Disease Classification: Oncology
Overview:
Stomach cancer is one of the common malignant tumors. It can occur in cardia area, pyloric area as well as the body of the stomach, with the pyloric area being the most common. According to the survey, the incidence of gastric cancer in China has a rising trend, and it is mostly seen in the age of 40-60 years, about three times more in men than in women. Clinical manifestations include loss of appetite, nausea and vomiting, discomfort and pain in the stomach and epigastric region, followed by epigastric mass, gagging and regurgitation, food infarction, black stools, vomiting of blood, anemia, and progressive emaciation.
Description of the disease
Gastric cancer is the most common gastric tumor, which is a malignant tumor originated from epithelium, i.e. gastric adenocarcinoma. Among the malignant tumors of the stomach, adenocarcinoma accounts for 95%. It is also the most common malignant tumor of the digestive tract, and even ranks among the top of all human malignant tumors. Although gastric cancer is a global disease, the incidence rate varies greatly between genders, different ages, countries and regions, various races, and even different periods in a region. Males are predominant, with the ratio of males to females being about 2-3:1. The age of onset of the disease is mostly in the middle-aged and old-aged, with fewer adolescents; roughly two-thirds of the patients are between the ages of 40-60, one-fourth of the patients are below the age of 40, and the rest are above the age of 60. People of color are generally more likely to develop the disease than Caucasians. North America, Western Europe, Australia, and New Zealand have a low prevalence, while Japan, Chile, Russia, and Iceland have a high prevalence. China's incidence rate is also high, and there are also large differences between different regions, generally the north and Inner Mongolia, and again for North China and East China, and to the south-central Hunan, Guangdong and Guangxi provinces and autonomous regions, as well as the southwest of Sichuan, Yunnan, Guizhou and other provinces of the lowest. The national average annual mortality rate is about 16/100,000 (21/100,000 for males and 10/100,000 for females), with a high incidence of up to 60-100/100,000, and a low incidence of less than 50-100,000 in the low incidence areas. With the continuous development of society and economy, the incidence rate of gastric cancer shows a decreasing trend. In the United States, the mortality rate was about 22/100,000 in the 1950s, and then decreased to below 3.7/100,000 in 1990; in Japan, there has been an obvious decreasing trend in recent years, and there are certain changes in certain regions of China. In 1972, the world population standardized incidence rate of gastric cancer in Shanghai Municipal District was 62/100,000 for men and 23.9/100,000 for women; in 1990, the incidence rate of gastric cancer in men declined to 45-100,000; and the incidence rates of men and women in 1995 reached 36/100,000 and 18/100,000, respectively. In the last 25 years, the incidence rate of gastric cancer in the Shanghai metropolitan area has been decreasing year by year, especially in men.
Symptoms and signs
Symptoms: Epigastric pain is the main symptom, which can be dull, burning, distending or severe pain, but it can also be only hunger-like discomfort. Typically, there is mild or moderate persistent pain under the raphe, which can be relieved by antacids or eating.DU about 2/3 of the pain is rhythmic: epigastric pain starts 1-3 hours after breakfast, and persists until lunch if no medication or food is taken. The pain returns 2-4 hours after eating, also requiring eating for relief, and about half have midnight pain, with the patient often waking up with pain in the north of DU.Regular pain can also occur in GU, but occurs earlier after a meal, about 1/2-1 hour after the meal, and disappears on its own by the time of the next meal. Midnight pain can also occur, but is not as common as DU.
Complications:
I. Bleeding Hemorrhage may occur in about 5% of patients, manifested by vomiting blood and/or black feces, and is occasionally the first symptom.
II. Pyloric or cardia obstruction Decided by the site of gastric cancer.
Third, perforation It is less common than benign ulcers, and mostly occurs in ulcerative type of cancer in the prepyloric region.
Aetiology of the disease
Although the etiology of gastric cancer has not yet been elucidated, it has been recognized that a variety of factors influence the above mentioned regulatory roles,**** which are also involved in the development of gastric cancer.
