Gastric stromal tumor (GST) is the most common type of gastrointestinal stromal tumor (GIST) and the most common type of tumor of mesenchymal origin. In 1998, Hierota et al. discovered the presence of mutations in the tyrosine protein kinase receptor (ck it) and the expression of the proto-oncogene protein CD117 in GIST, which gradually led to a clearer understanding of the origin, immunophenotypic characteristics, and histological diagnostic criteria of GIST, which was regarded as a non-epithelial clinical solid tumor with a non-epithelial origin, mostly in the gastrointestinal tract, positive for the proto-oncogene protein CD117, and rich in clostridial, epithelial, and epithelial forms. GST accounts for approximately 60% to 70% of GIST, much higher than the 20% to 30% of small intestine, 5% of colorectum, and less than 5% of esophagus, omentum, and mesentery. Although the pathology and immunohistochemistry of gastric mesenchymal tumors and other parts of the GI tract have commonalities, there are significant differences in clinical characteristics, treatment and prognosis, so the diagnosis and treatment of gastric mesenchymal tumors should be given adequate clinical attention. The clinical manifestation of GST lacks specificity. When the tumor is small (< 5 cm), there is often no clinical symptoms, but when the tumor is large (> 5 cm), there may be upper abdominal discomfort, vague pain, upper gastrointestinal bleeding or black stool, and most of the patients have bleeding as the first symptom. The clinical diagnosis of GST mainly relies on gastroscopy, gastrointestinal imaging, CT, and positron emission computed tomography (PETCT). Gastroscopy may reveal a submucosal bulging mass, usually with a smooth mucosal surface and a central depression or ulcer, and biopsy is often difficult to obtain tumor tissue, thus the pathology often returns chronic inflammation. Preoperative diagnosis by ultrasound endoscopy is very meaningful and can clarify the size and extent of the tumor, and in recent years it has been reported that fine needle aspiration biopsy with immunohistochemistry under ultrasound endoscopy can clarify the diagnosis. CT often shows endogenous or exogenous masses with heterogeneous density, necrotic cysts in the center, mild to moderate enhancement in the solid portion, and some foci of punctate calcification. The histology of GST is generally based on three main indicators: cell morphology, cell density, and cytodifferentiation, and there are generally three subtypes of GIST: spindle cell type (70%), epithelioid cell type (20%), and mixed type (10%). GST is mostly spindle cell type and epithelioid cell type. Tumors with higher cell density have a higher risk of malignancy. The risk of malignancy is significantly higher for >5 cells/50 HPF. Immunohistochemical diagnosis is important for GST because 90%-95% of GSTs have mutations in the ck it gene and expression of its protein CD117, thus once CD117 expression is positive, the diagnosis of GST is easily established. However, CD117 negativity does not exclude the diagnosis of GST. 75% of CD117 negative GST are positive for protein kinase theta (PKCtheta), 44% are positive for transmembrane glycoprotein CD34, and 40% are positive for smooth muscle actin (SMA). These can be used as auxiliary diagnostic indicators for GST. The risk of malignancy of GST is mainly based on tumor size and cytokinesis. According to the evaluation criteria published by the National Institutes of Health (NIH) in 2002, a tumor < 2 cm with a cytokinesis of < 5/50 H PF is considered very low risk; a tumor 2-5 cm with a cytokinesis of 5/50 H PF is considered low risk; a tumor < 5 cm with a cytokinesis of 6-10/50 HPF, or a tumor 5-10 cm with a cytokinesis of 5/50 HPF is considered low risk. ~ A tumor < 5 cm with a schizogram of 6-10/50 HPF, or a tumor 5-10 cm with a schizogram of 5/50 H PF is considered moderate risk; a tumor > 5 cm with a schizogram > 5/50 HPF, or any tumor > 10 cm, or any tumor with a schizogram > 10/50 HPF is considered high risk for malignancy. It is important for surgeons to be proficient in this assessment because it is the basis for the choice of the timing or mode of surgery, the determination of the extent of surgical resection, the establishment of postoperative treatment principles, and the prognosis of the patient. Papalambros et al. 2010 reported that very low-risk GST with a tumor < 2 cm and a fracture sign < 5/50 H PF had recurrence of the gastrointestinal anastomosis 8 years after surgery. Thus, it is clinically believed that GST is at risk of recurrence and metastasis, with liver metastases (65%), peritoneal metastases (50%), or both liver and peritoneal metastases (20%) predominating, and lymphatic metastases are rare. The above characteristics determine the choice of clinical