eMedicine Specialties > Oncology > Carcinomas of the Gastrointestinal Tract

Esophageal Cancer

Author: Piero Marco Fisichella, MD, Assistant Professor of Surgery, Stritch School of Medicine, Loyola University; Director, Esophageal Motility Center, Loyola University Medical Center
Coauthor(s): Marco G Patti, MD, Professor of Surgery, Director, Center for Esophageal Diseases, University of Chicago Pritzker School of Medicine
Contributor Information and Disclosures

Updated: May 7, 2009

Introduction

Background

Esophageal carcinoma was well described at the beginning of the 19th century, and the first successful resection was performed in 1913 by Frank Torek.1 In the 1930s, Ohsawa2 in Japan and Marshall3 in the United States were the first to perform successful 1-stage transthoracic esophagectomies with continent reconstruction.

Endoscopy demonstrating intraluminal esophageal c...

Endoscopy demonstrating intraluminal esophageal cancer.

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Endoscopy demonstrating intraluminal esophageal c...

Endoscopy demonstrating intraluminal esophageal cancer.


Pathophysiology

Esophageal carcinoma arises in the mucosa. Subsequently, it tends to invade the submucosa and the muscular layer and, eventually, contiguous structures such as the tracheobronchial tree, the aorta, or the recurrent laryngeal nerve. The tumor also tends to metastasize to the periesophageal lymph nodes and, eventually, to the liver, lungs, or both.

Media file 7 shows the staging of the disease based on tumor invasion of the esophageal wall (T), involvement of lymph nodes (N), and the presence of metastases (M). Unfortunately, by the time the first symptoms manifest, the cancer has already spread to lymph nodes (mediastinal, cervical, celiac) in most patients.

Frequency

United States

In the United States in 2008, the American Cancer Society estimates that there will be 16,470 new cases (12,970 men and 3,500 women) of esophageal cancer diagnosed; 14,280 persons (11,250 men and 3,030 women) are expected to die of the disease. Adenocarcinoma of the esophagus has the fastest growing incidence rate of all cancers in the United States. The incidence of esophageal carcinoma is approximately 3-6 cases per 100,000 persons, although certain endemic areas appear to have higher per-capita rates. The age-adjusted incidence is 5.8 cases per 100,000 persons.

The epidemiology of esophageal carcinoma has changed markedly over the past several decades in the United States. Until the 1970s, squamous cell carcinoma was the most common type of esophageal cancer (90-95%). It was located in the thoracic esophagus and affected mostly African American men who had a long history of smoking and alcohol consumption. Over the last 2 decades, the incidence of adenocarcinoma of the distal esophagus and gastroesophageal junction has progressively increased. Currently, it accounts for more than 50% of all new cases of esophageal cancer. Unlike squamous cell carcinoma, it affects mostly white men, and its pathogenesis is linked to gastroesophageal reflux disease (GERD) and the development of Barrett epithelium (Media file 1).

Cigarette smoking and alcohol may cause esophageal cancer and the two may act synergistically in this regard. A high-fat diet and obesity may increase the risk of esophageal cancer. Other risk factors include achalasia and Plummer-Vinson syndrome.

See related CME at Excess Body Weight Increases Risk for Many Cancers.

International

Esophageal cancer is the seventh leading cause of cancer death worldwide. Incidence of esophageal carcinoma can be as high as 30-800 cases per 100,000 persons in particular areas of northern Iran, some areas of southern Russia, and northern China. Unlike in the United States, squamous cell carcinoma is responsible for 95% of all esophageal cancers worldwide.

Race

In the United States, African-Americans have a higher incidence of esophageal cancer than whites.

Sex

Esophageal cancer is generally more common in men than in women, with a male-to-female ratio of 3-4:1.

Age

Esophageal cancer occurs most commonly during the sixth and seventh decades of life. The disease becomes more common with advancing age; it is about 20 times more common in those older than 65 years than in persons younger than 65 years.

