注: 有关食管癌筛查，食管癌治疗（成人）以及癌症筛查和预防研究的证据等级的单独PDQ总结也可从中获得。
在美国等西方国家，约90%的食管鳞状细胞癌由吸烟和饮酒引起。
胃食管反流/Barrett食管与食管腺癌风险增加相关。食管腺癌的其他危险因素，包括肥胖和使用抗胆碱药等药物通过松弛食管下括约肌引起胃食管反流病（GERD）。
基于确凿证据，吸烟和饮酒可增加患食管鳞状细胞癌的风险。在美国等西方国家，约90%的食管鳞状细胞癌由吸烟和饮酒引起。
影响程度：风险增加，中等程度。
基于确凿证据，避免吸烟与饮酒可降低食管鳞状细胞癌的发生风险。
影响程度：较大的积极获益。
基于一般证据，流行病学研究发现使用阿司匹林或其他NSAID可降低食管癌发生及死亡风险 (优势比[OR]，0.57；95%置信区间[CI]，0.47–0.71)。
影响程度：较少的积极获益。
基于确凿证据，NSAID的不良反应包括上消化道出血及严重的心血管事件，如心肌梗死、心衰、出血性卒中和肾损害。
影响程度：风险增加，程度较小。
基于一般证据，GERD与食管腺癌发生有关，尤其是GERD长期存在且症状严重时。
一项瑞典的病例对照研究发现，有复发性反流症状的患者的OR值为7.7，而长期具有严重症状的患者的OR值为43.5（95%CI，18.3-103.5）。
对共纳入1128例食管腺癌患者的5项病例对照研究进行荟萃分析发现，复发性烧心（OR，4.6；95%CI，3.3-6.6)，反流（OR，4.6；95%CI，3.4-6.1)或两者并存（OR，4.8；95%CI，3.4-6.8)使患癌风险显著增加。每日烧心和反流使患癌风险增加8倍（OR，8.0；95%CI，4.5-14.0)。
利用手术或内科治疗消除胃食管反流能否降低食管腺癌的发生风险尚不明确。
影响程度：未知。
基于一般证据，流行病学研究发现使用阿司匹林或其他NSAID可降低食管癌发生及死亡风险 (OR，0.57；95%CI，0.47–0.71)。
影响程度: 未知。
基于确凿证据，使用NSAID的不良反应包括上消化道出血及严重的心血管事件，如心肌梗死、心衰、出血性卒中和肾损害。
影响程度：风险增加，程度较小。
一项随机对照临床试验发现，对Barrett食管伴重度不典型增生患者行射频消融术可根治不典型增生和肠上皮化生，并降低疾病进展风险。
影响程度：对癌症死亡率的影响不明。
基于确凿证据，射频消融术的副作用包括食管狭窄（需扩张治疗）和上消化道出血，但其发生率较低。对Barrett食管患者，尤其对不伴有重度不典型增生的Barrett食管患者过度诊断或治疗，可能会导致严重副作用。
影响程度：如果缺乏经验的医生广泛采用上述方法，可能导致对食管狭窄（需扩张治疗）和上消化道出血的发生的低估。
Note: Separate PDQ summaries on Esophageal Cancer Screening, Esophageal Cancer Treatment (Adult), and Levels of Evidence for Cancer Screening and Prevention Studies are also available.
Smoking and drinking alcohol may account for roughly 90% of esophageal squamous cell carcinoma cases in Western countries like the United States.
Gastroesophageal reflux/Barrett esophagus is associated with an increased risk of esophageal adenocarcinoma. Other factors that may explain the increased risk of adenocarcinoma of the esophagus include obesity and the use of medications such as anticholinergics that can predispose to gastroesophageal reflux disease (GERD) by relaxing the lower esophageal sphincter.
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 carcinomas in Western countries like the United States.
Magnitude of Effect: Increased risk, moderate magnitude.
Based on solid evidence, avoidance of tobacco and alcohol would decrease the risk of squamous cell carcinoma.
Magnitude of Effect: Large positive benefit.
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 (odds ratio [OR], 0.57; 95% confidence interval [CI], 0.47–0.71).
Magnitude of Effect: Small positive.
