Head and neck cancer is more common in China, accounting for about 19.9%~30.2% of all malignant tumors in the body. Since most of them are in progressive or advanced stages when they are diagnosed, and the local recurrence rate is high (40-60%), the 5-year survival rate of head and neck cancer does not exceed 40% even with the application of current conventional classical treatments. In recent years, people have been studying the integrated treatment including surgery, radiotherapy, chemotherapy and biotherapy to improve the efficacy. Previous studies have shown that the adenoviral vector human recombinant P53 gene (rAd-p53) has a good therapeutic response in head and neck squamous carcinoma. From November 2004 to May 2005, we applied rAd-p53 combined with chemotherapy to treat 4 cases of advanced recurrent head and neck squamous carcinoma, and obtained better results as follows: The treatment of patients with advanced head and neck tumors requires a multidisciplinary and comprehensive treatment combining surgery, radiotherapy and chemotherapy, which has gained consensus. Although the survival rate of head and neck tumor patients has been improved and the survival period has been prolonged with the introduction of new drugs in recent years, for patients with recurrent local recurrence and distant metastases, the sensitivity of tumor to radiotherapy and chemotherapy has been significantly reduced after receiving repeated radiotherapy and chemotherapy, and the toxic side effects of treatment have further decreased the tolerance of patients. Therefore, reversing tumor resistance and improving sensitivity to radiotherapy and chemotherapy are particularly important for patients to gain access to further treatment. The p53 tumor suppressor gene is closely related to tumorigenesis, progression and patient prognosis. More than 50% of tumors have abnormalities of p53 gene mutations and deletions; especially in patients with head and neck squamous carcinoma, the incidence of p53 gene variants is as high as 95%. Previous research data indicate that wild-type p53 genes are involved in cell cycle regulation and induction of apoptosis. The introduction of wild-type p53 gene can increase the sensitivity of head and neck squamous carcinoma to radiotherapy and chemotherapy. rAd-p53 is a recombinant adenovirus constructed by genetic recombination, and its anti-tumor mechanism: 1. By introducing exogenous p53 gene expression, it can specifically cause apoptosis or put tumor cells in a severe hibernation state without damaging normal cells. 2. Highly expressed p53 protein and recombinant viral particles can effectively stimulate the body’s specific anti-tumor immune response, and local injection can cause 3. p53 protein can also play a “bystander effect” to kill tumor cells through cellular transmission and regulation of the immune system. 4. introduction of wild-type p53 can enhance the killing effect of radiotherapy and chemotherapy on tumor cells. rAd-p53 was applied by Clayman GL et al. The efficacy of rAd-p53 was evaluated in 17 patients with unresectable tumors: 2 patients had tumor shrinkage of more than 50%, 6 patients were stable for at least 3.5 months, and 9 patients had progressive disease. Of these, 17 patients with unresectable tumors were evaluated: 2 had tumor shrinkage of more than 50%, 6 were stable for at least 3.5 months, and 9 had progression. Among the surgically resectable cases, one case was pathologically confirmed to have pathological CR after surgery. The results showed that systemic or local application of rAd-p53 was safe, tolerated by patients, and had certain efficacy. The cytotoxic effect of rAd-p53 in combination with cisplatin on nasopharyngeal carcinoma cell lines was 25% higher than that of cisplatin alone, and about 50% of cells underwent apoptosis when the combination was used, while the apoptosis rate of either drug alone was quite low, and the two drugs interacted in a superimposed manner; when combined with doxorubicin, it enhanced the transfection of rAd-p53 in head and neck tumor cells and promoted the expression of p53 by enhancing exogenous p53 expression, promoting p53-mediated apoptosis in tumor cells and producing synergistic antitumor effects. It provides a theoretical basis for the clinical application of paclitaxel or cisplatin combined with p53 gene in the treatment of head and neck tumors. In our group, four patients with recurrent or metastatic head and neck tumors, whose lesions progressed after repeated surgery, radiation or chemotherapy, were treated with a single-week regimen of rAd-p53 gene combined with paclitaxel or Kenzyme plus cisplatin, and no serious toxic side effects were observed, and the efficacy was evaluated after two courses of treatment: two cases obtained sub-remission, two cases were stable, and the clinical symptoms of the four patients improved significantly, local pain symptoms were reduced, the dosage of morphine was reduced, and appetite was increased. Morphine dosage was reduced, appetite improved, weight increased, and KPS score improved by 10 points on average. Major adverse effects during treatment: all 4 patients developed fever with a temperature of about 38°C after drug administration, which was treated with symptomatic treatment or resolved on its own. All 4 patients had no liver or kidney function or myocardial damage, and all 4 cases had different degrees of myelosuppression, which was related to chemotherapy; there is no data proving that rAd-p53 aggravates chemotherapy drug’s There is no information that rAd-p53 aggravates the myelosuppression of chemotherapeutic agents; the leukocytes of 4 patients were recovered quickly by the adjuvant treatment of granulocyte colony-stimulating factor. Conclusion: The application of rAd-p53 was safe by intravenous infusion or local intratumoral injection and was tolerated by patients; p53 gene combined with chemotherapy is effective for advanced head and neck tumors and deserves further study.