Clinical

History

  • Dysphagia is the most common presenting symptom.
    • Dysphagia is initially experienced for solids, but eventually it progresses to include liquids.
    • A complaint of dysphagia in an adult should always prompt an endoscopy to help rule out the presence of esophageal cancer. A barium swallow study is also indicated.
  • Weight loss is the second most common symptom and occurs in more than 50% of people with esophageal carcinoma. Patients may experience bleeding.
  • Pain can be felt in the epigastric or retrosternal area. It can also be felt over bony structures, representing a sign of metastatic disease.
  • Hoarseness caused by invasion of the recurrent laryngeal nerve is a sign of unresectability. Patients may have a persisting cough.
  • Respiratory symptoms can be caused by aspiration of undigested food or by direct invasion of the tracheobronchial tree by the tumor. The latter is also a sign of unresectability.

See related CME at Diagnostic Evaluation of Dysphagia.

Physical

  • The goals of the workup are to establish the diagnosis and to stage the cancer.
  • The examination findings are often normal. Hepatomegaly may result from hepatic metastases.
  • Lymphadenopathy in the laterocervical or supraclavicular areas represents metastasis and, if confirmed by needle aspiration or biopsy findings, is a contraindication to surgery.
See related CME at Examining the Ears, Nose, and Oral Cavity in the Older Patient.

Causes

  • The etiology of esophageal carcinoma is thought to be related to exposure of the esophageal mucosa to noxious or toxic stimuli, resulting in a sequence of dysplasia to carcinoma in situ to carcinoma.
  • Other contributing factors for squamous cell carcinoma include the following: 
    • Vitamin or nutritional deficiencies have been recognized as contributing factors. In a high-risk country such as China, deficiencies in vitamin or microelement levels may play a role in causation. Riboflavin deficiency in China may contribute to a high incidence of esophageal cancer. 
    • In Western cultures, cigarette smoking and chronic alcohol exposure are the most common etiological factors for squamous cell carcinoma. 
    • Human papillomavirus infection has been recognized as a contributing factor. Helicobacter pylori infection has not been found to be associated with esophageal cancer.
    • Tylosis palmaris et plantaris is also implicated.
  • Gastroesophageal reflux disease (GERD) is the most common predisposing factor for adenocarcinoma of the esophagus.
    • As a consequence of the irritation caused by the reflux of acid and bile, 10-15% of patients who undergo endoscopy for evaluation of GERD symptoms are found to have Barrett epithelium.
    • Adenocarcinoma may develop in these patients, representing the last event of a sequence that starts with the development of GERD and progresses to (Barrett) metaplasia, low-grade dysplasia, high-grade dysplasia, and adenocarcinoma (Media file 1).
    • In 1952, Morson and Belcher first described a patient with adenocarcinoma of the esophagus arising in a columnar epithelium with goblet cells.4 In 1975, Naef et al emphasized the malignant potential of Barrett esophagus.5 With the premalignant nature of Barrett esophagus well established, many investigators have searched for markers of esophageal carcinoma that could facilitate earlier diagnosis and follow-up of tumor recurrence.
    • The risk of adenocarcinoma among patients with Barrett metaplasia has been estimated to be 30-60 times that of the general population.
    • The prognosis of esophageal cancer is still poor, as these cancers are found late. However, a better understanding of the molecular progression of Barrett metaplasia to dysplasia to adenocarcinoma sequence may improve the prognosis. Tilanus et al reviewed data from the published literature to address the molecular changes in the pathogenesis of Barrett esophagus-associated neoplastic lesions. He found that the progression of Barrett metaplasia to adenocarcinoma is associated with several changes in gene structure, gene expression, and protein structure.6  The oncosuppressor gene TP53 and various oncogenes, particularly erb -b2, have been studied as potential markers. Casson and colleagues identified mutations in the TP53 gene in patients with Barrett epithelium associated with adenocarcinoma.7  In addition, alterations in p16 genes and cell cycle abnormalities or aneuploidy appear to be some of the most important and well-characterized molecular changes. However, the exact sequence of events in the progression of Barrett esophagus to adenocarcinoma is not known. Probably multiple molecular pathways interact and are involved. 
    • A nationwide population-based case-control study performed in Sweden found an odds ratio of 7.7 (95% confidence interval, 5.3-11.4) for adenocarcinoma among persons with recurrent symptoms of reflux, as compared with persons without such symptoms, and an odds ratio of 43.5 (95% confidence interval, 18.3-103.5) among patients with long-standing and severe symptoms of reflux.
See related CME at Risk Factors for Development of Esophageal Cancer in BE: Implications for Management (Slides With Transcript).

