ABSTRACT
Esophageal adenocarcinoma is a highly aggressive cancer that is usually caught too late to avoid severe morbidity and death. Traditional endoscopic screening for adenocarcinoma’s precursor—Barrett esophagus—and subsequent surveillance are often ineffective for detecting early cancer, which can often be treated without esophagectomy. Current efforts are focused on better identifying patients at high risk as candidates for endoscopic screening and developing less invasive and cheaper detection methods to enable widespread screening in the primary care setting.
Emerging evidence indicates that heartburn is too common a symptom to be useful for determining need for Barrett esophagus screening; conversely, esophageal pain is commonly absent in patients with Barrett esophagus.
Endoscopy often fails to detect esophageal adenocarcinoma even when surveillance guidelines for Barrett esophagus are followed. Carefully following the Seattle Biopsy Protocols and repeating endoscopy within a year after initial diagnosis of Barrett esophagus may improve detection.
Several inexpensive, easily administered screening tools are being developed. Most involve swallowing a small device that collects esophageal mucosal cells as it is pulled back up for histologic evaluation and testing for cancer biomarkers.
Although we have come a long way in reducing the incidence of squamous cell carcinoma of the esophagus, likely due to declining rates of smoking and alcohol consumption, esophageal adenocarcinoma has become one of the most rapidly rising cancers in Western countries.1 The 5-year survival rate—about 22%—has changed little over the past 3 decades.2
Unfortunately, the incidence of esophageal adenocarcinoma is projected to increase in the coming decades in the United States,3 likely due to the anticipated continued rise in obesity,4 which is closely linked to esophageal adenocarcinoma. This may be due to gastroesophageal reflux disease associated with obesity, as well as inflammatory effects of metabolic syndrome on esophageal mucosa, leading to a leaky epithelium that allows more acid penetration even in the absence of reflux symptoms.
Esophageal adenocarcinoma is also becoming more common in younger individuals (≤ 50 years).5 These patients tend to have a more severe course due to later presentation, with 5-year death rates similar to those seen in patients older than 70.6
BARRETT ESOPHAGUS
Barrett esophagus is characterized by an encroachment of a columnar-type mucosa from the stomach into the distal esophagus (Figure 1 and Figure 2).7 It can appear as small pockets of metaplasia or can extend the whole length of the esophagus. Long-segment Barrett esophagus is defined as at least 3 cm of continuous metaplastic tissue in the esophagus.
Development of Barrett esophagus. The transformation from (A) normal squamous epithelium to (B) metaplastic columnar tissue is believed to be an adaptive phenomenon, probably an inflammatory response to acid exposure.
Normal vs Barrett esophagus on endoscopy and encroachment of columnar-type mucosa into the esophagus. (A) Normal appearance of the gastroesophageal junction. Outer pink-colored smooth tissue is squamous mucosa from the esophagus, and inner salmon-colored ridged tissue is stomach mucosa. As shown here, the limit of gastric folds—the gastroesophageal junction (white dashed line)—should coincide with the squamous columnar junction (blue solid line). (B) Long-segment Barrett esophagus, with encroachment of columnar-appearing mucosa into the esophagus. The Prague criteria circumferential extent (C) of Barrett mucosa (blue dashed line) is located 5 cm from the gastroesophageal junction (white dashed line), and the blue solid line represents its maximum extent (M) of 6.5 cm.
Reproduced from Dig Liver Dis, Vol 43 Suppl 4, Fiocca R, Mastracci L, Milione M, et al. Microscopic esophagitis and Barrett’s esophagus: the histology report, pages S319–S330; 2011, with permission from Elsevier.
The transformation from normal squamous epithelium to (metaplastic) columnar tissue is believed to be an adaptive phenomenon, probably an inflammatory response to acid exposure. The result is a mucosa more tolerant to acid, which likely feels better to the patient but is associated with progression to adenocarcinoma.8
Sawas et al9 proposed that there are 2 phenotypes of Barrett esophagus and adenocarcinoma:
The traditional type (46%), or slow pathway, is characterized by long segments of intestinal metaplasia in the esophagus. Patients tend to have severe obesity and metabolic syndrome. They characteristically slowly progress through gastroesophageal reflux disease symptoms and a histologic sequence of intestinal metaplasia, low-grade dysplasia, high-grade dysplasia, and cancer.
