Adenocarcinoma derived from gastric hamartomatous polyps

Seung Jong Oh1, Cheong A Oh, Dae Hoon Kim

  • 1Department of Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.

Summary

Gastric cancers can arise from hamartomatous polyps, even without a history of adenomatous polyposis coli. This case highlights de novo gastric cancers developing from these unique polyps.

Related Concept Videos

Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Barrett Esophagus-I: Introduction01:21

Barrett Esophagus-I: Introduction

Barrett's esophagus is a medical condition where the esophageal mucosa is significantly damaged by stomach acid or other digestive fluids, often due to long-term exposure associated with gastroesophageal reflux disease (GERD). In GERD, a weakened or abnormally relaxed lower esophageal sphincter allows stomach acid to flow persistently into the esophagus.
This constant acid exposure transforms the esophagus's pink mucosal lining (stratified squamous epithelium) into a type of lining more similar...
Cellular Adaptation IV: Dysplasia and Metaplasia01:24

Cellular Adaptation IV: Dysplasia and Metaplasia

DysplasiaDysplasia refers to abnormal changes in the size, shape, and organization of mature cells, characterized by pleomorphism, nuclear abnormalities, and increased mitotic activity. It commonly affects epithelial tissues, including the cervix, gastrointestinal tract, respiratory mucosa, and endometrium. Although it may occur alongside hyperplasia, dysplasia is not a true adaptive response but a preneoplastic change with potential to progress to cancer.When confined above the basement...
Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
Mucosal Barrier of the Stomach01:25

Mucosal Barrier of the Stomach

The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
Pyloric Obstruction01:11

Pyloric Obstruction

Pyloric obstruction, also referred to as gastric outlet obstruction, is a condition characterized by narrowing or blockage at the pylorus—the muscular valve regulating the flow of stomach contents into the duodenum. When this passage becomes impaired, the stomach cannot effectively empty its contents into the small intestine. This disruption leads to a range of gastrointestinal symptoms, including early satiety, bloating, epigastric pain, postprandial nausea, persistent vomiting, and...