Abstract】 The p53 gene is known as the “gene protector”, and its inactivation is closely related to the development of more than half of tumors. In 2003, the recombinant human p53 adenovirus injection was marketed under the trade name of “Imazan”, which is the first approved gene therapy drug for tumors in the world, and is composed of normal human p53 tumor suppressor gene and modified type 5 adenovirus gene. It is composed of normal human p53 tumor suppressor gene and modified type 5 adenovirus gene. The former is the main structure of Imazan to play the role of tumor therapy, while the latter mainly acts as a carrier, carrying the therapeutic gene p53 into the tumor cells. Recombinant human p53 adenovirus (rAd-p53) is a broad-spectrum anti-tumor drug, and several research papers have been published in China and abroad on the treatment of malignant solid tumors in all major systems. The clinical research progress is now reviewed. P53 gene is a recognized “gene protector”, and more than 60% of tumors in more than 100 human tumors are related to p53 gene mutation. The introduction of exogenous tumor suppressor gene (p53 gene) into tumor through adenoviral vector can inhibit the growth of tumor tissue through various anti-tumor mechanisms such as apoptosis, by-stander effects and inhibition of multidrug resistance gene (MDR) expression, which has become a new tumor treatment method. Currently, adenovirus-mediated p53 gene therapy has been applied to treat various malignant tumors, including: head and neck tumors, lung cancer, liver cancer, breast cancer, brain tumors, ovarian cancer, bladder cancer, prostate cancer, etc. The anti-tumor mechanism of action of “Imazan” is that the viral vector carries the therapeutic gene p53 into the target cells. At the nuclear level, p53 acts as a transcriptional regulator to regulate the expression of apoptosis-related genes in the nucleus, and at the cytoplasmic level, p53 initiates the apoptotic death receptor pathway and the mitochondrial apoptotic pathway. In addition, “Imazan” can also kill tumors through the “bystander effect” and inhibit tumor angiogenesis, and improve the sensitivity of radiotherapy and chemotherapy drugs. The replication-deficient adenovirus, which is the vector of “Imazan”, has stable physicochemical properties, high infection efficiency and low genotoxicity, and is safe for clinical application. Preclinical studies have shown that the introduction of wild-type p53 gene into tumor cells can induce cell cycle arrest, promote apoptosis, and inhibit tumor angiogenesis. Studies in animal models of transplantation tumors have shown that intratumoral injection of adenovirus-mediated wild-type p53 leads to apoptosis and tumor regression in tumor cells of various origins. These tumor types include non-small cell lung cancer, leukemia, glioblastoma, head and neck tumors, and tumors in the breast, liver, ovary, colon, and kidney.