GSC (gastric stump carcinoma), also known as post-surgical gastric cancer, was first proposed by Balfour in 1922 and refers to the primary tumor that occurs in the residual stomach more than 5 years after major gastrectomy for benign gastric or duodenal lesions, and some people include the cancer that occurs again in the residual stomach more than 10 years after gastric cancer surgery. Due to the prevalence of gastrectomy in the 1970s, the improvement of diagnostic techniques and the deepening of the understanding of the special precancerous state of the remnant stomach in recent years, the incidence of remnant gastric cancer has been increasing year by year, and the rate is reported to be 3-10% abroad. There are many factors affecting the occurrence of remnant gastric cancer and the etiology is complex. Preventive measures against the etiology are expected to reduce the incidence of remnant gastric cancer. This article briefly describes the epidemiology and prevention of residual gastric cancer. The epidemiology of residual gastric cancer is long and complex, and there are many factors affecting the occurrence of residual gastric cancer, the underlying causes of which are not yet fully understood. 1.1 Age and gender: the older the patient is at the time of the first operation, the shorter the interval between carcinomas; residual gastric cancer is more common in men, with the male:female ratio ranging from 4 to 9:1. The reasons for this phenomenon are unknown and may be related to the high mental stress, high incidence of ulcer disease and more surgical resections in men. 1.2 Postoperative interval time: the occurrence of residual gastric cancer is related to postoperative time. Generally speaking, the longer the time after major gastrectomy, the higher the incidence of residual gastric cancer. Some studies have shown that residual gastric cancer mostly occurs 10-20 years after surgery, and the risk of carcinoma increases greatly in those who are more than 10 years after surgery, especially 12 years after surgery, which is a significant feature of GSC. It is also believed that patients with major gastrectomy will inevitably develop residual gastric cancer as long as they survive long enough. 1.3 Anastomosis mode: The occurrence of residual gastric cancer is related to the mode of the first surgical anastomosis, which is most likely to occur after Billroth-II. The anatomy of the gastrointestinal tract is more altered after Billroth-II anastomosis, and the postoperative alkaline bile, pancreatic fluid and intestinal fluid are easily refluxed. The reflux must pass through the gastrointestinal anastomosis to enter the distal intestine, which causes great irritation to the anastomosis and gastric mucosa. The quantitative study of reflux after gastrointestinal anastomosis of different procedures showed that there were differences in the degree of reflux after different gastrointestinal anastomoses, and the reflux volumes were ranked from high to low as Billroth-II anastomosis, Billroth-Ⅰ anastomosis, and Roux-en-y anastomosis, with significant differences between the three and between the two. 1.4 Helicobacter pylori (Hp) infection is associated with the development of gastric cancer and has been classified as a class I carcinogen by WHO. Epidemiological surveys have shown that the incidence of gastric cancer is positively correlated with the rate of Hp infection. In residual gastric cancer, due to major gastrectomy, surgical reconstruction causes changes in the internal environment of the residual stomach, and Hp infection and alkaline reflux fluid have synergistic pathogenic effects, causing severe atrophy and intestinalization of the residual gastric mucosa and even leading to carcinogenesis. lee et al [8] found that HP infection is one of the causes of chronic active inflammatory cell proliferation in the residual gastric mucosa. seoane et al [9] showed that HP infection and the occurrence of residual gastric cancer closely related to the occurrence of residual gastric cancer. 1.5 Duodenogastric reflux After the majority of gastrectomy, the residual stomach has different degrees of duodenogastric reflux due to anatomical and physiological changes and loss of the anti-reflux effect of the pylorus. Due to the long-term reflux and immersion of alkaline intestinal fluid and bile, a series of pathological changes such as residual gastritis, intestinal glandular metaplasia, cystic degeneration of glands, atypical hyperplasia adenomatous changes, and thus carcinoma, occur in the gastric mucosa around the anastomosis. Low acid or even no acid and reduced gastrin in the remnant stomach facilitate the proliferation of bacteria, and the nitrosamines produced can further aggravate gastric mucosal damage [10]. 1.6 Decreased gastrin and digestive factors: gastrin can stimulate the synthesis of DNA, RNA and protein in the mucosa of the gastric acid-secreting site and duodenal mucosa, thus exerting a trophic effect on the gastric mucosa, and it is the main hormone responsible for cytokinetic changes in the gastric mucosa after gastric surgery.Kondo [11] suggested that the trophic effect of gastrin may be through increasing gastric mucosal blood flow, promoting gastric mucosa damaged by carcinogenic substances Healing of gastric mucosa damaged by carcinogenic substances, and increasing gastric acid secretion to inhibit the development of gastric cancer. After the removal of gastric sinus by major gastrectomy, the level of gastrin secretion is obviously low, and the role of gastrin in strengthening the gastric mucosal barrier, nutrition of gastric mucosal epithelial cells and resistance to H+ reverse diffusion is greatly weakened, so the mucosa and wall cells of the residual stomach lose the nutritional effect of gastrin, and the anti-injury mechanism of gastric mucosa is weakened to different degrees, which makes the residual stomach susceptible to cancer. In view of the factors affecting the occurrence of residual gastric cancer, patients who need to undergo gastric surgery or postoperative surgery due to gastric and duodenal lesions should take corresponding preventive measures to actively avoid the occurrence of residual gastric cancer. 2.1 Strictly grasp the indications for benign gastrectomy surgery The residual stomach after gastrectomy can be considered as the precancerous state of primary gastric cancer, so the indications for benign gastrectomy surgery should be strictly grasped. At present, the healing rate of peptic ulcer has been improved due to the wide application of H2 receptor blockers and gastric proton pump inhibitors. Eradication of Helicobacter pylori and anti-relapse measures have led to a gradual decrease in the recurrence rate and complications, and a significant reduction in refractory ulcers. The past view that early gastrectomy can prevent peptic ulcer malignancy should be discarded, and it is more appropriate to consider surgery after the age of 45 for patients with benign gastric disease who can be operated electively. In ulcer disease, especially duodenal bulb ulcer, gastrectomy should be performed at least 60% of the extent of gastrectomy to ensure that the purpose of surgical acid reduction is achieved. 2.2 Selection of gastrointestinal reconstruction Gastrointestinal reconstruction should reduce or avoid duodenal gastric reflux. Based on the highest rate of reflux after gastric surgery in Billroth-II style, gastrointestinal reconstruction after gastric surgery should avoid this operation as much as possible, and try to use long tab Roux-en-Y style or Billroth-II + Braun gastrojejunostomy or directly choose highly selective vagotomy in order to reduce or avoid duodenal gastric reflux and reduce the possibility of residual gastric cancer. 2.3 Enhanced radical treatment of HP If HP infection exists in the remnant stomach, it will lead to the development of remnant gastritis and remnant gastric cancer. Epidemiological data support that HP infection is etiologically linked to both chronic atrophic gastritis and intestinal epithelial hyperplasia. Currently, HP is considered a definite carcinogenic factor and a trigger for carcinogenesis of the gastric mucosa, so eradication of HP can significantly reduce the infiltration of inflammatory cells in the mucosal layer and has a preventive effect on the occurrence of remnant gastric cancer, so eradication of HP infection after gastrectomy is advocated. 2.4 Regular gastroscopy There is no positive correlation between residual gastric mucosal lesions and clinical symptoms, and early residual gastric cancer has no obvious symptoms, so patients 5 years after benign major gastrectomy should routinely undergo gastroscopy regardless of whether they have symptoms or not. It is recommended that patients more than 5 years after major gastrectomy should undergo gastroscopy once a year for early detection of residual gastric cancer and improvement of prognosis.