Oral Cancer

John (Gold)
John (Gold)

March 6th, 2006, 1:08 am #1

U.S. National Cancer Institute - SEER Cancer Stat Fact Sheets Cancer of the Oral
Cavity and Pharynx
The American Cancer Society estimates that 29,370 men and women (19,100 men and 10,270 women) will be diagnosed with and 7,320 men and women will die of cancer of the oral cavity and pharynx in 20051.

The following information is based on NCI's SEER Cancer Statistics Review2 and other statistics from NCI's analysis of SEER incidence data and NCHS mortality data.

Incidence & Mortality SEER Incidence From 1998-2002, the median age at diagnosis for cancer of the oral cavity and pharynx was 63 years of age3. Approximately 0.6% were diagnosed under age 20; 2.7% between 20 and 34; 7.7% between 35 and 44; 20.2% between 45 and 54; 23.0% between 55 and 64; 23.0% between 65 and 74; 17.1% between 75 and 84; and 5.8% 85+ years of age.

The age-adjusted incidence rate was 10.5 per 100,000 men and women per year. These rates are based on cases diagnosed in 1998-2002 from 13 SEER geographic areas. Incidence rates by race and sex were:
Race/Ethnicity Men Women
All Races 15.5 per 100,000 men 6.4 per 100,000 women
White 15.4 per 100,000 men 6.4 per 100,000 women
Black 19.0 per 100,000 men 6.1 per 100,000 women
Asian/Pacific Islander 11.9 per 100,000 men 5.8 per 100,000 women
American Indian/Alaska Native 8.9 per 100,000 men 3.8 per 100,000 women
Hispanic 9.2 per 100,000 men 3.9 per 100,000 women

US Mortality From 1998-2002, the median age at death for cancer of the oral cavity and pharynx was 68 years of age4. Approximately 0.2% died under age 20; 0.9% between 20 and 34; 3.7% between 35 and 44; 13.9% between 45 and 54; 22.3% between 55 and 64; 25.6% between 65 and 74; 22.5% between 75 and 84; and 10.9% 85+ years of age.

The age-adjusted death rate was 2.8 per 100,000 men and women per year. These rates are based on patients who died in 1998-2002 in the US. Death rates by race and sex were:
Race/Ethnicity Men Women
All Races 4.2 per 100,000 men 1.6 per 100,000 women
White 3.9 per 100,000 men 1.6 per 100,000 women
Black 7.1 per 100,000 men 1.9 per 100,000 women
Asian/Pacific Islander 3.5 per 100,000 men 1.4 per 100,000 women
American Indian/Alaska Native 3.6 per 100,000 men 1.2 per 100,000 women
Hispanic 2.9 per 100,000 men 0.8 per 100,000 women

Trends in Rates Trends in rates can be described in many ways. Information for trends over a fixed period of time, for example 1992-2002, can be evaluated by the annual percentage change (APC). If there is a negative sign before the number, the trend is a decrease; otherwise it is an increase. If there is an asterisk after the APC then the trend was significant, that is, one believes that it is beyond chance, i.e. 95% sure, that the increase or decrease is real over the period 1992-2002. If the trend is not significant, the trend is usually reported as stable or level. Joinpoint analyses can be used over a long period of time to evaluate when changes in the trend have occurred along with the APC which shows how much the trend has changed between each of the joinpoints.

The joinpoint trend in SEER cancer incidence with associated APC(%) for cancer of the oral cavity and pharynx between 1975-2002 was:
All Races Male and Female: 0.8 for 1975-1981; -1.2* for 1981-2002
All Races Male: -0.1 for 1975-1983; -1.5* for 1983-2002
All Races Female: 2.6* for 1975-1980; -1.0* for 1980-2002

The joinpoint trend in US cancer mortality with associated APC(%) for cancer of the oral cavity and pharynx between 1975-2002 was:
All Races Male and Female: -0.4 for 1975-1979; -1.7* for 1979-1993; -2.5* for 1993-2002
All Races Male: -1.8* for 1975-1991; -2.6* for 1991-2002
All Races Female: -0.9* for 1975-1990; -2.4* for 1990-2002

Survival & Stage Survival rates can be calculated by different methods for different purposes. The survival rates presented here are based on the relative survival rate, which measures the survival of the cancer patients in comparison to the general population to estimate the effect of cancer. The overall 5-year relative survival rate for 1995-2001 from 9 SEER geographic areas was 59.4%. Five-year relative survival rates by race and sex were: 61.1% for white men; 63.1% for white women; 34.3% for black men; 52.0% for black women.

The stage distribution based on historic stage shows that 34% of oral cavity and pharynx cancer cases are diagnosed while the cancer is still confined to the primary site (localized stage); 51% are diagnosed after the cancer has spread to regional lymphnodes or directly beyond the primary site; 10% are diagnosed after the cancer has already metastasized (distant stage) and for the remaining 5% the staging information was unknown. The corresponding 5-year relative survival rates were: 82.1% for localized; 51.3% for regional; 27.6% for distant; and 46.6% for unstaged.

