What is oncogene addiction? We are all familiar with drug addiction, but I am afraid this is the first time we have heard of genetic addiction, right? Addiction refers to the formation of a dependence on a substance or behavior that is difficult to overcome and can lead to psychological and physical problems if forced to stop. For example, drug addiction is caused by the repeated use (or consumption) of addictive drugs (or drugs), resulting in psychological and even physiological dependence on the drug, and if you do not continue to take it, it will bring obvious withdrawal symptoms, which are painful and accompanied by some abnormal physiological and psychological indicators, and can be fatal in serious cases. Oncogenic addiction is the dependence of tumor cells on overactive genes or pathways to achieve their growth and survival. Oncogenic addiction is relatively easy to understand. Some of the characteristics of cancer are caused by the activation of oncogenes or inactivation of oncogenes, and the maintenance of these characteristics is of course dependent on the function of these oncogenes. Just like a person who becomes arrogant and domineering because he has been promoted, if he is jerked off, see how he can still be wild? Why would cancer cells become dependent on certain common genes as well? Cancerous cells have many characteristics that distinguish them from normal cells. To put it simply (and generally), after a cell becomes cancerous, many of its behaviors have gone far beyond the normal range, and the original balance within the cell has been disturbed. In order to maintain the new balance, the cell either increases the “workload” of some genes or “mobilizes” others to correct the imbalance and resolve the stress. These mobilized genes, which may normally be obscure, unimportant, or even dispensable, are now “promoted and reused” to become “key players” in the life and death of cancer cells. For example, the growth of cancer cells is not limited, and the cells keep growing rapidly, so the demand for materials and energy increases greatly, and the reliance on “logistic transportation” becomes even greater; however, the increased vascular transportation capacity still cannot meet the demand, so cancer cells have to increase the glycolytic capacity for emergency, just like “The rapid proliferation of cancer cells requires DNA replication, which is out of control, so the cancer cells are busy and make mistakes repeatedly, which increases their reliance on “repairman”. The “tinkerer” is too busy, so he has to “bribe” members of the quality control department, such as p53, ATM or Chk2, etc. In short, there are more and more problems, and the “evil path” is going further and further. The system is constantly adjusting and forming a new balance. For example, the growth of cancer cells requires the synthesis of a large number of new proteins, and it is inevitable that substandard products (such as misfolded protein assembly) will be produced. At this time, it is necessary to usually hang around, idle “quality controller” followed by overtime, or supervise the production, or pick out the inferior products in time to destroy. The intracellular protein controller has two parts, one to assist protein assembly, called molecular chaperones, like some heat shock proteins; the other part is responsible for the “destruction process”, if the protein error can not be corrected that has to “destroy” (degradation). Under normal circumstances, protein production is not slow, everyone is orderly; after the cell cancer, it forces these mechanisms to speed up the rhythm, violating the labor law “5 + 2” “day and night”, working overtime, exhausted; which day these guys suddenly went on strike. When these guys suddenly go on strike, the crazy energy of cancer cells will come to an end. What is the relationship between oncogene addiction and lung cancer? What is the value of this concept? From the examples I have given, you may have realized that it is to help people realize that there are more potential defects (or weaknesses) in cancer cells so that we can use them to control cancer. Oncogene addiction provides a theoretical basis for molecular targeted therapy for lung cancer Many lung cancer cells rely on mutated EGFR, ALK fusion genes, ROS1 fusion genes or RET fusion genes to maintain their survival, and if, we can remove these lung cancer addiction genes, we can achieve the effect of treating lung cancer.