The formation and development of gastric cancer, from cancer to develop into cancer cells to go through a long process. Generally believed that this process can be divided into excitation, promotion, progression and metastasis in four stages. This is the theory of multi-stage tumors. This multi-stage cancerous tumors in the experimental stage and pathological evolution have been confirmed.
Excitation process is the role of normal cells by the carcinogen into after the process of latent tumor cells. Excitation process is relatively short, usually not reversible. Have confirmed that most of the carcinogens were mutagenic properties, so excited with the mutagenic properties of the process, which involves stimulating the event of genetic mutations. Promote the process of latent cancer cells by tumor promoters effect the process of cancer cells after the shift. To promote the early stages of reversible and irreversible late. Tumor promoters themselves do not have mutagenicity, tumor promotion process is further stimulate cell proliferation, and gradually form a clone of the selection process. In this process, stimulate cell growth out of control, escape from host immune surveillance, and gradually form a malignant phenotype, and then develop into invasive, metastatic cancer.
The formation and development of gastric cancer, gastric cancer occurs when, because of the characteristics of cancer cells, tumor cells continue to grow, reproduce, and continue to expand around the infiltration of tissues and organs, or through the blood, lymphatic and other channels to distant at the dissemination and transfer, and finally lead to the body tissues and organs function failure leading to death. Some statistics show that the natural history of gastric cancer for the 3_6 years. Speed the development of gastric cancer depends on two factors: the first is the degree of malignancy of cancer, the higher the malignant process, the faster the development of the tumor, the more short survival; followed by the immune status of patients, such as immune function poor, the more anti-tumor ability of poor development to rapid tumor growth and survival to short. In general, the tumors were expansive type of growth or mass infiltration of those low rate of lymph node metastasis, immune function is strong. The main performance is in the active immune cells around the tumor, the tumor is often accompanied by fibrous tissue wrapped; and invasive growth of cancer patients showed lymph node metastasis rate was higher activity of cancer cells in the immune response around the obvious.
Since tumor growth, tumor necrosis and ulceration of easy infiltration or tumor caused gastric damage and broken blood vessels stain, may cause upper gastrointestinal bleeding. When a small amount of bleeding and only a positive fecal occult blood or black stools. When the bleeding is heavy, can cause acute bleeding, this can be seen vomiting into a lot of brown blood and melena. If the depth of tumor invasion to the stomach through the stomach, can cause perforation caused by acute diffuse peritonitis, when the tumor to surrounding tissues and organs can be formed when the internal fistula puncture. Violations of tumor metastasis and invasion of intestine, can cause intestinal stenosis caused by complete or incomplete intestinal obstruction. When the gastric tumor growth and invasion, can cause stomach smaller or poor cardiac obstruction caused by Helicobacter pylori and gastric cardia. Sometimes these complications are more serious, if too late to rescue the poor or therapeutic effect, it can directly endanger the patient's life.
The formation and development of gastric cancer, with the rapid development of cell and molecular biology of gastric cancer research of the development process has entered the molecular level. Comprehensive analysis of gene over-expression occurred in the initial stage of carcinogenesis, such as the ras, met gene; gene mutation and cancer cells may be one of the main events start-up phase, this phase of the reversibility of the larger, such as ras, p53 gene ; gene amplification and rearrangement in the promotion stage of carcinogenesis, cancer cells may begin to differentiate the different biological behavior, which showed heterogeneity in their control from the body, such as erbB2, EGFR, mdrn2, met, akt2 isogenic; gene deletion has the potential to more severe genomic damage, not only led to the diversification of the biological behavior of cancer cells, and further lead to cancer cell proliferation and differentiation of the irreversibility of loss of control, prompting the rapid development of tumors, such as APC, p53, p16, nm23 gene. These again proved the occurrence and development of gastric cancer is a multi-stage, multi-step process.