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Esophageal Cancer Prevention (PDQ®)

Health Professional Version
Last Modified: 07/17/2014

Overview

Note: Separate PDQ summaries on Esophageal Cancer Screening, Esophageal Cancer Treatment, and Levels of Evidence for Cancer Screening and Prevention Studies are also available.

Squamous Cell Carcinoma of the Esophagus

Who is at risk?

Smoking and drinking alcohol may account for roughly 90% of esophageal squamous cell carcinoma cases in Western countries like the United States.[1]

Factors with adequate evidence of increased risk of squamous cell carcinoma of the esophagus

Cigarette smoking and drinking alcohol

Based on solid evidence, smoking cigarettes and drinking alcohol increases the risk of esophageal squamous cell carcinoma. Smoking and drinking alcohol may account for roughly 90% of esophageal squamous cell carcinoma in Western countries like the United States.[1]

Magnitude of Effect: Increased risk, moderate magnitude.

Study Design: Evidence from population-based case-control and cohort studies.
Internal Validity: Fair.
Consistency: Good.
External Validity: Fair.
Helicobacter pylori infection and gastric atrophy

Based on fair evidence, serum cytotoxin-associated gene A (CagA) antibodies and gastric atrophy are associated with an increased risk of esophageal squamous cell carcinoma (odds ratio [OR], 2.1; 95% CI, 1.1–4.0 and OR, 4.3; 95% confidence interval [CI], 1.9–9.6, respectively).[2]

Magnitude of effect: Unknown magnitude but probably small in terms of absolute risk.

Study Design: Evidence from cohort or case-control studies.
Internal Validity: Fair.
Consistency: Large study.
External Validity: Fair.
Factors with adequate evidence of decreased risk of squamous cell carcinoma of the esophagus

Avoidance of tobacco and alcohol

Based on solid evidence, avoidance of tobacco and alcohol would decrease the risk of squamous cell carcinoma.[1,3]

Magnitude of Effect: Large positive benefit.

Study Design: Evidence obtained from cohort or case-control studies.
Internal Validity: Fair.
Consistency: Multiple studies.
External Validity: Fair.
Chemoprevention

Aspirin and nonsteroidal anti-inflammatory drug (NSAID) use

Benefits

Based on fair evidence, epidemiologic studies have found that aspirin or NSAID use is associated with decreased risk of developing or dying from esophageal cancer (OR, 0.57; 95% CI, 0.47–0.71).[4]

Magnitude of Effect: Small positive.

Study Design: Evidence obtained from cohort or case-control studies.
Internal Validity: Fair.
Consistency: Good.
External Validity: Fair.
Harms

Based on solid evidence, harms of NSAID use include upper gastrointestinal bleeding and serious cardiovascular events, such as myocardial infarction, heart failure, hemorrhagic stroke, and renal impairment.

Magnitude of Effect: Increased risk, small magnitude.

Study Design: Evidence obtained from randomized controlled trials.
Internal Validity: Fair.
Consistency: Good.
External Validity: Fair.
Adenocarcinoma of the Esophagus

Factors with adequate evidence of increased risk of adenocarcinoma of the esophagus

Gastroesophageal reflux/Barrett esophagus

Based on fair evidence, an association exists between gastroesophageal reflux disease (GERD) and adenocarcinoma, particularly if the GERD is long-standing and symptoms are severe.[5,6] In a case-control study from Sweden, the OR for patients with recurrent reflux symptoms was 7.7, while the OR for patients with long-standing and severe symptoms was 43.5 (95% CI, 18.3–103.5).[7]

It is unknown whether elimination of gastroesophageal reflux by surgical or medical means will reduce the risk of adenocarcinoma of the esophagus.[7,8]

Magnitude of Effect: Unknown.

Study Design: Ecologic and descriptive studies.
Internal Validity: Fair.
Consistency: Good; multiple studies.
External Validity: Fair.
Interventions with adequate evidence of decreased risk adenocarcinoma of the esophagus

Aspirin and NSAID use

Benefits

Based on fair evidence, epidemiologic studies have found that aspirin or NSAID use is associated with decreased risk of developing or dying from esophageal cancer (OR, 0.57; 95% CI, 0.47–0.71).[4,9]

Magnitude of Effect: Positive; unknown magnitude.