I. Helicobacter pylori infection With the deepening of research, Helicobacter pylori infection (Hp) is considered to have a certain relationship with the occurrence of gastric cancer, and in 1994, the International Agency for Research on Cancer (IARC) under the World Health Organization declared that Hp is a class I (i.e., definite) carcinogen for human gastric cancer. A large number of epidemiological data suggest that Hp is a risk factor for the development of gastric cancer, and in the laboratory, Hp has been successfully induced gastric cancer in Mongolian gerbils directly.Hp has adhesion, and its secreted toxin has pathogenicity, leading to gastric mucosal lesions, which can be easily cancerous on the basis of the development of atrophy, intestinalization, and atypical proliferation since the development of active superficial inflammation, and it is a kind of nitrate reductant, which has the ability to catalyze the role of nitrosation in the carcinogenesis of gastric mucosa. Hp is also a nitrate reducer, which can catalyze the nitrosation process and play a carcinogenic role. Hp may induce gastric cancer a few years after infection, or even 20 or 30 years later.
Second, environmental factors: It is observed that the first generation of immigrants from high incidence areas to low incidence areas still maintains a high susceptibility to gastric cancer, while the second generation has a significant downward trend, and the third generation swears that the risk of gastric cancer is basically close to that of the local residents. This suggests that the onset of stomach cancer is related to environmental factors, and most likely carcinogens in the diet. Epidemiologists pointed out that eating more fresh vegetables, fruits, dairy products and proteins can reduce the risk of gastric cancer, while eating more moldy grains, moldy foods, salted vegetables, smoked and cured fish and meat, as well as excessive intake of salt, can increase the risk. For example, after eating food containing high concentration of nitrate for a long time (such as smoked and cured smoked fish and meat, salted vegetables, etc.), nitrate can be converted into nitrite by bacterial reductase enzyme in the stomach, and then combined with amine to form carcinogenic nitrosamines. Bacteria can enter the stomach along with partially spoiled and unfresh food, and low gastric acid secretion after chronic gastritis or partial gastrectomy can also result in a large number of bacterial reproduction. In the elderly, the atrophy of gastric acid secretory glands often causes low gastric acid secretion, which is conducive to the growth of bacteria. In normal people, the bacteria in the stomach is less than 103/ml, but in the above situation, the bacteria can proliferate to more than 106/ml, which will produce a large number of nitrite carcinogens. The carcinogenic substances can cause cancer when they act on the gastric mucosa for a long time.
Epidemiologic investigations have shown that gastric cancer is more prevalent in lower socioeconomic classes, which further supports the importance of environmental factors.
Third, genetic factors, genetic quality is also very important to the development of gastric cancer. The phenomenon of family aggregation of gastric cancer and the fact that it can occur in identical siblings support this view. More scholars believe that genetic quality makes carcinogens more likely to cause cancer in susceptible people.
Four, precancerous lesions and pre-cancerous state Pre-cancerous state refers to systemic or local diseases or states that are prone to malignant changes, while pre-cancerous lesions refer to the pathological histology that is more likely to be transformed into cancerous tissues. According to long-term clinical observation, the precancerous states of gastric cancer are: ① chronic atrophic gastritis; ② gastric polyps, hyperplasia type does not develop cancer, but adenocarcinoma type can, and broad-based adenomatous polyps >2cm are easy to develop cancer; ③ residual gastritis, especially the latter who undergoes Billroth Ⅱ type of gastrectomy, and the cancer often occurs more than 15 years after the operation; ④ pernicious anemia with significant atrophy of the gastric body; and ⑤ a small number of patients with gastric ulcers. While atypical hyperplasia is regarded as a precancerous lesion of gastric cancer, the gastric mucosa can be replaced by gastric-type mucosa, which is called gastrulation of gastric mucosa. There are small intestine type and large intestine type of gastrification. The large intestine type is also called incomplete intestinalization, in which it is assumed that the absorbed carcinogenic substances accumulate locally due to the incomplete enzyme system, leading to atypical cell proliferation and mutation into cancer. Therefore, the above pre-cancerous state and the complication of atypical deepening should be closely followed up.
Pathophysiology
Pathogenesis: Like all tissues in the human body, under normal conditions, the epithelial cells of the gastric mucosa maintain a dynamic balance between proliferation and cell death, which is the basis for its structural integrity and sound function. This balance depends on the regulation of oncogenes and oncogenes, as well as certain regulatory peptides, etc. Once out of control, multiple oncogenes are stimulated while oncogenes are inhibited, which accelerates the proliferation and increases the DNA damage that cannot be repaired, generating aneuploidy, and the death regulation mechanism cannot be activated to make the cells die of their own accord, and then they may gradually progress to cancer. Although the etiology of gastric cancer has not yet been elucidated, it has been recognized that a variety of factors may affect the above mentioned regulatory effects*** and participate in the pathogenesis of gastric cancer.
