What are the factors for the development of thyroid cancer?

  To date, the etiology of thyroid cancer is unclear. In clinical practice, it is believed that its development may be related to the following factors.  1. Iodine and thyroid cancer It is generally believed that iodine deficiency leads to endemic goiter, reduced synthesis of thyroid hormones, and increased levels of thyroid stimulating thyroid follicular hyperplasia, which increases the incidence of thyroid cancer, but mostly follicular thyroid cancer. In non-endemic goiter endemic areas, papillary thyroid carcinoma accounts for 85% of well-differentiated thyroid carcinoma, and high iodine diet may increase the incidence of papillary thyroid carcinoma.  Radiation and thyroid cancer Irradiation of the thyroid gland of laboratory rats with X-rays can promote the development of thyroid cancer in animals; on the other hand, the destruction of the thyroid gland and its inability to produce thyroxine can cause the secretion of thyroid stimulating hormone (TSH) in large quantities, which can also promote thyroid cell carcinogenesis. Children who have received radiation treatment to the upper mediastinum or neck for thyroid enlargement during infancy are especially prone to thyroid cancer because the cells of children and adolescents are proliferating vigorously and radiation is an additional stimulus to promote the formation of tumors. In Japan, the incidence of thyroid cancer increased after the atomic bombings in Nagasaki and Hiroshima.  3.Chronic stimulation of thyroid stimulating hormone and thyroid cancer TSH regulates the growth of thyroid follicular cells through cAMP-mediated signaling pathway, and thyroid cancer may occur. Increased serum TSH level induces nodular goiter, and thyroid follicular carcinoma can be induced after administration of mutagens and TSH stimulation. Moreover, clinical studies have shown that TSH inhibition 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.  4.The role of sex hormones and thyroid cancer The relationship between sex hormones and thyroid cancer has been emphasized because there are significantly more women than men among patients with well-differentiated thyroid cancer. Clinically, it is found that the tumor of adolescents is usually larger than that of adults, and the metastasis of cervical lymph nodes or distant metastasis of thyroid cancer occurs earlier in adolescents than in adults, but the prognosis is better than that of adults. The incidence of female increases significantly after the age of 10, and it is possible that the increase of estrogen secretion is related to the occurrence of thyroid cancer in young people. It is possible that the increase of estrogen secretion is related to the occurrence of thyroid cancer in young people. Some studies found that there are sex hormone receptors in thyroid tissue: estrogen receptor (ER) and progesterone receptor (PR), and there is ER in thyroid cancer tissue, but the effect of sex hormones on thyroid cancer is still inconclusive.  5. Other thyroid diseases and thyroid cancer (1) Nodular goiter: The incidence of thyroid cancer in nodular goiter can be as high as 4% to 17%. Nodular goiter is a TSH-induced hyperplasia of follicular epithelium in different parts of the thyroid gland, which results in papillary hyperplasia and vascular regeneration, and may lead to papillary thyroid cancer. After feeding rats or mice with drinking water and grain from iodine deficiency disease areas, increased serum TSH levels induce not only nodular goiter but also thyroid cancer in them, which is a risk factor for the development of thyroid cancer.  (2) Thyroid hyperplasia: It has been reported that congenital hyperplastic goiter is found to be not properly treated for a long time and eventually thyroid cancer occurs. Therefore, it is very important to detect congenital hyperplastic goiter in time and give thyroid hormone replacement therapy to eliminate the long-term stimulation of TSH.  (3) Thyroid adenoma: It is believed that the occurrence of thyroid cancer is related to solitary thyroid adenoma. If thyroid cancer is secondary to thyroid adenoma, the type should be predominantly 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 adenoma, but it is quite difficult to confirm the relationship between the two.  (4) Chronic lymphocytic thyroiditis (Hashimoto thyroiditis, HT): both Hashimoto’s disease. In recent years, thyroid cancer has been increasingly reported to be found in HT, with an incidence of 4.3% to 24%. HT and thyroid cancer can be two unrelated diseases coexisting in the thyroid gland. 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 and decreased thyroid hormone secretion, which feedback causes increased TSH. TSH continuously stimulates thyroid follicular cells, which overproliferate and become cancerous; it is also possible that TSH acts as a promoter and becomes cancerous while thyroid oncogenes are overexpressed; 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 thought that thyroid cancer did not occur in hyperthyroid patients. However, the incidence of thyroid cancer has been reported to be 2.5% to 9.6%. In contrast, the incidence of hyperthyroidism in thyroid cancer can be 3.3% to 19%. We should pay attention to the clinical situation of hyperthyroidism combined with thyroid cancer and be more alert to the existence of thyroid cancer.  6. Family factors and thyroid cancer Thyroid cancer is rarely an independent familial syndrome, but it can be part of a familial syndrome or a hereditary disease.