Study Design: Evidence obtained from cohort or case-control studies.
Internal Validity: Fair.
Consistency: Good.
External Validity: Fair.
Harms

Based on solid evidence, harms of NSAID use include upper gastrointestinal bleeding and serious cardiovascular events, such as myocardial infarction, heart failure, hemorrhagic stroke, and renal impairment.

Magnitude of Effect: Increased risk; small magnitude.

Study Design: Evidence obtained from randomized controlled trials.
Internal Validity: Good.
Consistency: Good.
External Validity: Good.
Ablation of Barrett esophagus with dysplasia

Benefits

A randomized controlled trial has found that radiofrequency ablation of Barrett esophagus with severe dysplasia may lead to eradication of both dysplasia and intestinal metaplasia and a reduced risk of disease progression.[10]

Magnitude of Effect: : Impact on cancer mortality not known.

Study Design: Evidence obtained from a randomized controlled trial.
Internal Validity: Good.
Consistency: Single study.
External Validity: Good.
Harms

Based on solid evidence, harms of radiofrequency ablation include esophageal stricture and requirement for dilatation and upper gastrointestinal hemorrhage but at low rates. It is possible that overdiagnosis and overtreatment of Barrett esophagus, particularly without severe dysplasia, could lead to a substantial number of harms.

Magnitude of Effect: The low rates of esophageal stricture and requirement for dilatation and upper gastrointestinal hemorrhage may be an understatement of the risks if this practice is widely adopted by less-experienced physicians.

Study Design: Evidence obtained from a randomized controlled trial.
Internal Validity: Good.
Consistency: Single study.
External Validity: Patients representative of a subset of people with dysplasia, particularly severe dysplasia; physicians may not be representative of practicing physicians because this is a new technology and requires specialized knowledge.
References
  1. Engel LS, Chow WH, Vaughan TL, et al.: Population attributable risks of esophageal and gastric cancers. J Natl Cancer Inst 95 (18): 1404-13, 2003.  [PUBMED Abstract]

  2. Ye W, Held M, Lagergren J, et al.: Helicobacter pylori infection and gastric atrophy: risk of adenocarcinoma and squamous-cell carcinoma of the esophagus and adenocarcinoma of the gastric cardia. J Natl Cancer Inst 96 (5): 388-96, 2004.  [PUBMED Abstract]

  3. 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]

  4. Corley DA, Kerlikowske K, Verma R, et al.: Protective association of aspirin/NSAIDs and esophageal cancer: a systematic review and meta-analysis. Gastroenterology 124 (1): 47-56, 2003.  [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. Fitzgerald RC: Molecular basis of Barrett's oesophagus and oesophageal adenocarcinoma. Gut 55 (12): 1810-20, 2006.  [PUBMED Abstract]

  7. Lagergren J, Ye W, Lagergren P, et al.: The risk of esophageal adenocarcinoma after antireflux surgery. Gastroenterology 138 (4): 1297-301, 2010.  [PUBMED Abstract]

  8. Spechler SJ, Goyal RK: The columnar-lined esophagus, intestinal metaplasia, and Norman Barrett. Gastroenterology 110 (2): 614-21, 1996.  [PUBMED Abstract]

  9. Liao LM, Vaughan TL, Corley DA, et al.: Nonsteroidal anti-inflammatory drug use reduces risk of adenocarcinomas of the esophagus and esophagogastric junction in a pooled analysis. Gastroenterology 142 (3): 442-452.e5; quiz e22-3, 2012.  [PUBMED Abstract]

  10. Shaheen NJ, Sharma P, Overholt BF, et al.: Radiofrequency ablation in Barrett's esophagus with dysplasia. N Engl J Med 360 (22): 2277-88, 2009.  [PUBMED Abstract]

Description of the Evidence



Background

Two histological types account for most malignant esophageal neoplasms: adenocarcinoma and squamous cell carcinoma. The epidemiology of these types varies markedly. In the 1960s, squamous cell carcinomas comprised over 90% of all esophageal tumors. The incidence of esophageal adenocarcinomas has risen markedly for the past 2 decades; it is now more prevalent than squamous cell carcinomas in the United States and Western Europe, with most tumors located in the distal esophagus.[1]

