By Jason Wasserman MD PhD FRCPC
November 2, 2025
Gastric dysplasia (also called glandular intraepithelial neoplasia) is a precancerous change that affects the inner lining of the stomach. In gastric dysplasia, the cells that normally cover the stomach wall begin to look and behave abnormally, but they have not yet spread into deeper layers of the stomach.
Gastric dysplasia can remain stable for years, but in some people it can progress to a type of stomach cancer called adenocarcinoma if it is not treated or monitored.
Gastric dysplasia begins in epithelial cells, which are the cells that form the thin inner lining of the stomach. These cells normally create glands, small pockets in the stomach wall that produce mucus and digestive juices. When the gland cells divide too quickly or develop genetic damage—changes in their DNA—they become disorganized and start to show abnormal features. These early changes are what pathologists refer to as dysplasia.
Gastric dysplasia can occur anywhere in the stomach, but it is most common in the antrum, which is the lower part of the stomach near where it connects to the small intestine.
Gastric dysplasia usually develops gradually as a result of long-term inflammation or irritation of the stomach lining.
Common causes include:
Chronic infection with Helicobacter pylori, a type of bacteria that causes ongoing inflammation in the stomach.
Smoking or heavy alcohol use, which damage the protective lining of the stomach.
Infection with Epstein–Barr virus (EBV), which can interfere with normal cell growth.
Genetic changes in key control genes such as CDH1 or APC, which regulate how cells grow, divide, and attach to one another. Mutations in these genes may occur by chance or, less commonly, be inherited.
People who have chronic atrophic gastritis (long-term inflammation with thinning of the stomach lining) or intestinal metaplasia (replacement of normal stomach cells with intestinal-type cells) also have a higher risk of developing gastric dysplasia.
Gastric dysplasia typically does not cause symptoms on its own. When symptoms occur, they are usually due to the inflammation or infection that led to the dysplasia.
Common symptoms include:
Persistent upper abdominal pain or discomfort.
Bloating or indigestion after eating.
Nausea or loss of appetite.
Fatigue from anemia (a low red blood cell count) caused by slow bleeding from small ulcers.
Because gastric dysplasia causes microscopic changes, it is usually detected during an endoscopy performed for another stomach problem, such as gastritis or reflux.
No. Gastric dysplasia is not cancer, but it is a precancerous condition. This means that the abnormal cells are limited to the surface lining and have not invaded deeper tissue or spread elsewhere.
If gastric dysplasia, particularly high grade dysplasia, is left untreated, it may progress to stomach cancer. Detecting and treating it early can prevent this progression.
The diagnosis of gastric dysplasia is made after a biopsy of the stomach lining is examined by a pathologist, a doctor who diagnoses diseases by studying tissue under the microscope.
The process leading to a biopsy usually starts when a patient has symptoms, a history of chronic gastritis, or an abnormal result on another test. Your doctor will perform a gastroscopy, also called an upper endoscopy, to examine the stomach lining and take small tissue samples for testing.
Before the procedure, your doctor reviews your symptoms, medical history, and any risk factors such as long-term H. pylori infection, smoking, or prior stomach ulcers. You will be asked to avoid eating or drinking for several hours so that your stomach is empty during the exam. A mild sedative or numbing spray may be used to make the procedure comfortable.
During the procedure, the doctor gently passes a thin, flexible tube with a camera (an endoscope) through your mouth, down your throat, and into your stomach. This allows direct visualization of the stomach lining on a monitor.
If any areas appear abnormal—such as red, raised, or discolored patches—the doctor removes several tiny samples of tissue (biopsies) using instruments passed through the endoscope. The samples are preserved in a special solution and sent to a pathology laboratory for analysis.
An endoscopy usually takes 10 to 20 minutes, and patients can go home afterward. Mild throat irritation or bloating may occur briefly but resolves within a day.
In the lab, a pathologist studies the biopsy under the microscope. Dysplasia is diagnosed when the glandular cells lining the stomach show abnormal nuclei (the dark centers of cells that contain genetic material), crowded growth, and irregular organization.
The pathologist also notes the mitotic activity, which means how many cells are dividing, and whether the glands appear organized or disorganized. These findings help determine whether the dysplasia is low grade or high grade.
Pathologists classify gastric dysplasia as low grade or high grade based on how abnormal the cells look and how quickly they are dividing.
In low grade dysplasia, the cells look only slightly abnormal. The nuclei, which hold the cell’s genetic material, are somewhat larger and darker than normal but remain organized. The glands retain much of their normal structure, and the mitotic activity—the number of dividing cells—is low.
The risk of low grade dysplasia progressing to stomach cancer is low (about 10% within one year). However, careful monitoring is important to make sure it does not progress.
In high grade dysplasia, the cells look much more abnormal. The nuclei are darker and vary widely in size and shape. The glands are crowded and irregular, with very little normal tissue separating them. The mitotic activity is high, meaning many cells are dividing, and some dividing cells appear abnormal (atypical mitoses).
High grade dysplasia has a much higher chance (up to 70% within one year if untreated) of progressing to stomach cancer, so it is usually removed or treated right away.
Pathologists recognize two main types of gastric dysplasia based on how the abnormal cells appear under the microscope.
Intestinal-type dysplasia is composed of cells that look similar to the cells that normally line the small intestine. It is often linked to H. pylori infection and intestinal metaplasia.
Foveolar-type dysplasia is made up of cells that resemble normal stomach lining cells (called foveolar cells) but that grow in an irregular way or divide too quickly.
Both types are precancerous and can progress to stomach cancer if untreated. The distinction between them can only be made by a pathologist examining a biopsy under the microscope.
The next steps depend on the grade of dysplasia and whether all abnormal tissue has been removed.
Low grade dysplasia: Treatment usually focuses on correcting underlying causes, such as eradicating H. pylori infection and avoiding smoking or alcohol. A follow-up endoscopy is recommended within 6 to 12 months to monitor for changes.
High grade dysplasia: The affected tissue is generally removed using a specialized endoscopic procedure such as endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD). If early cancer is suspected or the dysplasia cannot be completely removed, surgery may be necessary.
After treatment, patients continue with regular endoscopic surveillance to monitor for recurrence or new areas of dysplasia.
Your pathology report guides these decisions by describing the type, grade, and extent of removal of the dysplastic tissue.
What type and grade of dysplasia do I have?
Was Helicobacter pylori infection found in my biopsy?
Has the dysplastic area been completely removed, or do I need additional treatment?
How often should I have follow-up endoscopies?
What is my risk of developing stomach cancer?
Should I consider genetic testing based on my results or family history?