Gastrointestinal stromal tumors (GIST) are independent tumors that are not very rare clinically. 1. Basic research on gastrointestinal stromal tumors 1.1. Concept of GIST The tumor is located in the gastrointestinal tract and has a histological pattern of spindle cell epithelioid cells or pleomorphic cells. Immunohistochemical expression of KIT protein (CD117) is positive. Genetic presence of frequent c-kit gene mutations. Originates from a tumor of mesenchymal origin. Tumors can also occur in soft tissues of the abdominal cavity such as the omentum, mesentery, or retroperitoneum, all with the same morphologic, immune expression, and molecular genetic features as GIST. However, mesenchymal tumors with the above features occurring outside the gastrointestinal tract and abdominal cavity are rare. 1.2. History of GIST research From 1960 to 1980, spindle-shaped and epithelioid tumors of mesenchymal origin were discovered in the gastrointestinal tract and were considered smooth muscle tumors or smooth myoblastomas, and were classified as epithelioid smooth muscle sarcomas by WHO. After the development of immunohistochemistry in the 1980s, the immunophenotype was found to be mostly negative for desimin, negative or focally positive for smooth muscle actin (SMA), and often negative or weakly localized positive for S-100 protein. Electron microscopic findings do not show the typical myxomatous and neurological features. 1983 Mazur and Clark study determined to name this type of tumor after gastrointestinal mesenchymal tumor (GIST). [In 1993, CD34 was identified as a relatively specific immunohistochemical marker for GIST. [The KIT protein product (CD117) is a highly specific marker for GIST. These findings are of great value in determining the clinical diagnosis of GIST with certainty. Before the 1980s, GIST was histomorphologically similar to smooth muscle tumors and neurogenic tumors, and was thought to originate from smooth muscle or neural tissue. （GIST is an independent mesenchymal tumor biologically characterized by c-kit mutation and KIT protein (CD117) expression. The concept of gastrointestinal mesenchymal tumor (GIMT) differs from that of GIST in the range of tumors it contains, with approximately 73% of GIMT being GIST and the other GIMTs being smooth muscle tumors, smooth muscle sarcomas, lipomas, nerve sheath tumors, and gastrointestinal autonomic nerve tumors (GIST). Other GIMTs include smooth muscle tumor, smooth muscle sarcoma, lipoma, nerve sheath tumor and gastrointestinal autonomic nerve tumor (GANT). The tumors vary in size from 0.8cm to 20cm in diameter and can be solitary or multiple. The tumors are mostly located in the submucosa (60%), subplasma (30%) and muscularis (10%) of the gastrointestinal layer. The tumor is well-defined, without envelope, and grows into the lumen as a polyp-like mass often accompanied by ulcer formation, and grows outside the plasma membrane to form a subplasma mass. Clinical signs of gastrointestinal bleeding and palpable masses are common. In mesenchymal tumors located in the abdominal cavity, the mass is often large in size. The tumor has a nodular or lobulated gross morphology, with grayish-white and red sections, uniform, hard and tough texture, ulcer formation on the mucosal surface, visible hemorrhage, necrosis, mucinous changes and cystic changes. 1.5, histomorphological features GIST including those occurring outside the GI tract have the same histological morphology. There are basically two cell types, namely: most (70%) consist of spindle cells, a few (15%) consist of epithelioid cells, and a mixture of the two cell types (15%). From the proportion of the two cell types, there are two types of cells: spindle cell type, epithelioid cell type and mixed cell type. The majority of the three types are spindle cell type (60%-80%), followed by epithelioid cell type (10%-30%), and the least mixed type. There was no correlation between different cell types and tumor malignancy [6]. 1.6. Molecular genetic characteristics Mutations in the proto-oncogene c-kit function are common in GIST (80%). c-kit mutations can occur at multiple loci in exons 11, 9, 13 and 17, and PDGFRA mutations (platelet-derived growth factor receptor) are also present in those who do not show c-kit mutations. c-kit proto-oncogene mutations cause tyrosine kinase activation and trigger cellular disorder. Mutations in the c-kit proto-oncogene activate tyrosine kinase, triggering uncontrolled cell proliferation and inhibition of apoptosis, which are key to the pathogenesis of GIST and correlate with the malignancy and poor prognosis of GIST. The detection of c-kit and PDGFRA mutations in tumor tissues by PCR correlates with the efficacy of the molecularly targeted drug Imatinib, time to disease progression and overall survival rate. 2. Clinical studies of gastrointestinal mesenchymal tumors 2.1. Epidemiology of GIST The incidence of GIST was not recognized in the past, and it was difficult to count the incidence exactly. In recent years, the annual incidence rate is estimated to be 1 to 2/100,000 population, and the annual incidence of 6,500 new cases in the United States should exceed at least this number in China. In our hospital, there are more than 20 newly diagnosed patients in two years, and some hospitals in China report between 5 and 10 cases of GIST annually, which is not very rare. GIST accounts for 1% of malignant gastrointestinal tumors, 2.2% of malignant gastric tumors, 13.9% of malignant tumors of the small intestine, and only 0.1% of malignant tumors of the colorectum. 2.2. Clinical characteristics of GIST Sex is slightly more common in men than in women, or equal in both sexes. Prevalent age range 55 to 65 years (reported age ranges from 17 to 84 years). gist sites: stomach 60% to 70% most common, small intestine 20% to 30%, colorectal.