I. Helicobacter pylori infection With the deepening of research, Helicobacter pylori infection (Hp) is considered to have a certain relationship with the occurrence of gastric cancer, and in 1994, the International Agency for Research on Cancer (IARC) under the World Health Organization declared that Hp is a class I (i.e., definite) carcinogen for human gastric cancer. A large number of epidemiological data suggest that Hp is a risk factor for the development of gastric cancer, and in the laboratory, Hp has been successfully induced gastric cancer in Mongolian gerbils directly.Hp has adhesion, and its secreted toxin has pathogenicity, leading to gastric mucosal lesions, which can be easily cancerous on the basis of the development of atrophy, intestinalization, and atypical proliferation since the development of active superficial inflammation, and it is a kind of nitrate reductant, which has the ability to catalyze the role of nitrosation in the carcinogenesis of gastric mucosa. Hp is also a nitrate reducer, which can catalyze the nitrosation process and play a carcinogenic role. Hp may induce gastric cancer a few years after infection, or even 20 or 30 years later.
Second, environmental factors: It is observed that the first generation of immigrants from high incidence areas to low incidence areas still maintains a high susceptibility to gastric cancer, while the second generation has a significant downward trend, and the third generation swears that the risk of gastric cancer is basically close to that of the local residents. This suggests that the onset of stomach cancer is related to environmental factors, and most likely carcinogens in the diet. Epidemiologists pointed out that eating more fresh vegetables, fruits, dairy products and proteins can reduce the risk of gastric cancer, while eating more moldy grains, moldy foods, salted vegetables, smoked and cured fish and meat, as well as excessive intake of salt, can increase the risk. For example, after eating food containing high concentration of nitrate for a long time (such as smoked and cured smoked fish and meat, salted vegetables, etc.), nitrate can be converted into nitrite by bacterial reductase enzyme in the stomach, and then combined with amine to form carcinogenic nitrosamines. Bacteria can enter the stomach along with partially spoiled and unfresh food, and low gastric acid secretion after chronic gastritis or partial gastrectomy can also result in a large number of bacterial reproduction. In the elderly, the atrophy of gastric acid secretory glands often causes low gastric acid secretion, which is conducive to the growth of bacteria. In normal people, the bacteria in the stomach is less than 103/ml, but in the above situation, the bacteria can proliferate to more than 106/ml, which will produce a large number of nitrite carcinogens. The long-term effect of carcinogenic substances on the gastric mucosa can cause cancer. Epidemiologic surveys have shown that gastric cancer is more prevalent in lower socioeconomic classes, which supports the importance of environmental factors.
Third, genetic factors, genetic quality is also very important to the development of stomach cancer. The phenomenon of family aggregation of gastric cancer and the fact that it can occur in identical siblings support this view. More scholars believe that genetic quality makes carcinogens more likely to cause cancer in susceptible people.
Four, precancerous lesions and pre-cancerous state Pre-cancerous state refers to systemic or local diseases or states that are prone to malignant changes, while pre-cancerous lesions refer to the pathological histology that is more likely to be transformed into cancerous tissues. According to long-term clinical observation, the precancerous states of gastric cancer are: ① chronic atrophic gastritis; ② gastric polyps, hyperplasia type does not develop cancer, but adenocarcinoma type can, and broad-based adenomatous polyps >2cm are easy to develop cancer; ③ residual gastritis, especially the latter who undergoes Billroth Ⅱ type of gastrectomy, and the cancer often occurs more than 15 years after the operation; ④ pernicious anemia with significant atrophy of the gastric body; and ⑤ a small number of patients with gastric ulcers. While atypical hyperplasia is regarded as a precancerous lesion of gastric cancer, the gastric mucosa can be replaced by gastric-type mucosa, which is called gastrulation of gastric mucosa. There are small intestine type and large intestine type of gastrification. The large intestine type is also called incomplete intestinalization, in which it is assumed that the absorbed carcinogenic substances accumulate locally due to the incomplete enzyme system, leading to atypical cell proliferation and mutation into cancer. Therefore, the above pre-cancerous state and the complication of atypical deepening should be closely followed up.
