Retrospective development of anticancer drugs
Traditional anti-tumor drugs act on DNA replication and cell differentiation, and although they have serious side effects, they are still very effective in treating some cancers. In order to reduce side effects and increase the specificity of oncology drugs, some drugs targeting oncoprotein signaling pathways have been developed, and these drugs are limited in application due to their resistance to drug resistance. Nowadays, small molecule anticancer drugs that act on different cellular mechanisms are emerging. Their targets include chromosome modification, heat shock proteins, molecular chaperones and protein kinases. These targets are more common for cancer cells than normal cells. important. This article will review the development of anti-tumor drugs and compare the advantages and limitations of anti-cancer drugs that act on both tumor-dependent cellular mechanisms and signaling molecules.
Anti-tumor drugs can be roughly divided into three generations. The first generation: anti-tumor drugs mainly act on DNA replication and cell differentiation, such as modifying DNA and interfering with tubulin polymerization. The second generation: anti-tumor drugs mainly act on signaling molecules related to tumor growth. The most prominent receptors or kinases are BCR-ABL and BRAF. The third generation: the development of anti-tumor drugs no longer directly interferes with DNA replication or cell differentiation, and instead targets cell mechanisms that are more important for tumor cell growth, such as chromosome modification, heat shock proteins, molecular chaperones and proteins. Kinase and the like. Drugs targeting these targets have been marketed, such as the proteasome inhibitor bortezomib for the treatment of multiple myeloma. However, more and more researchers have confirmed that the mechanism of RNA and protein synthesis, intracellular transport, metabolic pathways and organelle completion are more important for the growth of tumor cells than normal cells.