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Esophageal Cancer Prevention (PDQ®)

  • Last Modified: 02/27/2014

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Summary of Evidence

Squamous Cell Carcinoma
        Avoidance of tobacco and alcohol
        Dietary factors
        Aspirin and nonsteroidal anti-inflammatory drug use
        Helicobacter pylori infection and gastric atrophy
Adenocarcinoma of the Esophagus
        Gastroesophageal reflux/Barrett esophagus
        Aspirin and nonsteroidal anti-inflammatory drug use
Ablation of Barrett Esophagus With Dysplasia

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

Avoidance of tobacco and alcohol

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

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).[1] 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.[2] Case-control studies have also suggested a significantly increased risk of cancer of the esophagus associated with alcohol abuse.

Description of the Evidence

  • Study Design: Evidence obtained from cohort or case-control studies.
  • Internal Validity: Fair.
  • Consistency: Multiple studies.
  • Magnitude of Effects on Health Outcomes: Large positive benefit.
  • External Validity: Fair.
Dietary factors

Based on fair evidence, diets high in cruciferous (cabbage, broccoli, cauliflower) and green and yellow vegetables and fruits are associated with a decreased risk of esophageal cancer.[3,4]

Description of the Evidence

  • Study Design: Evidence obtained from cohort or case-control studies.
  • Internal Validity: Fair.
  • Consistency: Multiple studies.
  • Direction and Magnitude of Effect: Small positive.
  • External Validity: Fair.
Aspirin and nonsteroidal anti-inflammatory drug use

Based on fair evidence, epidemiologic studies have found that aspirin or nonsteroidal anti-inflammatory drug (NSAID) use is associated with decreased risk of developing or dying from esophageal cancer (odds ratio [OR] = 0.57; 95% CI, 0.47–0.71).[5]

Description of the Evidence

  • Study Design: Evidence obtained from cohort or case-control studies.
  • Internal Validity: Fair.
  • Consistency: Good.
  • Magnitude of Effects on Health Outcomes: Large positive.
  • External Validity: Fair.

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.

Description of the Evidence

  • Study Design: Evidence obtained from randomized controlled trials.
  • Internal Validity: Good.
  • Consistency: Good.
  • Magnitude of Effects on Health Outcomes: Increased risk, small magnitude.
  • External Validity: Good.
Helicobacter pylori infection and gastric atrophy

Based on fair evidence, serum CagA antibodies and gastric atrophy are associated with an increased risk of esophageal squamous cell carcinoma (OR = 2.1; 95% CI, 1.1–4.0 and OR = 4.3; 95% CI, 1.9–9.6, respectively).[6]

Description of the Evidence

  • Study Design: Evidence obtained from cohort or case-control studies.
  • Internal Validity: Fair.
  • Consistency: Large study.
  • Magnitude of Effects on Health Outcomes: Unknown magnitude.
  • External Validity: Fair.
Adenocarcinoma of the Esophagus

Gastroesophageal reflux/Barrett esophagus

Based on fair evidence, an association exists between gastroesophageal reflux disease (GERD) and adenocarcinoma.[7,8] 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.

It is unknown whether elimination of gastroesophageal reflux by surgical or medical means will reduce the risk of esophageal adenocarcinoma.[8,9]

Description of the Evidence

  • Study Design: Ecologic and descriptive studies.
  • Internal Validity: Fair.
  • Consistency: Good; multiple studies.
  • Magnitude of Effects on Health Outcomes: Unknown.
  • External Validity: Fair.
Aspirin and nonsteroidal anti-inflammatory drug use

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).[5]

Description of the Evidence

  • Study Design: Evidence obtained from cohort or case-control studies.
  • Internal Validity: Fair.
  • Consistency: Good.
  • Magnitude of Effects on Health Outcomes: Positive; unknown magnitude.
  • External Validity: Fair.

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.

Description of the Evidence

  • Study Design: Evidence obtained from randomized controlled trials.
  • Internal Validity: Good.
  • Consistency: Good.
  • Magnitude of Effects on Health Outcomes: Increased risk, small magnitude.
  • External Validity: Good.
Ablation of Barrett Esophagus With Dysplasia

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]

  • Study Design: Evidence obtained from a randomized controlled trial.
  • Internal Validity: Good.
  • Consistency: Single study.
  • Magnitude of Effects on Health Outcomes: Impact on cancer mortality not known.
  • External Validity: Good.

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.

  • Study Design: Evidence obtained from a randomized controlled trial.
  • Internal Validity: Good.
  • Consistency: Single study.
  • Magnitude of Effects on Health Outcomes: 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.
  • External Validity: Patients representative of a subset of people with dysplasia, particularly severe dysplasia; physicians may not be representative of practicing physicians since this is a new technology and requires specialized knowledge.
References
  1. 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]

  2. 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. 

  3. Chainani-Wu N: Diet and oral, pharyngeal, and esophageal cancer. Nutr Cancer 44 (2): 104-26, 2002.  [PUBMED Abstract]

  4. Boeing H, Dietrich T, Hoffmann K, et al.: Intake of fruits and vegetables and risk of cancer of the upper aero-digestive tract: the prospective EPIC-study. Cancer Causes Control 17 (7): 957-69, 2006.  [PUBMED Abstract]

  5. 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]

  6. 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]

  7. 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]

  8. Fitzgerald RC: Molecular basis of Barrett's oesophagus and oesophageal adenocarcinoma. Gut 55 (12): 1810-20, 2006.  [PUBMED Abstract]

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