Pathology: According to the statistics of 1,686 cases in Shanghai and Beijing, the favorable sites of gastric adenocarcinoma are gastric antrum (58%), cardia (20%), gastric body (15%), whole stomach or most of stomach (7%). It can be categorized into early and progressive stages. Early gastric cancer refers to gastric cancer that is limited and does not exceed the depth of submucosa, regardless of whether it has localized lymph node metastasis or not. Progressive gastric cancer is called intermediate stage when its depth exceeds the submucosa and has invaded the muscular layer, and advanced stage when it has invaded the plasma layer or tissues outside the plasma layer.
Diagnostic examination
Laboratory examination: anemia is common, about 50% have iron deficiency anemia, which is caused by long-term blood loss; or caused by nutritional deficiency. If pernicious anemia is present, megaloblastic anemia is seen. Fecal occult blood test often shows persistent positive, easy to detect, and has the significance of auxiliary diagnosis. Some scholars take it as the first choice of gastric cancer screening. Gastric fluid analysis is of little significance. Although progressive gastric cancer can present acid-free or low gastric acid secretion due to the involvement of acid secretion area, this low gastric acid secretion state can overlap with normal people, so it is not listed as routine examination. Currently, the anisotropy of clinical markers used for gastric cancer is not strong. Serum carcinoembryonic antigen (CEA) is of little significance for diagnosis, although CEA is significantly elevated in gastric fluid in half of the patients, exceeding 100 ng/ml, but it also overlaps with that in gastric fluid of chronic atrophic gastritis. The gastric cancer-associated antigen used in late times is claimed to have a positive rate of more than half, but there is also a certain percentage of false positives.
X-ray barium meal examination: X-ray examination is still of great value in the diagnosis of gastric cancer. In recent years, gas-barium double contrast method, compression method and low-tension contrast technique are even applied, and high-density barium powder is used, which can clearly show the fine structure of the mucosa and is favorable to find micro lesions. Early gastric cancer can be manifested as limited shallow puddle of filling defects (Ⅰ, Ⅱa) with wide base and granular surface; or presenting a niche shadow (Ⅱc, Ⅲ) with irregular jagged edges, and interruption, deformation or fusion of mucosal striations concentrating toward it; or signs such as focal accumulation of barium in the mucosa and blurring of the gastric cell. For those who are suspected to have early gastric cancer, more X-ray films should be taken from different angles and carefully analyzed without sparing the tiny changes. The only X-ray diagnosis rate of progressive stage can be more than 90%. The mass that now enters into the gastric cavity shows a large and irregular filling defect. Ulcerative carcinoma mainly occurs on top of the mass, so its niche is located within the gastric contour, the diameter of the niche is often larger than 2.5cm, and the margin is not neat, which can show half-moon sign; the margin around the niche is not neat due to cancerous infiltration, and it is surrounded by a round and more transparent band, which is called ring embankment sign, and the adjacent mucous membrane is stiff, and peristaltic movement disappears without folds coalescence, or folds interruption can be seen. Stiffness of the gastric wall and loss of peristalsis are the X-ray features of invasive carcinoma. If the infiltration is extensive and only involves the gastric antrum, the peritoneal antrum is narrow, fixed and funnel-shaped, or there is scapular sign; if the whole stomach is involved, it is a fixed, small lumen, non-peristaltic, leathery stomach. Gastric cancer must be differentiated from gastric lymphoma. Gastric lymphoma is characterized by extensive involvement of the gastroduodenum, and X-ray shows coarse folds with multiple polypoid filling defects and multiple shallow niches.
Gastroscopy: gastroscopy combined with mucosal biopsy is currently the most reliable means of diagnosis. Experienced endoscopists can confirm the diagnosis of gastric cancer more than 95%, for this reason, more biopsy specimens should be taken, and some people suggest that more than 7 pieces must be taken. For early gastric cancer, gastroscopy is the best diagnosis method. Under the microscope, early gastric cancer may present a discolored mucosa, or the local mucosa becomes granular and rough, or mildly elevated or depressed; or there is a sense of stiffness, not soft, and biopsy should be performed for these slight changes. The size of the cancer should be estimated under the microscope, and those less than 1cm are called small gastric cancer, and those less than 0.5cm are called micro gastric cancer.
Early gastric cancer can be categorized into the following types according to Japanese scholars.
Type I (polypoid type) The lesion is elevated in the form of a small polyp, which is often wider than 2cm and without clitoris, accounting for about 15% of early gastric cancer.