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.
Based on fair evidence, an association exists between GERD and adenocarcinoma, particularly if the GERD is long-standing and symptoms are severe.
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).
A meta-analysis of 1,128 individuals with esophageal adenocarcinoma from five case-control studies reported statistically significant increases in risk with recurrent heartburn (OR, 4.6; 95% CI, 3.3–6.6), regurgitation (OR, 4.6; 95% CI, 3.4–6.1), or both (OR, 4.8; 95% CI, 3.4–6.8). Daily heartburn and regurgitation was associated with an eightfold increase in risk (OR, 8.0; 95% CI, 4.5–14.0).
It is unknown whether elimination of gastroesophageal reflux by surgical or medical means will reduce the risk of adenocarcinoma of the esophagus.
Magnitude of Effect: Unknown.
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).
Magnitude of Effect: Unknown magnitude.
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.
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.
Magnitude of Effect: Impact on cancer mortality not known.
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.
按照组织类型，食管癌主要分为腺癌和鳞状细胞癌。不同类型食管癌的流行病学特征具有显著差异。在20世纪60年代，鳞状细胞癌占所有食管癌病例的90%以上。而在过去20年内，食管腺癌的发病率明显上升，目前好发于食管远端的腺癌已取代鳞状细胞癌成为美国和西欧最常见的食管癌类型。
据估测，2020年美国食管癌新发病例和死亡病例将有18440例和16170例。新发病例中，预计有14350例男性患者，4090例女性患者。
在所有人种/种族中，发病率一般随年龄增长而增加。然而，食管鳞状细胞癌在55-69岁黑人男性中的发病率与其在70岁以上白人男性中的发病率相近，食管鳞状细胞癌在55-69岁黑人女性中发病率则稍高于其在70岁以上白人女性中的发病率。
虽然食管鳞状细胞癌的总发病率有所下降，但其在黑人男性中的发病率是白人男性的6倍以上。
据估计，2015年中国食管癌新发病例24.6万例，死亡18.8万例。新发病例中，预计有17.7万例男性患者，6.9万例女性患者。
中国的食管癌以鳞癌为主，发病率随年龄增长而增加，男性食管癌发病率远远高于女性。
中国食管癌的总发病率并未下降，但女性发病率有所下降，在2003~2007年女性发病率为6.24/10万，2015年降为5.92/10万。
相比之下，从20世纪70年代至20世纪90年代中期，食管腺癌的发病率迅速上升。
男性是食管腺癌的重要高危因素，女性的归因危险度较低。尽管来自性别的风险无法改变，但其他危险因素的影响有限。
在美国，食管鳞状细胞癌与过量吸烟及酗酒显著相关。吸烟的相对危险度为2.4，人群归因危险度为54.2%（95%置信区间[CI]，3.0-76.2）。
一些回顾性队列研究在调整吸烟因素后，发现酗酒者食管癌的发病风险是普通人群的2至7倍。
一些病例对照研究结果也显示酗酒会导致食管癌发生风险显著增加。
一项纳入221例食管鳞状细胞癌患者和695例对照的多中心病例对照研究发现：长期吸烟、饮酒和少吃蔬果对食管鳞状细胞癌的人群归因危险度分别为56.9%(95%CI，36.6%-75.1%)，72.4%(95%CI，53.3%-85.8%)和28.7%(95%CI，11.1%-56.5%)，合并人群归因危险度为89.4%(95%CI，79.1%-95.0%)。
中国食管癌的总患病率远高于美国，这与维生素A、维生素B2、α-胡萝卜素、β-胡萝卜素、维生素E、抗坏血酸和锌等营养素缺乏以及暴露于特定致癌物（例如N-亚硝基化合物）相关。
一项前瞻性、随机、安慰剂对照的食管癌化学预防研究共纳入610例中国食管癌高危人群。