Lifetime Risk Based on rates from 2000-2002, 1.02% of men and women born today will be diagnosed with cancer of the oral cavity and pharynx at some time during their lifetime. This number can also be expressed as 1 in 98 men and women will be diagnosed with cancer of the oral cavity and pharynx during their lifetime. These statistics are called the lifetime risk of developing cancer. Sometimes it is more useful to look at the probability of developing cancer of the oral cavity and pharynx between two age groups. For example, 0.72% of men will develop cancer of the oral cavity and pharynx between their 50th and 70th birthdays compared to 0.26% for women.

Prevalence On January 1, 2002, in the United States there were approximately 231,799 men and women alive who had a history of cancer of the oral cavity and pharynx -- 147,272 men and 84,527 women. This includes any person alive on January 1, 2002 who had been diagnosed with cancer of the oral cavity and pharynx at any point prior to January 1, 2002 and includes persons with active disease and those who are cured of their disease. Prevalence can also be expressed as a percentage and it can also be calculated for a specific amount of time prior to January 1, 2002 such as disgnosed within 5 years of January 1, 2002.

References All statistics in this report are based on SEER incidence and NCHS mortality statistics. Most can be found within:

Ries LAG, Eisner MP, Kosary CL, Hankey BF, Miller BA, Clegg L, Mariotto A, Feuer EJ, Edwards BK (eds). SEER Cancer Statistics Review, 1975-2002, National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2002/, based on November 2004 SEER data submission, posted to the SEER web site 2005.

See below for specific referenced tables

1 Table I-1 (http://seer.cancer.gov/csr/1975_2002/re ... ble.01.pdf)
2Oral Cavity and Pharynx Section (http://seer.cancer.gov/csr/1975_2002/re ... cavity.pdf)
3 Table I-11 (http://seer.cancer.gov/csr/1975_2002/re ... 1_2pgs.pdf)
4 Table I-13 (http://seer.cancer.gov/csr/1975_2002/re ... 3_2pgs.pdf)

John (Gold)
John (Gold)