The rapid pathway (54%) tends to occur in patients with mild obesity without metabolic syndrome. Small segments of Barrett esophagus, easily missed by endoscopy, may undergo a genomic catastrophe, with sudden conversion to an aggressive cancer. This phenotype is associated with poorer survival compared with the traditional phenotype.
WHY IS ESOPHAGEAL CANCER SO DEADLY?
Compared with other cancers, esophageal cancer continues to have an especially poor prognosis. Even patients initially diagnosed with stage 2 disease (invasion of muscle layer but not yet metastasized) have only about a 30% survival rate at 10 years.10
Anatomy predisposes to metastasis
Unless esophageal adenocarcinoma is caught at either its very earliest detectable point or at a precancerous stage, it is commonly incurable. The likeliest explanation for its extreme aggressiveness is that the lymphatic system routes right up into the mucosa. At T1a, in which the tumor is limited to the most superficial layer, there is an approximately 5% chance that it has already metastasized through the lymphatic system. For T1b (ie, the tumor is submucosal), the risk is as high as 20%.10
Risk is often overlooked
Another important reason for poor survival is that patients at risk of Barrett esophagus are often not identified and screened. Dulai et al11 found from a review of 12 studies (N = 1,503 cases) that only about 5% of patients undergoing resection for incident adenocarcinoma had a previously known diagnosis of Barrett esophagus.
The presenting symptom of esophageal adenocarcinoma is often dysphagia, at which point the disease has usually advanced to incurable cancer. Although reflux and heartburn have for decades been key criteria for eligibility for Barrett esophagus screening by most society guidelines, patients with the worst reflux frequently have the least severe symptoms, and vice versa. This paradoxical phenomenon reflects reduced sensitivity of the esophagus as acid exposure continues.12
Opportunities to refer at-risk patients for endoscopy are frequently missed in primary care settings. In a large retrospective cohort study, Vajravelu et al12 found that patients diagnosed with incident esophageal cancer tended to have multiple primary care visits in the 3 years before diagnosis.
Many patients take acid blockers nightly over years without reporting it to their doctor because the drugs are available over the counter and the symptoms are pretty well managed. Asking about nighttime symptoms is one of the most important questions a primary care physician can ask to identify increased risk of Barrett esophagus, because patients are likely to have chronic acid exposure.
EFFORTS TO IMPROVE SCREENING GUIDELINES
White men with central obesity are usually considered most at risk for developing Barrett esophagus,13 and the population fitting this description in the United States is large. Identifying patients for screening who develop the rapid phenotype is even more of a challenge: they are more likely to have only mild obesity, without metabolic syndrome. And because heartburn is so common, it is not specific, and as discussed above, symptoms tend to wane in time. Determining better ways to select candidates for screening is an active area of investigation.
Wenker et al14 developed the Houston-BEST (Barrett’s Electronic Screening Tool) Barrett esophagus risk prediction model adaptable for incorporation into electronic health records. Risk factors include male sex, age 50 or older, White or Hispanic ethnicity, smoking, elevated body mass index, history of gastroesophageal reflux disease, and family history of esophageal cancer. Although this model improves Barrett detection rates, it ignores women (who appear to be only protected until menopause), other ethnic groups, and individuals without obesity, thus excluding many vulnerable at-risk people.
Sawas et al15 examined the sensitivity criteria for screening patients with Barrett esophagus from the American College of Gastroenterology and the British Society of Gastroenterology using 2 cohorts of patients. By eliminating the presence of reflux symptoms, while including women, and considering proton pump inhibitor use, detection of esophageal adenocarcinoma significantly improved.
Rubenstein et al16 used artificial intelligence tools to develop the Kettles Esophageal and Cardia Adenocarcinoma Prediction (K-ECAN) tool. In addition to the expected risk factors, performance was improved by adding novel ones, eg, features of metabolic syndrome (lower high-density lipoprotein cholesterol and higher low-density lipoprotein cholesterol), chronic obstructive pulmonary disease, lower serum bicarbonate, higher white blood cell count (possibly indicative of systemic inflammation), lower sodium, lower blood urea nitrogen, and lower alanine transaminase.