Incidence and Mortality

In 2014, it is estimated that 18,170 Americans will be diagnosed with esophageal cancer and 15,450 will die of this malignancy. Of the new cases, it is estimated that 14,660 will occur in men and 3,510 will occur in women.[2] 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.[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] In contrast, the incidence of adenocarcinoma of the esophagus rapidly increased from the 1970s to the mid-1990s.[4]

Male gender is an important predictor of adenocarcinoma of the esophagus. The attributable risk is low enough in women that, although the risk from gender is not modifiable, other risk factors necessarily have limited impact.[4]

Squamous Cell Carcinoma of the Esophagus

Factors with adequate evidence of increased risk of squamous cell carcinoma of the esophagus

Smoking cigarettes and drinking alcohol

In the United States, squamous cell carcinoma of the esophagus is strongly associated with tobacco and alcohol abuse. The relative risk associated with tobacco use is 2.4, and the population attributable risk is 54.2% (95% confidence interval [CI], 3.0–76.2).[5,6] Retrospective cohort studies adjusted for tobacco use have shown a twofold to sevenfold increase in risk of esophageal cancer in alcoholics compared with rates for the general population.[5] Case-control studies have also suggested a significantly increased risk of cancer of the esophagus associated with alcohol abuse.

In a multicenter, population-based, case-control study of 221 patients with esophageal squamous cell carcinoma and 695 controls, ever-smoking, alcohol consumption, and low fruit and vegetable consumption accounted for 56.9% (95% CI, 36.6%–75.1%), 72.4% (95% CI, 53.3%–85.8%), and 28.7% (95% CI, 11.1%–56.5%) of esophageal squamous cell carcinomas, respectively, with a combined population attributable risk of 89.4% (95% CI, 79.1%–95.0%).[7]

In China, where the overall prevalence of esophageal carcinoma is much higher than in the United States, esophageal cancer is associated with deficiencies of nutrients, such as retinol, riboflavin, alpha-carotene, beta-carotene, alpha-tocopherol, ascorbate and zinc, and with exposure to specific carcinogens (e.g., N-nitroso compounds).[5]

Factors with adequate evidence of decreased risk of squamous cell carcinoma of the esophagus

Chemoprevention

A prospective, placebo-controlled, esophagus chemoprevention study randomly assigned 610 high-risk Chinese patients.[8] Patients were aged 35 to 64 years and received either placebo or combined low-dose retinol (15 mg or 50,000 IU) plus riboflavin (200 mg) and zinc gluconate (50 mg) for 13.5 months. Standard histological evaluations (including two endoscopic biopsies) were conducted for 93% of all entered patients. Micronuclei from esophageal cells were obtained before therapy began and after the 13.5 months of treatment. Serum levels of vitamin A, beta-carotene, riboflavin, and zinc were obtained at 0, 2, and 13.5 months.

The second report of this study presented micronuclei frequency results.[9] A statistically significant reduction in the mean percentage of micronucleated esophageal cells occurred in the active-treatment group compared with the placebo group. The pattern of cell proliferation, another potential intermediate endpoint marker, also improved.[10]

Aspirin and nonsteroidal anti-inflammatory drug (NSAID) use

A systematic review and meta-analysis of the association between aspirin and NSAID use and esophageal cancer identified two cohort and seven case-control studies published between 1980 and 2001.[11] Pooled results showed a protective association between aspirin/NSAID use and esophageal cancer (odds ratio [OR], 0.57; 95% CI, 0.47–0.71). The association with aspirin use was statistically significant (OR, 0.50; 95% CI, 0.38–0.66); the association with NSAIDs was borderline significant (OR, 0.75; 95% CI, 0.54–1.0). Aspirin/NSAID use was associated with lower risk of both adenocarcinoma (OR, 0.67; 95% CI, 0.51–0.87) and squamous cell carcinoma (OR, 0.58; 95% CI, 0.43–0.78).[11]

Adenocarcinoma of the Esophagus

Factors associated with increased risk of adenocarcinoma of the esophagus

Male gender

Male gender is an important predictor of adenocarcinoma of the esophagus. The attributable risk is low enough in women that, although the risk from gender is not modifiable, other risk factors necessarily have limited impact.