March 6th, 2006, 1:18 am #2

Oral Cavity and Pharynx Cancer Gina L. Day, Ph.D.*[/size]
* From the Epidemiology and Extramural Programs Branch, Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland[/size]
Nearly 30,000 new cases of oral cancer--cancers of the lip, tongue, mouth, and pharynx--were estimated for the United States in 1994, and about 7,900 people died of the disease (Boring et al., 1994). These cancers account for almost 4 percent of all malignancies. Except for salivary gland tumors, which are rare, almost all oral cancers are squamous cell carcinomas and share a common etiology. Overall five-year relative survival for oral cancer has remained stable at 40 to 50 percent for several decades. Prognosis varies considerably according to the site of the tumor, stage of disease at treatment, gender, and the age of the patient.
In Americans, oral cancer is two to three times more common among males than females. Over 90 percent of cases occur in persons over age 45, with an average age of 64 for whites and 57 for blacks. Like most epithelial tumors, risk of oral cancer increases with age. This cancer occurs more frequently in blacks than whites. During 1987-91, the average annual age-adjusted incidence rate for oral cancer in the United States was 15.8 cases per 100,000 persons per year among white men, 6.2 among white women, 23.7 among black men, and 6.5 among black women (Ries et al., 1994). The most commonly involved sites are the tongue, floor of mouth, gum and other parts of the mouth, lip, tonsil (oropharynx), and hypopharynx. Among white males, the gums and the floor of the mouth are the most frequently affected sites. Among black males, the most common site is the pharynx, or throat. In this country, differences in alcohol and tobacco use account for the bulk of the racial differences in oral cancer (Day et al., 1993). The highest oral cancer rates in the world (world standardized rates > 40/100,000) are reported in parts of France, India, and Southeast Asia (Parkin et al., 1992).
Tobacco and alcohol account for approximately three-fourths of all oral cancers in the U.S. (Blot et al., 1988) and are the primary causes of these cancers in most Western countries (IARC 1986, 1988). In some parts of the country, smokeless tobacco use contributes to the high rates of gum and buccal cancers (Surgeon General, 1986). Recent epidemiologic evidence indicates that smoking and drinking are independent risk factors for oral cancer that produce a synergistic effect when combined. In the largest population-based case-control study of oral cancer yet conducted (Blot et al., 1988), strong positive trends in risk were observed according to amount and duration of each type of tobacco and for amount of alcohol consumption. Relative to nonsmokers, heavy cigarette smokers (40+/day for 20+ years) experienced a four-fold risk (men) and ten-fold risk (women) after adjusting for alcohol intake. After controlling for smoking, moderate drinkers (15-29 alcoholic drinks/week) had a three-fold risk of oral cancer and heavy drinkers (> 30 drinks/week) experienced an eight- to nine-fold risk. Combined heavy smoking and drinking resulted in a greater than 35-fold excess risk.
The decline in risk of oral cancer following cessation of smoking is particularly rapid, providing further evidence of the role of smoking. In the study by Blot and coworkers, the risk of quitters was less than half that of continuing smokers five years following cessation of smoking, and little or no elevation in risk was found among those who had quit smoking for ten or more years. The chewing of quids containing betel leaves, tobacco, and lime and the smoking of bidi (a tobacco preparation rolled in betel leaf) contribute to the majority of cases in parts of India and Southeast Asia (Mahboubi and Sayed, 1982; Jayant and Deo, 1986). In the southern United States, use of snuff is the primary cause of cancers arising in the cheek and gum (Winn et al., 1981). Among users of snuff, cancerous lesions typically arise at the site where smokeless tobacco, or quid, is held in contact with the buccal mucosa or gingiva. Although not as prevalent as cigarette smoking, habitual use of pipes, cigars, and smokeless tobacco is associated with relative risks for cancers of the mouth as great as that for cigarette smoking.
Among other potential etiologic factors, recent epidemiologic studies have indicated that diet may play an important role in the origins of these cancers. Findings have pointed to the protective effects of a diet consistently high in fresh fruits; vegetables; vitamins A, C, and E; and carotenoids, even with adjustment for alcohol intake and smoking (McLaughlin et al., 1988; Franco et al., 1989; Gridley et al., 1990; Franceschi et al., 1991; La Vecchia et al., 1991). A reduced risk of oral cancer associated with vitamin E supplementation has been shown in one study (Gridley et al., 1992). Poor dentition and oral hygiene, trauma due to ill-fitting dentures or jagged teeth, and use of mouthwashes high in alcohol content may enhance oral cancer risk (Winn et al., 1991). Iron deficiency anemia, a relatively common disorder, may produce atrophic oral changes (as seen in patients with Plummer-Vinson syndrome) that may predispose to malignant transformation. Certain generalized skin diseases, such as syphilis and erosive lichen planus, have been implicated as a contributory factor in the development of cancers of the tongue (Mahboubi and Sayed, 1982). DNA viruses, including human papillomaviruses and herpes simplex viruses, have been suggested as possible risk factors, but their role remains to be clarified (Maden, 1992).
Associations with other factors, such as urban residence, lower socioeconomic status, and social instability have been found (Greenberg et al., 1991); however, these factors are highly correlated with patterns of exposure to the major risk factors, tobacco and alcohol. Although some early studies have suggested that certain occupational groups, including textiles, metal, and steel workers, as well as persons exposed to asbestos and polyvinyl chloride, have a higher than expected rate of oral cancer (Mahboubi and Sayed, 1982), available epidemiologic evidence indicates that the occupational component does not play a large role in oral cancer etiology. Outdoor work (or sunlight exposure) has been linked to lip cancer, and an increased risk of salivary gland tumors has been associated with ionizing radiation (Mahboubi and Sayed, 1982).
Oral leukoplakia is the most common precancerous lesion, with a small percent of such lesions ultimately becoming malignant. Oral cancer is also characterized by an exceptionally high incidence of subsequent tumors in the same site or adjacent sites in the upper digestive and respiratory tracts. Major determinants of new primaries following oral cancer are high levels of tobacco smoking and alcohol drinking (Day et al., 1994).
Based on available information, oral cancer is highly preventable. Quitting smoking and limiting alcohol intake would greatly limit deaths from this disease.
Blot WJ, McLaughlin JK, Winn DM, et al.: Smoking and drinking in relation to oral and pharyngeal cancer. Cancer Res 48:3282-7, 1988.

Boring CC, Squires TS, Tong T, et al.: Cancer Statistics 1994. CA Cancer J Clin 44:7-26, 1994.

Day GL and Blot WJ: Second primary tumors in patients with oral cancer. Cancer 70:14-19, 1992.

Day GL, Blot WJ, Austin DF, et al.: Racial differences in risk of oral and pharyngeal cancer: Alcohol, tobacco, and other determinants. J Natl Cancer Inst 85:465-473, 1993.

Day GL, Blot WJ, Shore RE, et al.: Second cancers following oral and pharyngeal cancer: the role of tobacco and alcohol. J Natl Cancer Inst 86:131-137, 1994.

Franceschi S, Bidoli E, Baron AE, et al.: Nutrition and cancer of the oral cavity and pharynx. Int J Cancer 40:20-25, 1991.

Franco EL, Kowalski LP, Oliviera BV, et al.: Risk factors for oral cancer in Brazil: a case-control study. Int J Cancer 43:992-1000, 1989.

