The traditional classification is based on the source of antitumor drugs and the mechanism of action of their drugs, which are classified into six major groups, including alkylating agents, antimetabolites, antitumor antibiotics, botanicals, miscellaneous, and hormone balancing drugs. According to the different targets of antitumor drugs on each phase of DNA synthesis (G1 phase), DNA synthesis (S phase), DNA synthesis (G2 phase) and mitosis (M phase) in the cell proliferation cycle, they are divided into two major categories: cell cycle specific drugs and cell cycle non-specific drugs. 1, cell cycle-specific drugs: the action characteristics are limited to a certain phase of the cell proliferation cycle, in a certain period of time to play its killing effect. The use of slow or continuous intravenous injection, intramuscular injection, oral administration, etc. will play a greater role. The main drugs include antimetabolites and phytochemicals, such as menadione, which acts in the G1 phase. The drugs acting in the S phase are fluorouracil, methotrexate, etc. Drugs acting in G2 phase such as pinyamycin and nitrosoureas. Drugs acting in the M phase such as vincristine, paclitaxel and camptothecin. 2, cell cycle non-specific drugs: no selection of direct action on each phase of the cell proliferation cycle, the effect is stronger, can quickly kill tumor cells, its dose and efficacy is positively correlated, to an intravenous injection is appropriate. Such drugs include alkylating agents, platinum and anti-tumor antibiotics, such as nitrogen mustard, cyclophosphamide, melphalan, cisplatin, carboplatin, oxaliplatin, doxorubicin, actinomycin-D, carazolam, etc. With the in-depth research of antitumor drugs and further understanding of the mechanism of action of drugs at the molecular level, clinical drugs are classified as follows: I. Cytotoxic drugs: (1) Alkylating agents: such as nitrogen mustard (HN2), cyclophosphamide (CTX) and so on. Can make the nucleophilic group in the cell alkylation reaction, causing DNA in the replication of nucleobase mispairing, causing cryptographic interpretation of the wrong. The disruption of DNA structure and function can lead to cell division, proliferation arrest or death. However, there are a few damaged cells whose DNA has been repaired and survived, resulting in the emergence of drug resistance. (2) Platinum compounds: such as cis-chloroplatinum (DDP), oxaliplatin (OXA), etc. It can bind to DNA and then destroy its structure and function. (3) Anthracyclines: such as doxorubicin (ADM), pirarubicin (THP), etc. They can be embedded between DNA base pairs, interfere with the transcription process and prevent the formation of mRNA. (4) Antibiotics that damage DNA: such as mitomycin (MMC), bleomycin (BLM), etc. It can make DNA single-strand break and prevent the synthesis of DNA. (2) Antibiotic drugs that act on nucleic acid transcription: such as actinomycin-D (ACD), arabinosin (ACLA), etc. Non-specific antitumor drugs produced by microorganisms can have a killing effect on each phase of the cell cycle. 3.Anti-metabolic drugs affecting nucleic acid biosynthesis: they are cell cycle specific drugs, which prevent DNA synthesis and inhibit cell division and proliferation at different stages respectively. According to the different biochemical processes they interfere with are divided into: (1) dihydrofolate reductase inhibitors: such as methotrexate (MTX). (2) Thymidylate synthase inhibitors: such as fluorouracil (5-FU). (3) Nucleotide reductase inhibitors: such as hydroxyurea (HU). (4) DNA polymutase inhibitors: such as Ara-C (Ara-C). (5) Inhibitors of purine nucleotide interactions: such as mercaptopurine (6-MP). (4) Phytopharmaceuticals that affect protein synthesis and interfere with mitosis: (1) Vincristine (VCR), paclitaxel (TAX), etc.: affect microtubule protein assembly, interfere with the formation of the spindle in mitosis, and cause proliferating cells to stop at mid-division. (2) High trichostatin: interferes with nucleoproteasome function and prevents protein synthesis. (3) Menthylase: degrades menthylase in blood, making cells lack this amino acid, affecting amino acid supply and preventing protein synthesis. 5, topoisomerase inhibitors: including topoisomerase I inhibitors such as irinotecan (CPT-11) and topoisomerase II inhibitors such as etoposide (VP-16) . It can directly inhibit topoisomerase and prevent the replication of DNA and RNA synthesis. 6, other cytotoxic drugs: such as vincristine, bortezomib, etc. Drugs affecting endocrine balance Tumors originating from hormone-dependent tissues, such as breast cancer, prostate cancer, endometrial cancer, thyroid cancer, etc., still partially retain their dependence on hormones and receptors. These tumors can be reduced in size by hormone therapy, or by resection of the endocrine glands. The endocrine therapy used in clinical practice can directly or indirectly change the hormonal balance of the body and the internal environment of tumor occurrence and development through the feedback effect of pituitary gland to achieve the effect of tumor suppression. These endocrine drugs include estrogen, progesterone and their antagonists. Tamoxifen, which is commonly used in breast cancer clinic, is an estrogen-modulating agent that achieves therapeutic effects by competing with the receptors on the surface of tumor cells and interfering with the stimulation of estrogen on breast cancer. Adrenocorticotropic hormones are used to treat acute lymphoblastic leukemia and malignant lymphoma by affecting the metabolism of fatty acids and causing lymphocyte degradation. 1.Sex hormone drugs: including androgenic drugs such as methyltestosterone; estrogenic drugs such as haloestrol, etc. 2.Sex hormone modulators: including anti-estrogen drugs such as tamoxifen (TAM), toremifene, etc.; anti-androgen drugs such as flutamide, bicalutamide, etc. 3.Aromatase inhibitors: such as letrozole, exemestane, etc. 4, progesterone drugs: such as methyl progesterone, methylepregnanolone. 5.Gonadotropin-releasing hormone drugs: such as goserelin, treprostin, etc. 6.Adrenocorticotropic hormone drugs: such as prednisone, dexamethasone, etc. 7. Other hormone drugs: such as thyroxine, etc. Biological response modifiers are a class of biological antitumor drugs with a wide range of biological and antitumor activities. The mechanism of action of these drugs is to enhance the immune function of the body and regulate it. 1.Cellular immune enhancers: such as interleukin-2, thymidine, etc. 2. Macrophage enhancers: such as interferon, adenovirus P53, etc. Molecularly targeted drugs Among the molecularly targeted drugs, one class is monoclonal antibodies produced by genetic engineering technology. Through the high selectivity, affinity and antibody-dependent cytotoxic effect on the receptor, they can kill tumor cells or inhibit the proliferation of tumor cells. Another class of drugs are those that act on transduction pathways. Small molecule compounds that block or inhibit intracellular signal transduction pathways. 1.Monoclonal antibody drugs: such as trastuzumab, rituximab, cetuximab, bevacizumab, etc. 2, the role of transduction inhibition drugs: such as gefitinib, sorafenib, erlotinib, lapatinib, etc. V. Chinese medicine preparations Ginseng capsule, compound zebrano capsule, compound bitter ginseng injection, arsenious acid, chingqi fuzheng granules, etc. Adjuvant therapeutic drugs 1.Blood-raising drugs: such as recombinant human granulocyte colony-stimulating factor, erythropoietin, interleukin D11, etc. 2, analgesic drugs: such as indomethacin, tramadol, morphine, etc. 3, anti-vomiting drugs: such as domperidone, granisetron, toltesetron, etc. 4.Bone destruction inhibiting drugs: such as pamidronate disodium, zoledronic acid, etc.