What are the causes of thyroid cancer Nowadays, many people are suffering from thyroid diseases, especially thyroid cancer. They are often confused as to how they develop nail cancer. Today, let me sort out some important causes for you! 1. Iodine and thyroid cancer Iodine is an essential trace element. Iodine deficiency leads to a decrease in thyroid hormone synthesis and an increase in thyroid stimulating hormone (TSH) level, which stimulates thyroid follicular hyperplasia and hypertrophy, resulting in goiter and thyroid hormone, which increases the incidence of thyroid cancer, and opinions are still not unanimous. And high iodine diet may increase the incidence of papillary thyroid cancer. 2.Radiation and thyroid cancer Irradiation of the thyroid gland of laboratory rats with X-rays can promote the development of thyroid cancer in animals, which can lead to the deformation of the nucleus and a great reduction in the synthesis of thyroxine, resulting in carcinogenesis; on the other hand, the thyroid gland is destroyed and cannot produce endocrine hormone, and the resulting large secretion of TSH can also promote thyroid cell carcinogenesis. TSH also regulates the growth of thyroid follicular cells through cAMP-mediated signaling pathway, which may lead to thyroid cancer. Increased serum TSH level induces nodular goiter, and thyroid follicular carcinoma can be induced after giving mutagen and TSH stimulation. Moreover, clinical studies have shown that TSH suppression therapy plays an important role in the treatment of differentiated thyroid cancer after surgery, but whether TSH stimulation is a causative factor for the development of thyroid cancer remains to be confirmed. The relationship between sex hormones and thyroid cancer has been emphasized because there are significantly more women than men with well-differentiated thyroid cancer. It is possible that the increased secretion of estrogen is related to the occurrence of thyroid cancer in young people. Therefore, some people have studied sex hormone receptors in thyroid cancer tissues and found that there are sex hormone receptors in thyroid tissues: estrogen receptor (ER) and progesterone receptor (PR), and ER in thyroid cancer tissues, but the effect of sex hormones on thyroid cancer is still inconclusive. 5.Goitre-producing substances and thyroid cancer Animal experiments have confirmed that prolonged use of goitre-producing substances can induce thyroid cancer and also hinder the synthesis of thyroid hormones, increase TSH secretion, stimulate thyroid follicular hyperplasia, and may produce thyroid neoplasia with diffuse enlargement of the thyroid gland, and cause thyroid tumors. Other thyroid diseases and thyroid cancer (1) Nodular goiter The occurrence of thyroid cancer in nodular goiter has always been valued as a risk factor for the development of thyroid cancer, and the incidence of thyroid cancer in nodular goiter can be as high as 4% to 17%. It is not clear. (2) Thyroid hyperplasia The relationship between thyroid hyperplasia and thyroid cancer is still unclear, but it has been reported that congenital hyperplastic goiter without proper long-term treatment eventually develops into thyroid cancer. (3) Thyroid adenoma Most people think that thyroid cancer occurs with solitary thyroid adenoma, and if thyroid cancer is secondary to thyroid adenoma, the type of thyroid cancer should be mainly follicular carcinoma, but the fact is that papillary thyroid carcinoma accounts for the majority of cases, and patients with follicular thyroid carcinoma often have a history of previous adenoma, but it is quite difficult to confirm the relationship between them, even with histological observation. The relationship between them is difficult to confirm, even with histological observation. (4) Chronic lymphocytic thyroiditis In recent years, there have been more and more reports of thyroid cancer found in HT, with incidence rates ranging from 4.3% to 24%, with wide variation, and the actual incidence is more difficult to estimate because HT mostly does not require surgical treatment. On the other hand, focal HT may also be an immune response of the body to thyroid cancer. It is possible that HT leads to destruction of thyroid follicular cells, hypothyroidism, and decreased thyroid hormone secretion, which feedback causes increased TSH, which continuously stimulates thyroid follicular cells, and thyroid follicular cells overproliferate and become cancerous; it is also possible that TSH acts as a promoting factor and becomes cancerous while thyroid oncogenes are overexpressed; it is also believed that HT and It has also been suggested that HT and thyroid cancer share a common background of autoimmune abnormalities. (5) Hyperthyroidism Because of the low level of serum TSH in hyperthyroid patients, it was previously believed that thyroid cancer does not occur in hyperthyroid patients or the incidence of thyroid cancer is consistent between hyperthyroid patients and the general population (0.6% to 1.6%), and the incidence of thyroid cancer is 2.5% to 9.6%. The actual incidence of hyperthyroidism is unclear either because the thyroid gland is large or because there are already thyroid nodules, and most of them are treated with medication. Therefore, we should pay attention to the clinical situation of hyperthyroidism combined with thyroid cancer and be more alert to the existence of thyroid cancer. 7. Familial factors and thyroid cancer Thyroid cancer is less often seen as an independent familial syndrome, but can be part of a familial syndrome or hereditary disease. A few families have a tendency to develop multifocal well-differentiated thyroid cancer. Thyroid cancer is associated with familial colonic polyposis (e.g. Gardner syndrome), including colonic adenomatous polyps combined with soft tissue, most often with fibromatosis, combined with fibrosarcoma. It is an autosomal dominant disease, caused by mutations in the APC gene located on chromosome 5q21 to q22, the latter being a signaling protein involved in the regulation of cell proliferation, which can be carcinogenic in a small number of individuals when stimulated by TSH.