Gastroesophageal reflux disease (GERD)

The most important epidemiological difference between squamous cell carcinoma and adenocarcinoma is the strong association between GERD and adenocarcinoma. The results of a population-based case-controlled study suggest that symptomatic gastroesophageal reflux is a risk factor for adenocarcinoma of the esophagus. The frequency, severity, and duration of reflux symptoms were positively associated with increased risk of adenocarcinoma of the esophagus.[12] In a case-control study from Sweden, the OR was 7.7 for patients with recurrent reflux symptoms, while the OR for patients with long-standing and severe symptoms was 43.5 (95% CI, 18.3–103.5).[12] The probable mechanism is that long-standing GERD is associated with the development of Barrett esophagus, a condition in which an abnormal intestinal-type epithelium replaces the stratified squamous epithelium that normally lines the distal esophagus; Barrett esophagus is considered a precursor of esophageal adenocarcinoma.[13] The intestinal-type epithelium of Barrett esophagus has a characteristic endoscopic appearance that differs from squamous epithelium.[14] Dysplasia in Barrett epithelium represents a neoplastic alteration of the columnar epithelium that may progress to invasive adenocarcinoma.[15]

A population-based cohort study in Sweden shows that patients with Barrett esophagus develop adenocarcinoma of the esophagus at about 1.2 cases per 1000 person-years of follow-up monitoring, which is about 11.3 times higher than in the general population. Thus, while the relative risk may be elevated, the absolute risk is still not high. Furthermore, over half of the cases of adenocarcinoma of the esophagus are not associated with GERD symptoms.

Helicobacter Pylori

An interesting hypothesis associates the rise in the incidence of adenocarcinoma of the esophagus to a declining prevalence of H. pylori infection in Western countries. Reports have suggested that gastric infection with H. pylori may protect the esophagus from GERD and its complications.[16] According to this theory, H. pylori infections that cause pangastritis also cause a decrease in gastric acid production that protects against GERD.[17] Patients whose duodenal ulcers were treated successfully with antibiotics developed reflux esophagitis twice as often as patients whose infections persisted.[18] Other suggested factors to explain the increased risk of adenocarcinoma of the esophagus include obesity [19] and the use of medications such as anticholinergics that can predispose to GERD by relaxing the lower esophageal sphincter.[20]

Interventions with adequate evidence of decreased risk of adenocarcinoma of the esophagus

Aspirin and NSAID use

A systematic review and meta-analysis of the association between aspirin and NSAID use and esophageal cancer identified two cohort and seven case-control studies published between 1980 and 2001.[11] Pooled results show a protective association between aspirin/NSAID use and esophageal cancer (OR, 0.57; 95% CI, 0.47–0.71). The association with aspirin use was statistically significant (OR, 0.50; 95% CI, 0.38–0.66); the association with NSAIDs was borderline significant (OR, 0.75; 95% CI, 0.54–1.0). Aspirin/NSAID use was associated with lower risk of both adenocarcinoma (OR, 0.67; 95% CI, 0.51–0.87) and squamous cell carcinoma (OR, 0.58; 95% CI, 0.43–0.78).[11]

Radiofrequency ablation in dysplastic Barrett esophagus

A randomized controlled trial [21] assessed whether radiofrequency ablation (vs. sham ablation) could eradicate dysplastic Barrett esophagus and decrease the rate of neoplastic progression in patients with Barrett esophagus and dysplasia. Among patients with low-grade dysplasia, eradication of dysplasia occurred in 90.5% of the treatment group compared with 22.7% in the control group; in the high-grade dysplasia group, rates were 81.0% in the treatment group compared with 19.0% in the control group. Additionally, 77.4% of patients in the ablation group had complete eradication of intestinal metaplasia, compared with 2.3% in the control group. Patients in the ablation group had less disease progression, and although cancer was not a primary outcome because expected numbers were small, there were fewer cancers in the ablation group (1.2% vs. 9.3%; P = .045). The complication rate was relatively low; among 84 treated patients, there was one upper gastrointestinal hemorrhage and five strictures that were easily treated.[21]

This study suggests that the treatment of patients with Barrett esophagus and dysplasia may ablate Barrett esophagus and prevent disease progression, but the study provides only weak evidence about whether treatment reduces the outcome of esophageal cancer (because it was not designed to answer that question). Evidence from the study suggests that ablation does not simply coagulate and hide dangerous cells under the surface of the esophagus (those cells could later evolve to cancer). A question entirely separate from this study is whether patients should be screened for Barrett esophagus (this study focused on treatment of patients with Barrett who had been identified as having dysplasia). Furthermore, the study does not discuss the net benefits and harms of an overall program of screening (e.g., of screening patients with GERD or certain GERD symptoms) and the surveillance of patients with Barrett esophagus. The potential for overdiagnosis and overtreatment may be considerable if physicians used results of this study to treat patients with Barrett esophagus and no dysplasia.