Type II (superficial type) is divided into three subtypes, which together account for 75%.
Type IIa (elevated superficial type) The lesion rarely rises above the mucosal surface, with a height of not more than 0.5cm, small area and flat surface.
Type IIb (flat superficial type) The lesion is equal to the mucosa, but the surface is rough and granular.
Type IIc (superficially depressed type) The most common, shallowly pitted lesion has a rough, uneven undersurface and is seen as an interruption or fusion of the axial folds of the polymerized mucosa.
Type III (ulcerative type) accounts for about 10% of early gastric cancer. The mucosal ulceration is deeper than that of type IIc, but it does not exceed the submucosa, with peripheral polymerization, and the folds are interrupted, fused, or changed into a pestle shape.
Sometimes it is not easy to recognize early gastric cancer, but it can be sprayed with 0.5% Meilan under endoscopy, and the lesion will be colored, which will help to guide the biopsy site. Nowadays, magnifying endoscopy has been introduced, which can observe micro lesions more carefully and improve the diagnosis rate of early gastric cancer. Most of the progressive gastric cancer can be diagnosed from visual observation. The tumor may appear as an uneven lump with dirty surface, which often oozes blood and ulcers; or it may appear as an irregular large ulcer, the bottom of which is covered with dirty moss and oozes blood, and the edge of the ulcer often appears as a nodular elevation without polymeric folds, and there is no peristaltic movement at the lesion.
The introduction of an ultrasound probe from the gastroscope for examination is called ultrasound endoscopy, which is able to detect tumors growing outside the lumen, to clarify the depth of invasion of the tumor, as well as to understand whether there is any peripheral proliferation or metastasis.
Diagnosis: Diagnosis mainly depends on X-ray barium meal examination and gastroscopy with biopsy. Early diagnosis is a prerequisite for the radical treatment of gastric cancer. To achieve this goal, gastroscopy should be performed early or regularly in the following cases: ① people over 40 years old, especially men, who have recently experienced dyspepsia, or suddenly vomiting or black feces; ② people who are to be diagnosed as benign ulcers but lack of gastric acid in gastric peptide stimulation test; ③ people who are known to have chronic atrophic gastritis, especially type A, accompanied by intestinal and atypical hyperplasia, and who should set up a plan for regular follow up; ④ people who have been treated for two months with no effect on the gastric ulcer; and ④ people who have been treated for two months with no effect on the gastric ulcer. Gastric ulcer after two months of treatment is ineffective, X-ray examination shows that the ulcer instead of increasing in size, should be immediate gastroscopy. Prognosis: If progressive gastric cancer is allowed to develop, it usually takes about one year on average from the appearance of symptoms to death. Early gastric cancer develops slowly, sometimes it can stay in the mucosa for a long time (even several years) without developing deeper. The pattern of early gastric cancer transforming into advanced gastric cancer is still unclear.
The 5-year survival rate of gastric cancer after radical surgery depends on the depth of gastric wall invasion, the extent of lymph node involvement and the way of tumor growth. The prognosis of early gastric cancer only involving the mucosal layer is good, and the 5-year survival rate after surgery can reach more than 95%; if the submucosal layer has been involved, the prognosis is a little bit worse due to local lymph node metastasis, and the 5-year survival rate is about 80%. If the tumor appears in the form of mass, the resection rate is high, and it is better than that of diffuse type with early metastasis. Leathery stomach has a poor prognosis. If the tumor has invaded the muscularis propria but no lymph node metastasis is found at the time of surgery, the 5-year survival rate is still up to 60%-50%; if the tumor has reached the plasma layer and there is local lymph node metastasis, the prognosis is not good, and the 5-year survival rate is only 20% on average; in cases where there has been distant dissemination, the 5-year survival rate is 0.
Treatment Options
One, Surgery is the only possible means to cure gastric cancer. The effect of surgery depends on the stage of gastric cancer, the depth of invasion and the extent of spread of the cancer. For early gastric cancer, partial gastrectomy is the first choice, and if there is local lymph node metastasis, it should be cleared at the same time, which still has good effect. For patients with progressive stage, if no distant metastasis is found, surgical resection should be performed as far as possible, and some of them need extended radical surgery. For those with distant metastases, gastrectomy is generally not performed, and only palliative surgery (such as gastrostomy, gastrojejunostomy) is performed to ensure the patency of the digestive tract and improve nutrition.
