In 2013, it is estimated that 17,990 Americans will be diagnosed with esophageal cancer and 15,210 will die of this malignancy. Of the new cases, it is estimated that 14,440 will occur in men and 3,550 will occur in women.
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 for 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.. 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. 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), 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.
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. According to this theory, H. pylori infections that cause pangastritis also cause a decrease in gastric acid production that protects against GERD. Patients whose duodenal ulcers were treated successfully with antibiotics developed reflux esophagitis twice as often as those in whom infection persisted. Other factors that have been suggested to explain the increased risk of esophageal adenocarcinoma include obesity  and use of medications, such as anticholinergics that can predispose to GERD by relaxing the lower esophageal sphincter.