研究对象的年龄在35-64岁之间，随机分为试验组和对照组，试验组联合服用低剂量维生素A（15mg或50,000IU）、维生素B2（200 mg）和葡萄糖酸锌（50 mg）共13.5个月。93%的研究对象接受了标准组织学评估，并在试验开始前及开始13.5个月后进行食管细胞的细胞微核检测，在第0个月（试验前）、第2个月及第13.5个月分别检测血清中维生素A、β-胡萝卜素、维生素B2和锌的浓度。
该项研究发表的第二份报告列出了细胞微核结果。
研究人员通过比较含微核的食管细胞所占比例发现试验组含微核的食管细胞比例显著低于安慰剂组。试验组的另一间接终点指标即细胞增殖情况亦有改善。
一项关于阿司匹林/其他NSAID与食管癌的荟萃分析共纳入1980年至2001年发表的2项队列研究和7项病例对照研究。
汇总数据显示，使用阿司匹林/其他NSAID可降低食管癌的发生风险（OR，0.57；95%CI，0.47-0.71）。阿司匹林对降低食管癌的发生风险具有统计学意义（OR，0.50；95%CI，0.38-0.66），而其他NSAID无显著差异（OR，0.75；95%CI，0.54-1.0）。阿司匹林/其他NSAID既可降低食管腺癌的发生风险（OR，0.67；95%CI，0.51-0.87），也可降低食管鳞状细胞癌的发生风险（OR，0.58；95%CI，0.43-0.78）。
食管鳞状细胞癌和腺癌的显著流行病学差异之一是GERD与食管腺癌的发生存在强相关。一项基于人群的病例对照研究显示症状性GERD是食管腺癌的危险因素。反流症状的发生频率、严重程度、持续时间均与食管腺癌的发生风险呈正相关。
一项瑞典的病例对照研究发现，有复发性反流症状的患者的OR值为7.7，而长期具有严重症状的患者的OR值为43.5（95%CI，18.3-103.5）。
对共纳入1128例食管腺癌患者的5项病例对照研究进行荟萃分析发现，复发性烧心（OR，4.6；95%CI，3.3-6.6)，反流（OR，4.6；95%CI，3.4-6.1)或两者并存（OR，4.8；95%CI，3.4-6.8)使患癌风险显著增加。每日烧心和反流使患癌风险增加8倍（OR，8.0；95%CI，4.5-14.0)。
长期存在的GERD与Barrett食管发生发展相关，可能由于异常的肠上皮化生逐渐代替食管远端的正常复层鳞状上皮所导致；而Barrett食管是食管腺癌的癌前病变。
Barrett食管的肠型上皮具有与鳞状上皮截然不同的典型内镜下表现。
Barrett食管上皮的不典型增生代表柱状上皮癌变，可进展为浸润性腺癌。
瑞典的一项基于人群的队列研究显示，Barrett食管患者在随访监测中食管腺癌发病率为1.2/1000人年，比普通人群高约11.3倍。因此，虽然相对危险度可能升高，但绝对危险度仍然不高。此外，一半以上的食管腺癌患者无GERD症状。
一项关于阿司匹林/其他NSAID与食管癌的荟萃分析共纳入1980年至2001年发表的2项队列研究和7项病例对照研究。
汇总数据显示，使用阿司匹林等NSAID可降低食管癌的发生风险（优势比[OR]，0.57；95%CI，0.47-0.71）。阿司匹林对降低食管癌的发生风险具有统计学意义（OR，0.50；95%CI，0.38-0.66），而NSAID对降低食管癌的发生风险无显著性差异（OR，0.75；95%CI，0.54-1.0）。阿司匹林/NSAID既与食管腺癌的发生风险降低有关（OR，0.67；95%CI，0.51-0.87），也与食管鳞状细胞癌的发生风险降低有关（OR，0.58；95%CI，0.43-0.78）。
一项随机对照试验评估了射频消融术（与假消融术相比）是否能根除Barrett食管伴不典型增生并降低其癌变风险。研究发现，Barrett食管伴轻度不典型增生的患者中，治疗组的不典型增生根治率达到了90.5%，对照组为22.7%；Barrett食管伴重度不典型增生的患者中，治疗组和对照组的不典型增生根治率分别为81.0%和19.0%。此外，消融组中77.4%的患者完全根治肠上皮化生，而对照组仅有2.3%完全根治。消融组中，疾病进展的患者较少。尽管因为预期患癌人数较少，未将癌症作为主要结局，但消融组的癌症发生率更低（1.2%比9.3%；P=0.045），并发症发生率也相对较低。在84例接受治疗的患者中，仅出现1例上消化道出血和5例食管狭窄，这些情况均易于治疗。
本项研究表明，消融术能根除Barrett食管伴不典型增生患者的不典型增生并抑制疾病进展，但该研究提供的关于消融术治疗可降低食管癌发生风险的证据较为薄弱（实际上，研究设计并未旨在解答这一问题）。该研究还表明，消融术并不是简单地将危险细胞（这些细胞可能演变成癌症）凝固并隐藏在食管表面下。本研究未关注患者是否应接受Barrett食管筛查（本研究主要关注Barrett食管伴不典型增生的治疗），此外，本研究未讨论整体筛查计划（例如，筛查GERD患者或有某些GERD症状的患者）和Barrett食管监测的利弊。如果临床医生仅根据该研究结果对不伴有不典型增生的Barrett食管患者进行治疗，则可能出现过度诊断和过度治疗。
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.
