The exact cause of the disease is still difficult to determine, but from epidemiological investigations, experimental tumor studies and clinical observations, the occurrence of thyroid cancer may be related to the following factors Radiological damage: Irradiation of thyroid gland of laboratory rats with x-ray can induce the development of thyroid cancer in animals. Experimentally, 131 i can cause changes in the metabolism of thyroid cells, deformation of the nucleus and a great reduction in the synthesis of thyroxine. It can be seen that on the one hand, radiation causes abnormal division of thyroid cells, leading to cancer; on the other hand, it destroys the thyroid gland and cannot produce endocrine hormone, and the resulting large secretion of thyroid stimulating hormone (tsh) can also promote thyroid cell carcinogenesis. In clinical practice, there are many facts that indicate that thyroid gland development is related to the action of radiation. Of particular interest is the fact that children who have been treated with radiation to the upper mediastinum or neck during infancy for thyroid enlargement or lymphoglandular proliferation are particularly susceptible to thyroid cancer, because the cells of children and adolescents are highly proliferative and radiation is an additional stimulus that predisposes them to tumor formation. Adults are less likely to develop thyroid cancer after neck radiation therapy. Iodine and tsh Excessive iodine intake or iodine deficiency can alter the structure and function of the thyroid gland: for example, the incidence of thyroid cancer in endemic areas of Switzerland is 20 times higher at 2 per 1,000 than in non-endemic areas such as Berlin. Conversely, a diet high in iodine also predisposes to thyroid cancer. Iceland and Japan, the countries with the highest iodine intake, have higher rates of thyroid cancer detection than other countries. This may be related to the factor that tsh stimulates thyroid hyperplasia. It has been shown that long-term tsh stimulation can contribute to thyroid hyperplasia, nodule formation and carcinogenesis. Other thyroid lesions: There are clinical reports of thyroid adenocarcinoma, chronic thyroiditis, nodular goiter or certain toxic goiters becoming cancerous, but the relationship between these thyroid lesions and thyroid cancer is not yet certain. For example, most thyroid adenomas are of follicular type and only 2-5% are papillary; if thyroid adenoma is transformed from adenoma, most of them should be of follicular type, but in fact, more than half of thyroid adenomas are cephalic carcinomas, so it is assumed that the incidence of thyroid adenoma carcinoma is also small. Genetic factors: About 5-10% of medullary thyroid carcinomas have obvious family history and are often combined with pheochromocytoma and other intercalary tumors, so it is presumed that the occurrence of such carcinomas may be related to chromosomal genetic factors.