Novel approaches may prove useful
Tumor markers are being identified that could help focus screening efforts. Januszewicz et al17 showed that p53 antibodies, a marker of cancer aggressiveness and detectable by immunochemistry of endoscopic biopsy tissue, can be especially useful for assessing increased risk in patients with a diagnosis of Barrett esophagus indefinite for dysplasia. It is the most used biomarker at present and can also be detected in serum.
Methylation markers may soon serve as useful diagnostic biomarkers, as they are well known to be an important part of the cancer process.18
Diehl et al19 developed an extensively tested tissue systems pathology test based on quantitative image features derived from biomarkers and morphology to better predict cancer risk in patients with Barrett esophagus.
The future gold standard screen may involve a blood test to identify a microRNA signature for detecting esophageal cancer. It is currently useful with squamous carcinoma,20 and is promising for Barrett esophagus, dysplasia, and adenocarcinoma.21
IMPROVING ENDOSCOPIC SURVEILLANCE PRACTICES
Unfortunately, endoscopic findings of a precancerous esophageal lesion can be subtle and easily overlooked, especially by a busy or inexperienced gastroenterologist. Even with an optimal screening technique, cancer is often missed. A meta-analysis of 24 studies (N = 820 cases of newly diagnosed esophageal adenocarcinoma) found that 25% of cancers were detected within 1 year after the index endoscopy that found Barrett esophagus.22
In a population-based study in the Netherlands, Peters et al23 found that most patients who were identified with Barrett esophagus and subsequently diagnosed with malignancy received the diagnosis within 5 to 6 years, and among those, the vast majority developed the malignancy during the first year. In a meta-analysis of 22 studies involving nearly 18,000 patients with Barrett esophagus with minimum follow-up of 3 years, about 80% of those diagnosed with adenocarcinoma or high-grade dysplasia at the index endoscopy or within 1 year of Barrett follow-up were considered to have prevalent rather than incident disease.24
One explanation for the cancer appearance within a year after endoscopy noted in many studies is that the tissue goes from metaplasia to cancer very rapidly. Probably a better explanation is that the cancer was missed during the initial endoscopy when Barrett esophagus was diagnosed. This is even more likely with cancers developing in ultrashort segments of esophageal intestinal metaplasia.
Codipilly et al25 found in a meta-analysis that patients under surveillance for Barrett esophagus had a 25% reduction in all-cause mortality, with rates not too different from patients not under surveillance.
The more recently published Barrett’s Oesophagus Surveillance Study (BOSS)26 found no difference at 10 years in the rate of esophageal adenocarcinoma diagnosis between people with Barrett esophagus undergoing biennial surveillance and those undergoing only “at need” endoscopy (for presence of new symptoms). Although this study had some flaws, it turned the field upside down, calling into question the usefulness of surveillance for patients with Barrett esophagus. No one advocates for abandoning the surveillance practice, but refining guidelines and clinical practices may be in order.
It is interesting that after the first year of negative findings confirming the diagnosis of Barrett esophagus without dysplasia or cancer, the incidence of developing progression is less than 0.4% annually, and that only 1 in 2,500 patients diagnosed with Barrett esophagus go on to develop cancer.22
Lessons that might be gleaned from these studies include the following:
A more careful first endoscopy would likely save lives
After an initial diagnosis of Barrett esophagus, routinely performing a second screen within the year to try to catch a missed cancer might be a wise practice
Continued surveillance after 6 years may not be the best use of resources.
IMPROVING ENDOSCOPIC ASSESSMENT
Simple but important strategies to optimize endoscopic practices could likely significantly increase catch rates of Barrett esophagus and esophageal adenocarcinoma:
Carefully inspect the esophagus at the rate of 1 minute/cm
Follow the Seattle Biopsy Protocol for surveillance of Barrett esophagus (biopsy all 4 quadrants of affected columnar mucosa every 1–2 cm, plus targeted biopsies of visible lesions)
Use virtual chromoendoscopy
Become an expert or refer to an expert
Repeat endoscopy within 1 year after index diagnosis of Barrett esophagus.
