Barrett's Esophagus (cont.)
In this Article
- Barrett's esophagus facts
- What is Barrett's esophagus?
- Why is there so much interest in Barrett's esophagus?
- What causes Barrett's esophagus?
- Who develops Barrett's esophagus?
- What is the specific abnormality in the inner lining (epithelium) of Barrett's esophagus?
- What about the cancer that occurs in Barrett's esophagus?
- What is dysplasia in Barrett's esophagus?
- What is the risk of developing adenocarcinoma of the esophagus in Barrett's?
- What are the symptoms of Barrett's esophagus?
- How is GERD with or without Barrett's esophagus treated?
- Why is it important to screen patients with GERD to diagnose Barrett's esophagus?
- Why is it critical to be accurate in the diagnosis of Barrett's esophagus?
- What does endoscopic biopsy surveillance in Barrett's esophagus involve?
- How is high grade dysplasia managed?
- How is low grade dysplasia managed?
- What are the experimental approaches for treatment of high grade dysplasia?
- What experimental options are there for Barrett's esophagus WITHOUT dysplasia?
- What does the future hold for Barrett's esophagus?
- Find a local Gastroenterologist in your town
What is dysplasia in Barrett's esophagus?
Dysplasia is a change in the cells lining the esophagus in which the cells actually show abnormal changes in their structure and appearance. When these changes become severe enough, (going from low-grade to high-grade dysplasia) the cells begin appear malignant (like cancer cells). However, unlike cancer these cells remain in place and don't invade tissues outside of the lining. Dysplasia occurs as a series of cell changes as Barrett's esophagus progresses to Barrett's-associated cancer. Patients with Barrett's are monitored with endoscopy and biopsies (surveillance) to detect these cellular changes (the dysplasia) or at worst, early cancer so that they may be treated. Currently, there is no way to predict which patients with Barrett's esophagus will develop dysplasia.
Dysplasia also has been identified adjacent to tumors of the gastrointestinal tract other than esophageal adenocarcinoma. For example, dysplasia is found in half the cases of stomach cancer and in colon cancer, in which the dysplasia is visible as so-called adenomatous polyps. Additionally, dysplasia is the same early warning cell change that pathologists look for in PAP smears of the cervix that predict cervical cancer.
Implications of dysplasia for cancer risk
Dysplasia is considered premalignant. This means that if dysplasia has been demonstrated on several occasions, it is believed that the patient will develop cancer if he or she lives long enough. Dysplasia is categorized as being high grade or low grade. When high grade dysplasia is diagnosed, cancer may already be present, and if not, the risk of developing cancer sooner is greater than with the lesser grades of dysplasia.
In follow-up biopsies of patients with dysplasia, the condition may not be detected again in some patients, whereas in others, low grades of dysplasia are found. This absence or decrease of dysplasia may be due factors such as sampling variations, the removal of tiny foci (groups of cells) of dysplasia with the initial biopsy, or actual biological reversal. The exact reason(s) are unknown.
Using molecular techniques, some changes, referred to as biomarkers, can be detected in biopsy specimens before dysplasia develops. These changes are similar to those that are observed in other cancers. Biomarkers include changes in the DNA content of cells, in the genes and chromosomes, and in growth factors. A number of these biomarkers can be shown to appear before and during the occurrence of dysplasia. The ultimate goal is to find a magic marker that can tell us which patients among those with no dysplasia or low grade dysplasia are more likely to develop high grade dysplasia or cancer. Such patients then can be followed by surveillance more closely than others.
At present, all patients with Barrett's esophagus, from the surveillance point of view, are treated in the same manner. The availability of biomarkers would separate (stratify) Barrett's patients based on their risk for cancer. Such stratification would allow doctors to do biopsies more frequently in the minority of patients who are at greater risk of cancer and less frequently in those predicted to have a lower risk of cancer.
Another use for proven biomarkers would be to help confirm the pathologist's interpretation of dysplasia on biopsies.
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