Biological characteristics Lung cancer can be divided into two categories: small cell lung cancer and non-small cell lung cancer, based on the efficacy of radiotherapy and chemotherapy. Small cell lung cancer accounts for about 20% of all lung cancers. Non-small cell lung cancer includes three major tissue types: adenocarcinoma, squamous carcinoma and large cell carcinoma. The long-term survival of patients with small cell lung cancer depends mainly on the response to radiotherapy and chemotherapy, while the long-term survival of non-small cell lung cancer depends mainly on its resectability. There are a large number of molecular biological differences between small cell lung cancer and non-small cell lung cancer. For example, small cell lung cancer is rich in L-dopa decarboxylase, bombesin, and enzyme neuron-specific enolase, while it is less expressed in non-small cell lung cancer. Even in the same small cell lung cancer, the expression of various molecular biological markers varied. Small cell lung cancers of variants with lower levels of these markers proliferate significantly faster than classic small cell lung cancers. In addition, about 20% of non-small cell lung cancers contain dopa decarboxylase, and the prognosis of this group of patients is significantly worse than that of other patients with the same stage. Therefore, APUD components can appear in any tissue type of lung cancer, and because of the large difference in prognosis, lung cancer can be classified into neuroendocrine lung cancer and non-neuroendocrine lung cancer, and this classification is very beneficial for prognosis judgment and treatment plan development. A series of molecular biological changes occur during the development of lung cancer, which constantly regulate tumor growth and also affect the efficacy of lung cancer treatment. In 2000, Hanahan proposed six characteristics of tumor molecular biology: ① activation of growth signaling pathways without external stimulation; ② insensitivity to growth inhibitory signals; ③ evasion of apoptosis; ④ ability to proliferate indefinitely; ⑤ induction of vasculogenesis; ⑥ ability to invade and metastasize. . EGFR is a transmembrane tyrosine kinase receptor that binds to ligands and forms dimers, which in turn activates downstream signaling pathways such as Ras-Raf-MARK and PI3K. EGFR overexpression is mainly seen in non-small cell lung cancers, but less commonly in small cell lung cancers. The importance of EGFR pathway research is to apply the theory of molecular biology to clinical practice, to guide clinical diagnosis and treatment, and to change the treatment mode of a certain type of lung cancer, which is a successful example of translational medicine. EGFR mutations have been shown in clinical trials to be a predictor of the efficacy of first-line EGFR-tyrosine kinase inhibitor (TKI) therapy in advanced lung adenocarcinoma. In addition to the proven EGFR mutations as clinical predictive markers, new molecular markers have become a hot research topic. For example, EML4-ALK fusion gene can predict the efficacy of ALK-targeted drugs, ERCC1/BRCA1 predict the efficacy of platinum-based chemotherapy, thymidine synthase (TS) predict pemetrexed, and RNA nucleotide reductase 1 (RRM1) predict the efficacy of gemcitabine. Epidemiological characteristics Lung cancer was a rare disease worldwide at the beginning of the 20th century and jumped to the top of the list of causes of cancer deaths worldwide over a 50-year period starting in the 1930s. lung cancer incidence rates decreased slightly in some developed countries in the 1990s, while they are continuing to rise in a wider range of developing countries. The incidence of lung cancer in China has been on the rise. In Beijing, for example, the lung cancer incidence rate rose from 38.79 per 100,000 to 60.65 per 100,000 between 2000 and 2009, an increase of 56.35%. in 2008, the incidence rate of lung cancer in Beijing was 72.38% for men and 43.08% for women. It is noteworthy that worldwide, the increase in lung cancer incidence is more pronounced among women than men. Even in some developed countries, the incidence of lung cancer in men has been controlled, while the incidence in women continues to rise. This is associated with the increase in smoking rates in the female population. Lung cancer incidence and mortality rates vary significantly by race; in 2001, the incidence of lung cancer among black, white, Asian, and Hispanic men in the United States was 109 per 100,000, 87 per 100,000, 50 per 100,000, and 52 per 100,000, respectively. Blacks had the highest mortality rate and Asians had the lowest mortality rate among males. Among women, the highest mortality rates were among whites and blacks, and lower mortality rates were among Asians and Hispanics. In the early 21st century, adenocarcinoma accounted for 47% of all lung cancers, including 52% in women and 42% in men. Another notable change is the steady decline in the incidence of small cell lung cancer, with statistics from Parkin et al. in 2002 showing that small cell lung cancer and large cell lung cancer accounted for 20% and 9% of all lung cancers, respectively. This is closely related to changes in smoking rates and smoking patterns in the population.