Wani et al27 assessed adherence to the Seattle Protocol when sampling for Barrett esophagus. Compliance ranged from 80% (for segment lengths up to 4 cm) to 38% (> 8–25 cm segment lengths), indicating that patients with increasing risk of dysplasia—associated with longer length of Barrett segment—are given less scrutiny and are therefore likelier to have a cancer overlooked.
Davis et al28 conducted a systematic review and meta-analysis of patients newly diagnosed with Barrett esophagus in a community facility who were subsequently sent to an expert center. After review by an expert gastrointestinal pathologist, they found that 27% had previously undetected visible lesions and 59% had pathologic grade change.
In the future, it is likely that machine learning will improve on human examination of endoscopic findings. de Groof et al29 demonstrated a multistep deep-learning system that can detect cancer in patients with Barrett esophagus more accurately than endoscopists. Beuque et al30 and Faghani et al31 developed artificial intelligence models that are better able to distinguish dysplastic grades and determine progression risk from esophageal biopsies. This is especially important for identifying criteria for future screening and for making treatment decisions.
NONINVASIVE TOOLS PROMISE SCREENING EXPANSION
For screening at-risk patients, new devices are emerging that are less invasive and less expensive than endoscopy and do not require anesthesia or gastroenterology expertise.32 The goal is to make screening for esophageal cancer as convenient as Papanicolaou tests for cervical cancer. While a given test may not be totally accurate, it could help identify patients in need of endoscopy. In many cases, the tests can be performed by a nurse practitioner, and the patient can go home immediately afterwards.
Promising tools include the following:
Transnasal endoscopy, using a device similar to (although much thinner) a standard endoscope, with camera and biopsy capabilities. It is passed through the nose in an awake patient, requiring only topical anesthesia.
EsoCheck, a textured balloon attached to a thin catheter that can be swallowed. When it reaches the stomach, the balloon expands and its ridged surface collects esophageal mucosa cells as it is pulled back up. EsoCheck comes with a DNA biomarker panel to assay collected cells. Together, they achieve 85% specificity and 85% sensitivity for detecting Barrett esophagus and esophageal adenocarcinoma.33
Cytosponge, a 2-cm–long gel-covered capsule attached to a string and swallowed, releasing a mesh sponge that collects cells as it is retracted. Efficacy data are strong from the Barrett’s Oesophagus Trial 3 (BEST3)34 in the United Kingdom, which found that screening high-risk individuals with the Cytosponge improved detection of Barrett esophagus compared with standard management. The BEST4 trial is now underway, with the goal of screening 120,000 people.
For the first time, these tools offer the opportunity to bring esophageal screening widely to the public to increase the chance that esophageal cancer can be detected early enough to make a survival difference. One model consists of a mobile van equipped with such devices, allowing community outreach inexpensively on a large scale.35
EARLY TREATMENT CAN IMPROVE SURVIVAL AND AVOID ESOPHAGECTOMY
Identifying cancer early in the disease has become critical, as effective endoscopic treatments are now available, obviating the need for esophagectomy. Several methods of endoscopic eradication therapy exist, involving “burning off” Barrett epithelium and early cancers, with the goal of having the esophagus repopulate with normal squamous mucosa.
Ablative techniques include multifocal nitrous oxide cryoballoon, cryotherapy with liquid nitrogen or carbon dioxide, and argon plasma coagulation.36 Long-term data from more than 2,500 patients with dysplastic Barrett esophagus indicated that radiofrequency ablation was effective in preventing esophageal adenocarcinoma.37
Endoscopic mucosal or submucosal resection can also be performed, involving injecting saline into the submucosa, lifting off the early visible lesion, putting a snare around it, and removing it.
INDIVIDUALS CAN REDUCE THEIR RISK
Efforts can be made by individuals to reduce the risk of developing Barrett esophagus and esophageal cancer. These include not smoking, having a healthy diet,38 and avoiding obesity. It is also important for individuals at high risk to get screened for Barrett esophagus.
DISCLOSURES
Dr. Katzka has disclosed being an advisor for Takeda, Regeneron, and Apogee Therapeutics.
Footnotes
Medical Grand Rounds articles are based on edited transcripts from Medicine Grand Rounds presentations at Cleveland Clinic. They are approved by the author but are not peer-reviewed.
- Copyright © 2026 The Cleveland Clinic Foundation. All Rights Reserved.
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