More on Esophageal Cancer

Overview: Esophageal Cancer
Differential Diagnoses & Workup: Esophageal Cancer
Treatment & Medication: Esophageal Cancer
Follow-up: Esophageal Cancer
Multimedia: Esophageal Cancer
References
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Further Reading

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Keywords

esophageal cancer, esophagus cancer, Barrett epithelium, Barrett's epithelium, Barrett esophagus, Barrett's esophagus, gastrointestinal reflux disease, GERD, esophageal adenocarcinoma, esophagus adenocarcinoma, esophagus carcinoma, esophageal carcinoma, reflux disease, squamous cell carcinoma

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Contributor Information and Disclosures

Author

Piero Marco Fisichella, MD, Assistant Professor of Surgery, Stritch School of Medicine, Loyola University; Director, Esophageal Motility Center, Loyola University Medical Center
Piero Marco Fisichella, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, Association for Academic Surgery, Society for Surgery of the Alimentary Tract, and Society of American Gastrointestinal and Endoscopic Surgeons
Disclosure: Nothing to disclose.

Coauthor(s)

Marco G Patti, MD, Professor of Surgery, Director, Center for Esophageal Diseases, University of Chicago Pritzker School of Medicine
Marco G Patti, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Surgeons, American Gastroenterological Association, American Medical Association, American Surgical Association, Association for Academic Surgery, Pan-Pacific Surgical Association, Society for Surgery of the Alimentary Tract, Society of American Gastrointestinal and Endoscopic Surgeons, Southwestern Surgical Congress, and Western Surgical Association
Disclosure: Nothing to disclose.

Medical Editor

Philip Schulman, MD, Chief, Medical Oncology, Department of Medicine, Memorial Sloan-Kettering Cancer Center; Clinical Professor, Department of Medicine, New York University School of Medicine
Philip Schulman, MD is a member of the following medical societies: American Association for Cancer Research, American College of Physicians, American Society of Hematology, and Medical Society of the State of New York
Disclosure: celgene Honoraria Speaking and teaching; Amgen Honoraria Speaking and teaching; genetech/idec Honoraria Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Wendy Hu, MD, Consulting Staff, Department of Hematology/Oncology and Bone Marrow Transplantation, Huntington Memorial Medical Center
Wendy Hu, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Blood and Marrow Transplantation, American Society of Hematology, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

CME Editor

Rajalaxmi McKenna, MD, FACP, Consulting Staff, Department of Medicine, Southwest Medical Consultants, SC, Good Samaritan Hospital, Advocate Health Systems
Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis
Disclosure: Nothing to disclose.

Chief Editor

Jules E Harris, MD, Clinical Professor of Medicine, Division of Hematology/Medical Oncology, Department of Internal Medicine, University of Arizona College of Medicine at Tucson; Consulting Staff, Arizona Cancer Center
Jules E Harris, MD is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Association of Immunologists, American Society of Hematology, and Central Society for Clinical Research
Disclosure: GlobeImmune Salary Consulting; Amplimed Consulting fee Consulting; FibroGen Consulting fee Consulting

 
 
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