Tumors have been discovered in humans for more than 3000 years and have been found on the bones of primitive humans. Tumors have been described since the beginning of written records. The word “tumor” is found in the oracle bone inscriptions excavated at Yinxu. In the West, the word cancer appeared earlier than madicine, which is derived from crab, probably referring to the crab-like behavior that tends to infiltrate and metastasize. Scientific oncology began in the 19th century after the discovery of microscope, and in 1858, Virchow pointed out in his book “Cytopathology” that “cancer is a disease of cells”, which pushed the study of cancer to the cellular level. Watson and Crick proposed the double helix structure of DNA based on the summary of others’ experiments, which brought the research to the molecular level. In the 1960s, the first specific abnormal chromosome Ph was found in the cells of patients with chronic granulocytic leukemia, and since then many chromosomal abnormalities of cancer have been found one after another, and it has become indisputable that cancer is a genetic disease. It is well known that one of the major achievements of modern molecular biology is the discovery of proto-oncogenes and the ability of proto-oncogenes to activate into cancer-causing oncogenes, for which Varmus and Bishop were awarded the Nobel Prize in Physiology and Medicine in 1989. Most of the proteins encoded by proto-oncogenes are cell growth factors and growth factor receptors, important signal transduction proteins, nuclear regulatory proteins and cell cycle regulatory proteins, which are important for normal cell growth. When a proto-oncogene is attacked as a target gene by a carcinogen, the proto-oncogene is activated to become an oncogene with the ability to promote cell transformation in two ways: (1) by structural changes (mutations) that produce oncoproteins with abnormal functions; (2) by changes in the structure of the proto-oncogene that are not altered, but by changes in the level of regulation that result in overexpression of the gene and production of excess normal growth-promoting proteins. Both of these approaches can lead to an excessive or sustained presence of cell growth stimulating signals that transform the cells. In contrast to the encoded proteins that promote cell growth, the products of another class of genes in cells under normal conditions – tumor suppressor genes – can inhibit cell growth. Their loss of function may also promote cell transformation. The most known oncogenes are the Rb gene and the p53 gene. It is important to note that proto-oncogenes, oncogenes, and oncogenes are actually genes that play a positive or negative role in regulating cell growth and differentiation and are inherent within the cells of the body. They play an important role in maintaining the normal function of the organism. If abnormal changes occur, they may cause cell transformation and tumor development. The development of malignant tumor is a long-term multi-factorial formation in a staged process. It is the result of the combined action of proto-oncogene, oncogene and carcinogens (physical, chemical and biological). Normal cells are constantly attacked by carcinogens over a long period of time, which eventually leads to mutation of genes and the formation of cancer cells. The essential differences between cancer cells and normal cells can be summarized as follows: (1) cancer cells have abnormalities in the regulation and control of the two biological processes of cell proliferation and cell differentiation, which cause cancer cells to grow and divide without functional differentiation; (2) cancer cells have variability, including variation in karyotype, growth rate, differentiation, nutritional requirements and infiltration and metastatic behavior. The variability of cancer cells constitutes the heterogeneity of cancer cells. It is rooted in the genetic instability of cancer cells. According to the central law of inheritance, the above-mentioned changes in the biological behavior of cancer cells are closely linked to their genetic alterations. The transformation of normal cells into cancer cells is a complex process, and individual genetic alterations are not yet sufficient to cause complete malignant transformation of cells. Multiple genetic alterations, including activation of several oncogenes, inactivation of two or more oncogenes, and alterations in apoptosis regulation and DNA repair genes, are required for complete malignant transformation of cells. In the case of colon cancer, for example, the critical steps in the evolution from normal epithelial overgrowth of the colon to colon cancer are mutation of oncogenes and inactivation of oncogenes. I think: in a sense the cancerous tissue is adapting to the local stimulation of carcinogenic substances. Because external carcinogenic substances, especially some physical and chemical factors, have harmful effects on cells, under the long-term effect of these substances, normal cells must strengthen the repair in order to adapt to the damage, which requires the activation of some genes to synthesize some necessary substances such as enzymes, proteins, etc. When the mutation of genes occurs, cancer cells may be formed, but at this time, cancer cells are no longer regulated and controlled by the body, which eventually leads to the death of the body. However, cancer cells are no longer regulated and controlled by the organism, which eventually leads to the death of the organism. The occurrence and development of tumor is a very complex problem. In addition to the role of external carcinogenic factors, internal factors of the body also play an important role, the latter including the host’s response to the tumor and the impact of the tumor on the host. This enables us to understand why under the same external carcinogenic factors, some individuals are prone to develop cancer while others do not; under the same exposure to external carcinogenic factors, some individuals develop cancer early while others develop cancer late; in rare cases, some tumors can fade and heal on their own. When normal cells are exposed to the long-term and continuous effects of external harmful factors, depending on the intensity of the external harmful factors, normal cells can have the following outcomes: 1. Cells can show adaptation, adapting to environmental changes through proliferation, hypertrophy and chemotaxis. These changes are mostly pathological and some of them are precancerous, such as endometrial hyperplasia caused by excessive estrogen stimulation, which increases the risk of endometrial cancer in such patients. In addition, chemosis is a more important abnormal proliferation that can become cancerous, such as pseudostratified ciliated columnar epithelial squamification of tracheal and bronchial mucosa in long-term smokers, and intestinal epithelial chemosis of gastric mucosa in chronic gastritis, all of which can lead to cancer. But some of the above damage is reversible, once the stimulus is eliminated, some can be restored to normal, and some are carcinogenic. 2.Cell death: There are two types of cell death, necrosis and apoptosis. After the cell is damaged, the cell starts to repair and if the repair is wrong, the apoptosis process is started. Apoptosis is controlled by apoptosis genes and apoptosis inhibiting genes, if apoptosis inhibiting genes are activated and apoptosis genes are inactivated, the cells will not die, such as the inactivation of oncogenes P53, bax and bcl-xs and the activation of apoptosis inhibiting genes bcl-2 and bcl-xl found in the test of tumor patients. Some of the cancerous cells were recognized by the immune system and thus eliminated, while those that evaded the immune system to attack the cancer cells formed cancer nests. The discovery of telomeres and telomerase also provided the basis for proving that cancer is a genetic disease. Telomeres are a special structure at the end of linear chromosomes in eukaryotic cells consisting of a complex of DNA and terminal DNA-binding proteins at the end of the telomeric chromosome. The length of telomeres is inversely correlated with the age of the cell; the older the cell, the shorter the telomeres. The maintenance of telomere length is achieved by telomerase action. Under normal conditions, telomerase activity is present in germ cells and stem cells, while in other cells telomerase activity cannot be detected. As somatic cells divide, telomeres shorten and cells move toward aging. In contrast, telomerase is reactivated in tumor cells, and the cells divide and multiply endlessly.