References
  1. Holmes RS, Vaughan TL: Epidemiology and pathogenesis of esophageal cancer. Semin Radiat Oncol 17 (1): 2-9, 2007.  [PUBMED Abstract]

  2. American Cancer Society: Cancer Facts and Figures 2014. Atlanta, Ga: American Cancer Society, 2014. Available online. Last accessed May 21, 2014. 

  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. Hur C, Miller M, Kong CY, et al.: Trends in esophageal adenocarcinoma incidence and mortality. Cancer 119 (6): 1149-58, 2013.  [PUBMED Abstract]

  5. Oesophagus. In: World Cancer Research Fund, American Institute for Cancer Research: Food, Nutrition and the Prevention of Cancer: A Global Perspective. Washington, DC: The Institute, 1997, pp 118-129. 

  6. 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]

  7. Engel LS, Chow WH, Vaughan TL, et al.: Population attributable risks of esophageal and gastric cancers. J Natl Cancer Inst 95 (18): 1404-13, 2003.  [PUBMED Abstract]

  8. Muñoz N, Wahrendorf J, Bang LJ, et al.: No effect of riboflavine, retinol, and zinc on prevalence of precancerous lesions of oesophagus. Randomised double-blind intervention study in high-risk population of China. Lancet 2 (8447): 111-4, 1985.  [PUBMED Abstract]

  9. Muñoz N, Hayashi M, Bang LJ, et al.: Effect of riboflavin, retinol, and zinc on micronuclei of buccal mucosa and of esophagus: a randomized double-blind intervention study in China. J Natl Cancer Inst 79 (4): 687-91, 1987.  [PUBMED Abstract]

  10. Yang GC, Lipkin M, Yang K, et al.: Proliferation of esophageal epithelial cells among residents of Linxian, People's Republic of China. J Natl Cancer Inst 79 (6): 1241-6, 1987.  [PUBMED Abstract]

  11. Corley DA, Kerlikowske K, Verma R, et al.: Protective association of aspirin/NSAIDs and esophageal cancer: a systematic review and meta-analysis. Gastroenterology 124 (1): 47-56, 2003.  [PUBMED Abstract]

  12. 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]

  13. Spechler SJ, Goyal RK: The columnar-lined esophagus, intestinal metaplasia, and Norman Barrett. Gastroenterology 110 (2): 614-21, 1996.  [PUBMED Abstract]

  14. Van Dam J, Brugge WR: Endoscopy of the upper gastrointestinal tract. N Engl J Med 341 (23): 1738-48, 1999.  [PUBMED Abstract]

  15. Reid BJ, Blount PL, Rabinovitch PS: Biomarkers in Barrett's esophagus. Gastrointest Endosc Clin N Am 13 (2): 369-97, 2003.  [PUBMED Abstract]

  16. 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]

  17. 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]

  18. 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]

  19. Lagergren J: Controversies surrounding body mass, reflux, and risk of oesophageal adenocarcinoma. Lancet Oncol 7 (4): 347-9, 2006.  [PUBMED Abstract]

  20. 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]

  21. Shaheen NJ, Sharma P, Overholt BF, et al.: Radiofrequency ablation in Barrett's esophagus with dysplasia. N Engl J Med 360 (22): 2277-88, 2009.  [PUBMED Abstract]

Changes to This Summary (07/17/2014)

The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.

This summary was comprehensively reviewed and extensively revised.

This summary is written and maintained by the PDQ Screening and Prevention Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ NCI's Comprehensive Cancer Database pages.

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About This PDQ Summary



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This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about esophageal cancer prevention. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.

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National Cancer Institute: PDQ® Esophageal Cancer Prevention. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: http://cancer.gov/cancertopics/pdq/prevention/esophageal/HealthProfessional. Accessed <MM/DD/YYYY>.

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