data suggest zinc supplementation should be more thoroughly explored in human prevention clinical trials for UADT cancer. ' 2007 Wiley-Liss, Inc.Key words: zinc deficiency; upper aerodigestive tract cancer; chemoprevention; COX-2; COX-2 null mice Upper aerodigestive tract (UADT) cancer, including esophageal and oral cancer, is an important cause of morbidity and mortality worldwide. 1 With a 5-year survival of 10%, esophageal cancers are deadly. The prognosis of oral cancer, the major site being the tongue, is equally dismal, with an increasing incidence worldwide, particularly in young adults. 2 Patients with oral cancer have a high mortality rate, because of field cancerization effects that result in second primary tumors, particularly in the esophagus. 3,4 Thus, new chemopreventive and therapeutic approaches are much needed to prevent and treat these deadly cancers.While chronic alcohol consumption and tobacco use are the major risk factors for UADT cancer, epidemiologic and clinical studies have implicated dietary zinc deficiency (ZD) in the etiology of esophageal squamous cell carcinoma (SCC) and head and neck SCC. [5][6][7][8][9] In 2005, Abnet et al. 10 provided the strongest evidence of an a...

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“…Squamous cell carcinoma (SCCa) is responsible for over 90% of cases with an estimated incidence of 3.0/100,000 in the United States [1,2]. Males with a history of tobacco and alcohol use are at greatest risk and commonly present with early stage lesions.…”

Section: Introductionmentioning

confidence: 99%

Improved Early Stage (T1/2) Oral Tongue Cancer Medial Pathology Margins Using Horizontal Mattress Suture Technique

Vasan¹

2017

BJSTR

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The epidemiology of tongue cancer: a review of global incidence

Cited by 135 publications

References 49 publications

Current topics in the epidemiology of oral cavity and oropharyngeal cancers

Current topics in the epidemiology of oral cavity and oropharyngeal cancers

Prevention of upper aerodigestive tract cancer in zinc‐deficient rodents: Inefficacy of genetic or pharmacological disruption of COX‐2

Improved Early Stage (T1/2) Oral Tongue Cancer Medial Pathology Margins Using Horizontal Mattress Suture Technique

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