The exact cause is still difficult to be sure, but from epidemiological investigations, experimental tumor studies and clinical observations, the occurrence of thyroid cancer may be related to the following factors 1.Radiation damage Irradiating the thyroid gland of experimental rats with X-rays can induce the development of thyroid cancer in animals. It is proved that 131I can change the metabolism of thyroid cells, deform the nucleus and greatly reduce 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 prevents it from producing 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 thyrotoxicosis 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. For example, in the 1998 Chernobyl leak, the incidence of thyroid cancer was 100 times higher in children living in Belarus and Ukraine than elsewhere. The chance of thyroid cancer occurring in adults after neck radiation therapy is uncommon. 2. Iodine and TSH Excessive iodine intake or iodine deficiency can change the structure and function of the thyroid gland. For example, the incidence of thyroid cancer in Switzerland is 20 times higher than that in non-endemic areas such as Berlin, where the incidence of endemic goiter is 2 per 1,000. 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 of TSH stimulating thyroid hyperplasia. Experiments have shown that long-term TSH stimulation can contribute to thyroid hyperplasia, nodule formation and cancerous changes. 3. Other thyroid lesions There are clinical reports of thyroid adenocarcinoma, chronic thyroiditis, nodular goiter or some toxic goiters becoming cancerous, but the relationship between these thyroid lesions and thyroid cancer is not yet certain. For example, most of the thyroid adenomas are follicular type, and only 2-5% are papillary; if thyroid cancer is transformed from adenoma, most of them should be follicular type, but in fact, more than half of the thyroid cancers are papillary cancers, so it is assumed that the incidence of thyroid adenoma carcinoma is very small. Genetic factors About 5-10% of medullary thyroid carcinomas have obvious family history and are often combined with pheochromocytoma, etc. It is presumed that the occurrence of such carcinomas may be related to chromosomal genetic factors. Cellular genes carry genetic information from both parents. An abnormal gene has been found in some types of thyroid cancer, such as medullary carcinoma which may be born with an abnormal gene that causes tumors. Family members may also inherit this abnormal gene, and such patients and their family members (parents, children, grandchildren, brothers, sisters, nieces and nephews) should be examined for the presence of the abnormal gene. Such tests are credible, and surgical removal of the thyroid gland may reduce the chance of developing medullary carcinoma, provided the abnormal gene is detected in family members, including those in whom no tumor is found.