Incidence and Mortality
Risk Factors

Incidence and Mortality

Annually, it is estimated that 16,470 Americans will be diagnosed with esophageal cancer and 14,280 will die of this malignancy. Of the new cases, it is estimated that 12,970 will occur in men and 3,500 will occur in women.[1]

Two histological types account for the majority of malignant esophageal neoplasms: adenocarcinoma and squamous carcinoma. The epidemiology of these types varies markedly. In the 1960s, squamous cell cancers comprised over 90% of all esophageal tumors. The incidence of esophageal adenocarcinomas has risen markedly over the past 2 decades, such that it is now more prevalent than squamous cell cancer in the United States and Western Europe, with most tumors located in the distal esophagus.[2]. Although the overall incidence of squamous cell carcinoma of the esophagus is declining, this histologic type remains six times more likely to occur in black males than in white males.[3] Incidence rates generally increase with age in all racial/ethnic groups. In black men, however, the incidence rate for those aged 55 to 69 years is close to that of whites aged 70 years and older. In black women, aged 55 to 69 years, the incidence rate is slightly higher than that of white women aged 70 years and older.

While risk factors for squamous cell carcinoma of the esophagus have been identified (such as tobacco use, alcoholism, malnutrition, and infection with human papillomavirus),[4] the risk factors associated with esophageal adenocarcinoma are less well defined. The most important epidemiological difference between squamous cell cancer and adenocarcinoma, however, is the strong association between gastroesophageal reflux disease (GERD) and adenocarcinoma. The results of a population-based case-controlled study suggest that symptomatic gastroesophageal reflux is a risk factor for esophageal adenocarcinoma. The frequency, severity, and duration of reflux symptoms were positively associated with increased risk of esophageal adenocarcinoma.[5]

An interesting hypothesis relates the rise in the incidence of esophageal adenocarcinoma to a declining prevalence of Helicobacter pylori infection in Western countries. Reports have suggested that gastric infection with H. pylori may protect the esophagus from GERD and its complications.[6] According to this theory, H. pylori infections that cause pangastritis also cause a decrease in gastric acid production that protects against GERD.[7] Patients whose duodenal ulcers were treated successfully with antibiotics developed reflux esophagitis twice as often as those in whom infection persisted.[8] Other factors that have been suggested to explain the increased risk of esophageal adenocarcinoma include obesity [9] and use of medications, such as anticholinergics that can predispose to GERD by relaxing the lower esophageal sphincter.[10]

GERD is a risk factor for esophageal adenocarcinoma because long-standing GERD is associated with Barrett esophagus, the condition in which an abnormal intestinal epithelium replaces the stratified squamous epithelium that normally lines the distal esophagus.[11] The intestinal-type epithelium of Barrett esophagus has a characteristic endoscopic appearance that differs from squamous epithelium.[12] Dysplasia in Barrett epithelium represents a neoplastic alteration of the columnar epithelium that may progress to invasive adenocarcinoma.[13]

References

1. American Cancer Society.: Cancer Facts and Figures 2008. Atlanta, Ga: American Cancer Society, 2008. Also available online. Last accessed October 1, 2008. 
   
   
2. Holmes RS, Vaughan TL: Epidemiology and pathogenesis of esophageal cancer. Semin Radiat Oncol 17 (1): 2-9, 2007.  [PUBMED Abstract]
   
   
3. Devesa SS, Blot WJ, Fraumeni JF Jr: Changing patterns in the incidence of esophageal and gastric carcinoma in the United States. Cancer 83 (10): 2049-53, 1998.  [PUBMED Abstract]
   
   
4. Siemiatycki J, Krewski D, Franco E, et al.: Associations between cigarette smoking and each of 21 types of cancer: a multi-site case-control study. Int J Epidemiol 24 (3): 504-14, 1995.  [PUBMED Abstract]
   
   
5. Lagergren J, Bergström R, Lindgren A, et al.: Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med 340 (11): 825-31, 1999.  [PUBMED Abstract]
   
   
6. O'Connor HJ: Review article: Helicobacter pylori and gastro-oesophageal reflux disease-clinical implications and management. Aliment Pharmacol Ther 13 (2): 117-27, 1999.  [PUBMED Abstract]
   
   
7. Graham DY, Yamaoka Y: H. pylori and cagA: relationships with gastric cancer, duodenal ulcer, and reflux esophagitis and its complications. Helicobacter 3 (3): 145-51, 1998.  [PUBMED Abstract]
   
   
8. Labenz J, Blum AL, Bayerdörffer E, et al.: Curing Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis. Gastroenterology 112 (5): 1442-7, 1997.  [PUBMED Abstract]
   
   
9. Lagergren J: Controversies surrounding body mass, reflux, and risk of oesophageal adenocarcinoma. Lancet Oncol 7 (4): 347-9, 2006.  [PUBMED Abstract]
   
   
10. Lagergren J, Bergström R, Adami HO, et al.: Association between medications that relax the lower esophageal sphincter and risk for esophageal adenocarcinoma. Ann Intern Med 133 (3): 165-75, 2000.  [PUBMED Abstract]
    
    
11. Spechler SJ, Goyal RK: The columnar-lined esophagus, intestinal metaplasia, and Norman Barrett. Gastroenterology 110 (2): 614-21, 1996.  [PUBMED Abstract]
    
    
12. Van Dam J, Brugge WR: Endoscopy of the upper gastrointestinal tract. N Engl J Med 341 (23): 1738-48, 1999.  [PUBMED Abstract]
    
    
13. Reid BJ, Blount PL, Rabinovitch PS: Biomarkers in Barrett's esophagus. Gastrointest Endosc Clin N Am 13 (2): 369-97, 2003.  [PUBMED Abstract]
    
    

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