Greenberg RS, Haber MJ, Clark WS, et al.: The relation of socioeconomic status to oral and pharyngeal cancer. Epidemiology 2:194-200, 1991.

Gridley G, McLaughlin JK, Block G, et al.: Diet and oral and pharyngeal cancer among blacks. Nutr Cancer 14: 219-225, 1990.

Gridley G, McLaughlin JK, Block G, et al.: Vitamin supplement use and reduced risk of oral and pharyngeal cancer. Am J Epidemiol 135:1083-1092, 1992.

IARC (1986): IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans, vol 38, Tobacco Smoking. Lyon, 1986.

IARC (1988): IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans, vol 44, Alcohol Drinking. Lyon, 1988.

Jayant K and Deo MG: Oral cancer and culture practices in relation to betel quid and tobacco chewing and smoking. Cancer Detect Prev 9:207-213, 1986.

La Vecchia C, Negri E, D'Avanzo B, et al.: Dietary indicators of oral and pharyngeal cancer. Int J Epidemiol 20:39-44, 1991.

Maden C, Beckman AM, Thomas DB, et al.: Human papillomavirus, herpes simplex virus and the risk of oral cancer in men. Am J Epidemiol 135:1093-1102, 1992.

Mahboubi E and Sayed GM: Oral Cavity and Pharynx. pp. 583-595. In Cancer Epidemiology and Prevention (Schottenfeld D, Fraumeni JF Jr, eds.). Philadelphia: W.B. Saunders, 1982.

McLaughlin JK, Gridley G, Block G, et al.: Dietary factors in oral and pharyngeal cancer. J Natl Cancer Inst 80:1237-1243, 1988.

Parkin DM, Muir CS, Whelan S, et al. (eds.): Cancer Incidence in Five Continents, vol VI. IARC Scientific Publication No. 120. World Health Organization, International Agency for Research on Cancer, Lyon, 1992.

Ries LAG, Miller BA, Hankey BF, et al.: SEER Cancer Statistics Review, 1973-1991: Tables and Graphs, National Cancer Institute. NIH Publ. No. 94-2789, Bethesda, MD, 1994.

Surgeon General: The Health Consequences of Using Smokeless Tobacco. Department of Health and Human Services, NIH Publ. No. 86-2874, Bethesda, MD, 1986.

Winn DM, Blot WJ, McLaughlin JK, et al.: Mouthwash use and oral conditions in the risk of oral and pharyngeal cancer. Cancer Res 51:3044-47, 1991.

Winn DM, Blot WJ, Shy CM, et al.: Snuff dipping and oral cancer among women in the southern United States. N Engl J Med 305:745-749, 1981.

Joined: November 11th, 2008, 7:22 pm

October 6th, 2010, 2:45 pm #3

The aetiology of upper aerodigestive tract
cancers among young adults in Europe:
the ARCAGE study

Journal:  Cancer Causes Control. 2010 Sep 11. [Epub ahead of print]

Macfarlane TV, Macfarlane GJ, Oliver RJ, Benhamou S, Bouchardy C, Ahrens W, Pohlabeln H, Lagiou P, Lagiou A, Castellsague X, Agudo A, Merletti F, Richiardi L, Kjaerheim K, Slamova A, Schejbalova M, Canova C, Simonato L, Talamini R, Barzan L, Conway DI, McKinney PA, Znaor A, Lowry RJ, Thomson P, Healy CM, McCartan BE, Marron M, Hashibe M, Brennan P.


BACKGROUND: The incidence of cancers of the upper aerodigestive tract (UADT) is increasing throughout the world. To date the increases have been proportionally greatest among young people. Several reports have suggested that they often do not have a history of tobacco smoking or heavy alcohol consumption.

OBJECTIVE: To determine the contribution of lifestyle factors to the etiology of UADT cancers occurring in those aged less than 50 years.

METHODS: A case-control study was conducted in 10 European countries. Cases were cancers of the oral cavity and pharynx, larynx and esophagus, and hospital or population controls were age and sex matched.

RESULTS: There were 356 cases younger than 50 years and 419 controls. Risk was strongly related to current smoking [odds ratio (OR) 5.5 95%; confidence interval (CI) (3.3, 9.2)], and risk increased with number of pack-years smoked. Risk was also related to alcohol consumption for both current (OR 1.8; 0.97, 3.3) and past (OR 3.4; 1.6, 7.4) drinkers, and risk increased with number of drink-years. Persons frequently consuming fruits and vegetables were at significantly reduced risk.

CONCLUSIONS: Risk factors already identified as being important for UADT cancers in adults are also important influences on risk in younger adults. The implication of these results is that the public health message in preventing UADT cancers remains the same to young and old alike.

http://www.springerlink.com/content/b34 ... lltext.pdf