In 2020, it is estimated that 18,440 Americans will be diagnosed with esophageal cancer and 16,170 will die of this malignancy. Of the new cases, it is estimated that 14,350 will occur in men and 4,090 will occur in women.
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.
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.
In contrast, the incidence of adenocarcinoma of the esophagus rapidly increased from the 1970s to the mid-1990s.
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.
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).
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.
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%).
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).
A prospective, placebo-controlled, esophagus chemoprevention study randomly assigned 610 high-risk Chinese patients.
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.
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.
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.
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).
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.
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).
A meta-analysis of 1,128 individuals with esophageal adenocarcinoma from five case-control studies reported statistically significant increases in risk with recurrent heartburn (OR, 4.6; 95% CI, 3.3–6.6), regurgitation (OR, 4.6; 95% CI, 3.4–6.1), or both (OR, 4.8; 95% CI, 3.4–6.8). Daily heartburn and regurgitation was associated with an eightfold increase in risk (OR, 8.0; 95% CI, 4.5–14.0).
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.
The intestinal-type epithelium of Barrett esophagus has a characteristic endoscopic appearance that differs from squamous epithelium.
Dysplasia in Barrett epithelium represents a neoplastic alteration of the columnar epithelium that may progress to invasive adenocarcinoma.
A population-based cohort study in Sweden shows that patients with Barrett esophagus develop adenocarcinoma of the esophagus at about 1.2 cases per 1,000 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.
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.
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).
A randomized controlled trial 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.
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.
定期审查PDQ癌症信息并及时更新。本节整理了截至上述日期对该总结所做的最新更改。
2020年新发病例与死亡病例的最新预测数据（引用自美国癌症协会，参考文献2）。
该总结由PDQ筛查和预防编委会撰写和维护，该委员会在编辑方面独立于NCI。本总结为独立的文献综述，不作为NCI或NIH的政策声明。关于总结政策和PDQ编委会在维护PDQ总结中作用的更多信息，请参见关于本PDQ总结和 PDQ® - NCI综合性癌症数据库网页。
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.
Updated statistics with estimated new cases and deaths for 2020 (cited American Cancer Society as reference 2).
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.
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.
This summary is reviewed regularly and updated as necessary by the PDQ Screening and Prevention Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
Board members review recently published articles each month to determine whether an article should:
Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.
Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website's Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.
Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Screening and Prevention Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary].”
The preferred citation for this PDQ summary is:
PDQ® Screening and Prevention Editorial Board. PDQ Esophageal Cancer Prevention. Bethesda, MD: National Cancer Institute. Updated
Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online, a collection of over 2,000 scientific images.
The information in these summaries should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.
More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website’s Email Us.
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.
This summary is reviewed regularly and updated as necessary by the PDQ Screening and Prevention Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
Board members review recently published articles each month to determine whether an article should:
Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.
Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website's Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.
Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Screening and Prevention Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary].”
The preferred citation for this PDQ summary is:
PDQ® Screening and Prevention Editorial Board. PDQ Esophageal Cancer Prevention. Bethesda, MD: National Cancer Institute. Updated
Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online, a collection of over 2,000 scientific images.
The information in these summaries should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.
More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website’s Email Us.