treatment for GST. Surgical treatment of GST is the first choice of treatment for GST. The indications for surgical treatment are: tumors < 2 cm can be observed clinically, but patients should be informed that the risk of malignancy cannot be ruled out despite the small size of the tumor, so regular observation is required; tumors > 2 cm are strongly recommended for surgical treatment. The principle of surgical resection is to ensure an en bloc resection (R0 resection) with negative margins, while avoiding tumor breakdown and tumor cell implantation in the peritoneal cavity. The choice of surgical approach depends on the size and location of the tumor and its relationship to the surrounding organs. In general, for small tumors and if the location allows, local excision or wedge resection can be performed, and the cut edge should generally be 1~2 cm from the tumor margin, and if necessary, frozen pathology should be sent to confirm the negative cut edge. If the tumor is large or located near the cardia or pylorus, partial gastrectomy is recommended. For larger tumors located in the lesser curvature, total gastrectomy can be performed if necessary. Several case studies have shown that there is no significant difference in patient survival after partial resection and partial gastrectomy. If the tumor is tightly adherent to surrounding organs, omentum and other tissues, it is recommended to remove the whole piece with the adherent organs or tissues. Local lymph nodes should be resected together if they are enlarged, but routine regional lymph node dissection is not recommended. Laparoscopic surgery is suitable for GST with small tumors, limited tumors, and little possibility of intraoperative tumor rupture. Endoscopic or laparoscopic tumor excision or resection is not recommended. Generally, R0 resection of low to moderate risk GST < 5 cm can achieve a 5-year survival rate of 50% to 80%. However, for moderate to high-risk GSTs > 5 cm, R0 resection alone is difficult to achieve radical cure, and the postoperative recurrence rate of metastasis is more than half. Most recurrences occur within 2 years after surgery, and liver metastases and intra-abdominal metastases are the most common, so regular postoperative ultrasound or CT review is important. For high and medium risk GST, it is recommended to review every 3-4 months until 3 years, then every 6 months until 5 years, and then every year; for very low and low risk GST, it is recommended to review every 6 months until 5 years. The introduction of imatinib (Glevec) in combination with surgical targeted therapy has revolutionized the clinical management of G IST. Imatinib is a tyrosine kinase inhibitor that can target and block the downstream signal transduction mediated by ck it to inhibit tumor growth. It has been clinically proven to be effective up to 75%~80%. The ACOSOG (Z9001) study showed that imatinib 400 m g/d was effective for all tumor sizes and improved recurrence-free survival (RFS). The improvement in recurrence-free survival was more pronounced in larger tumors (>10 cm), but no improvement in overall survival was observed. The duration of treatment remains controversial, with the general consensus being to stop at least 2 years of continuous use. However, there are cases of recurrence after 1 year of discontinuation, so there is still a debate on the issue of tumor resistance and whether it can effectively improve the cure rate and overall survival rate. In case of recurrence after drug discontinuation, surgery is recommended as the first choice, and postoperative adjuvant therapy is recommended because patients can still benefit from imatinib treatment after surgical reduction of tumor load and slow down the duration of tumor resistance. If surgery is lost, the dose can be increased to 600 m g/d, or the second-line drug sunitinib (Sutent) can be used instead. Sunitinib is a newly available multi-targeted agent, and 65% of patients with imatinib resistance may benefit from sunitinib treatment. Imatinib neoadjuvant therapy: neoadjuvant therapy is not recommended for patients with large tumors and clear peripheral invasion that makes R0 resection difficult, or where surgery may severely compromise peripheral organ function. Neoadjuvant therapy should be administered strictly to determine whether it can achieve tumor shrinkage and clinical reduction, and therefore regular CT or PETCT evaluation should be performed before and after neoadjuvant therapy to select the best time for surgery. If the tumor shrinks, surgery should be performed as soon as it can be safely removed, rather than waiting for the maximum effect of imatinib. Surgery should generally be performed within 12 months of drug administration to avoid unnecessary treatment, accelerated drug resistance, or delay in surgical treatment.