Small cell lung cancer (SCLC) accounts for about 15-20% of all lung cancers. Compared with non-small cell lung cancer, its biological behavior is worse, its disease develops rapidly, and it is prone to early metastasis, and about 60%-70% of patients are already in advanced stages when diagnosed. It is currently thought to be associated with smoking, environmental and genetic factors. There is increasing evidence that autocrine growth rings, proto-oncogenes and oncogenes are associated with the development of small cell lung cancer. It is believed that SCLC originates from Kulchistky cells in the bronchial epithelium and mucus glands, and the tumor cells have a clear neuroendocrine differentiation tendency and cause some abnormal endocrine syndromes such as abnormal antidiuretic hormone syndrome, Cushing’s syndrome and carcinoid syndrome in clinical practice. (I) Molecular mechanisms of small cell lung carcinogenesis The pathogenesis of SCLC has not been fully validated yet, but the abnormal proliferation of neuroendocrine cells in the lung was one of the first hypotheses. decarboxylase activity, calcitonin, etc. GFI1, which is associated with neuroendocrine cell differentiation, is also expressed in SCLC. 85% of SCLC produce at least one of the following three proteins: gastrin-releasing peptide, interneurin B, and receptors, such as belladonna (peptide) receptor subtype 3. The binding of the peptide to the receptor activates an autocrine growth loop that stimulates cell growth. Similarly, SCLC also expresses KIT proteins, and KIT protein kinase activity affects the pathophysiology of many tumors, with KIT expression rates in SCLC ranging from 28-88% [1, 2], which are examples of the existence of an autocrine growth loop in SCLC pathogenesis and are currently important targets for immune and molecularly targeted therapies for SCLC. myc oncogene encodes a nuclear phosphoprotein that promotes cell growth leading to accelerated cell cycle. Myc protein is overexpressed in 15-30% of small cell lung cancers. c-myc antisense DNA in combination with retinoic acid inhibits cell proliferation by downregulating Myc expression. Receptor tyrosine kinase c/met is associated with SCLC, whereas EGF receptor is rarely expressed in SCLC, and 75% of SCLC have Bcl-2 expression. VEGF-mediated angiogenesis has a more important role in the development and progression of SCLC compared to NSCLC, and VEGF expression and microvessel counts are associated with patient prognosis, and tumor angiogenesis is also associated with matrix metalloproteinases produced and released by SCLC. The study of the molecular mechanisms of SCLC development may help us to find new treatments, improve the efficacy of chemotherapy, develop new target drugs and early diagnosis. (II) Staging, prognosis and prognostic factors of small cell lung cancer Staging is particularly important for the diagnosis, treatment and prognosis of small cell lung cancer patients. Information to be collected for staging of primary SCLC includes: complete medical history and physical examination, pathology section consultation, chest X-ray, CT of chest and upper abdomen (including liver and adrenal glands), brain MR or CT, bone scan, blood electrolytes, creatinine, urea nitrogen, liver function (including lactate dehydrogenase), etc. Positron tomography (PET) is not currently used as a routine test necessary for clinical staging of SCLC, except as a clinical study. The clinical staging criteria of SCLC can be adopted from the TNM staging of AJCC/UICC, while the classification of limited stage and extensive stage by the Veterans Administration Lung Study Group (VALG) is widely recommended because it is more convenient for clinical guidance. The so-called limited stage SCLC refers to the lesion that is confined to one side of the chest cavity and can be included by the same radiation field, while the opposite is called extensive stage SCLC. Patients with limited stage of primary small cell lung cancer account for about 30-40% of the total number of patients, of whom 60-90% are sensitive to first-line treatment regimens such as EP and CAV regimens, and about 40-70% achieve complete remission (CR) (3), with a median survival (MST) of about 17 months and a disease-free survival (DFS) rate of 12-25% at 5 years. 12-25%, with CR rates of more than 20% for extensive SCLC combined with chemotherapy, MST of more than 7 months, 5-year DFS of 2%, and treatment-related mortality of less than 5%. Poor prognostic factors include poor PS score, diagnosis of extensive stage, weight loss, and larger tumor load. Patients with limited-stage small cell carcinoma with a good PS score or who are female, less than 70 years of age, with LDH within normal values and stage I suggest a better prognosis, while patients with extensive-stage small cell lung cancer with normal LDH values and a single metastasis suggest a better prognosis [4]