Two, endoscopic treatment For early gastric cancer, there are endoscopic electrocautery, laser or microwave for local cauterization, or stripping biopsy resection (saline is injected into the mucous membrane at the cancerous foci to make the foci separate from the muscular layer, and then electrocautery is performed), but it is not as reliable as surgery because of the metastasis of the early gastric cancer to the local lymph nodes. However, because early gastric cancer may have local lymph node metastasis, so it is not as reliable as surgery. Those who cannot be operated in middle or advanced stage can also be treated with laser, microwave or local injection of antitumor drug, anhydrous ethanol or immune enhancer under endoscopy. For cardia tumors with obstruction, endoscopic endoprosthesis can be placed to rebuild the channel.
Three, chemotherapy Anti-tumor drugs are often used to assist surgical treatment, and are used before, during and after surgery to inhibit the spread of cancer cells and kill the remaining cancer cells, so as to improve the effect of surgery. Generally speaking, chemotherapy is not given for early stage cancers, but it is necessary to give chemotherapy for those who can be surgically resected for intermediate and advanced cancers, and it is often given for a single dose of 5-FU, 5-FU, mitomycin, and 5-FU, as per the case, starting from 2-4 weeks after the surgery. -FU), mitomycin (MMC), or tegafur (FT-207), or a combination of chemotherapy. Combination chemotherapy may be tried in patients who cannot undergo surgery without radical resection. Gastrointestinal tumors have poor effect on chemotherapy, and gastric cancer is relatively better than others. Commonly used chemotherapeutic agents are 5-FU, MMC, adriamycin (ADM), nitrosoureas (e.g., CCNU, MeCCNU), and cisplatin (DDP), etoposide (pedunculated ethoside, VP-16), and with hydroxycamptothecin. These drugs, single-use effect is poor, the efficiency (tumor shrinkage of at least 50%) is only 10-20%, combined application is slightly better. There are a variety of combination regimens, but to date there is no ideal pairing. There are also interventional arterial chemotherapy via femoral artery cannulation to the corresponding arterial branches, the adverse effects of drugs are smaller than those of systemic drugs, but it is invasive treatment, and the operation is more complicated.
Four, other therapies High-energy intravenous nutritional therapy is also commonly used as an adjuvant therapy, preoperative and postoperative applications to improve the patient's system, so that more tolerant of surgery and chemotherapy. Available immune enhancers such as BCG (BCG), levamisole, lysostaphin preparations (OK-432) to improve the patient's immunity, but the effect is not certain. Currently, there are also research reports on the trial of micro viruses to treat gastric cancer.
The Chinese medicine Fuzheng Cancer Formula (Astragalus, Codonopsis, Atractylodes Macrocephalae, Xianhe Cao, Semen Coicis, Corydalis alba, Quartz, Hepatica, Ipomoea, Ishimitra, and Scorched Glycyrrhiza) is unique to our country, and it can be applied in conjunction with it.
At present, considerable attention is paid to the role of Hp in the development of gastric cancer, and patients with early gastric cancer can be treated with anti-Hp therapy after surgery.
Prevention
Because the cause of the disease is not known, there is a lack of effective primary prevention (removal of the cause) measures. However, according to epidemiological investigations, eating more fresh vegetables and fruits, eating more meat and drinking more dairy products, less salty and preserved foods, reducing salt intake, food storage in the refrigerator, seems to have a certain preventive effect. Daily intake of vitamin C can reduce the formation of nitrosamines in the stomach. Active eradication of Hp is also one of the important possible means of preventing gastric carcinogenesis. For patients with chronic atrophic gastritis, especially those with intestinalization and atypical hyperplasia should be given active treatment, and regular endoscopic follow-up examinations should also be carried out; for those with moderate atypical hyperplasia who have not improved after treatment, as well as those with severe atypical hyperplasia, it is appropriate to give preventive surgical treatment. It is still an important topic to find early gastric cancer by census and resect it in time (secondary prevention). As China is a vast country with a large population, a comprehensive census is impossible. It is not possible to conduct a comprehensive census because of the vast area of our country and the large population. It is a feasible way to select high-risk groups for regular screening in high-incidence areas, so a gastric cancer prevention and control network should be set up in high-incidence areas, and endoscopists should be trained vigorously to carry out universal screening for high-risk groups.