1.Iodine and thyroid cancer
Iodine is an essential trace element, and it is generally believed that iodine deficiency is endemic goiter. Iodine deficiency leads to reduced synthesis of thyroid hormones and increased levels of thyroid stimulating thyroid follicular hyperplasia and hypertrophy, resulting in goiter and the appearance of thyroid hormones, which increases the incidence of thyroid cancer. There is no consensus on the opinion, but it is mostly follicular thyroid cancer, which is not the most common type of thyroid cancer There is no significant change in the incidence of thyroid cancer before and after iodized salt prophylaxis, and the proportion of papillary thyroid cancer increases after the implementation of effective iodized salt prophylaxis, with more intake of foods containing very high iodine and a high iodine diet may increase the incidence of thyroid The incidence of papillary carcinoma. Yang Hui, Department of Nuclear Medicine, Henan Cancer Hospital
2.Radiation and thyroid cancer
Irradiation of thyroid gland of laboratory rats with X-rays can promote the development of thyroid carcinoma in animals, and the nucleus is deformed and the synthesis of thyroxine is greatly reduced, leading to carcinoma; on the other hand, the thyroid gland is destroyed and cannot produce endocrine hormone, and the resulting large secretion of thyroid stimulating hormone (TSH) can also promote thyroid cell carcinoma.
In clinical practice, many facts show that thyroid gland development is related to the effect of radiation. Children who have received radiation therapy to the upper mediastinum or neck during infancy due to thymus enlargement or lymphadenopathy 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 adults, thyroid cancer is less likely to occur after neck radiation therapy.
3. Chronic stimulation of thyroid stimulating hormone and thyroid cancer
Thyroid follicles are highly differentiated and have the function of polyiodine and synthesis of thyroglobulin. TSH also 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, and clinical studies have shown that TSH inhibitory therapy in differentiated thyroid cancer plays an important role in the treatment process after surgery, but whether TSH stimulation is a causative factor for the development of thyroid cancer remains to be confirmed.
4. 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 with well-differentiated thyroid cancer. Clinical comparison of the tumor sizes of well-differentiated thyroid cancer reveals that the tumors of young people are usually larger than those of adults, and the cervical lymph node metastasis or distant metastasis of thyroid cancer occurs earlier in young people than in adults, but the prognosis is better than that of adults. It is possible that the increased secretion of estrogen is related to the occurrence of thyroid cancer in young people, so some people study the 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 possibly produce neoplastic thyroid gland with diffuse enlargement of the thyroid gland, which can cause thyroid tumors.
6.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 associated with the development of thyroid cancer, and the incidence of thyroid cancer in nodular goiter can be as high as 4% to 17%.
The reasons for believing that there is no necessary association between thyroid cancer and nodular goiter are.
(1) Comparing the cytohistological changes of nodular goiter and thyroid carcinoma, nodular goiter is a lesion of the thyroid follicles that manifests as highly dilated follicles with flattened follicular wall cells, dilated follicles that converge into nodules of variable size filled with large amounts of colloid and incomplete fibrous envelope around the nodules. However, the most common type of thyroid cancer is not follicular thyroid cancer but papillary thyroid cancer.
②Comparing the age of onset of nodular goiter and thyroid cancer, we found that the age of onset of thyroid cancer was significantly lower than that of nodular goiter, which does not seem to support that thyroid cancer is secondary to nodular goiter.
(iii) Comparing the incidence of nodular goiter and thyroid cancer, the incidence of nodular goiter in the population was 40,000 per 1 million, while thyroid cancer was only 40 per 1 million, much lower than the 4% to 17% incidence of thyroid cancer in nodular goiter; the high incidence of thyroid cancer in nodular goiter is related to the cases selected for surgical treatment, some of which were even suspected clinically to have malignant thyroid lesions, and thus is not universally relevant.
Nevertheless, the presence of thyroid cancer in nodular goiter is indisputable. 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 (angiogenesis). level increases, which not only induces nodular goiter, but also thyroid cancer in nodular goiter, including papillary thyroid cancer and follicular thyroid cancer, the incidence of which is as high as 15.6% and is a risk factor for the development of thyroid cancer.
(2) Thyroid hyperplasia: The relationship between thyroid hyperplasia and thyroid cancer is still unclear, but some reports found that congenital hyperplastic goiter without proper treatment for a long time eventually develops thyroid cancer.
(3) Thyroid adenoma: Most people believe 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 the two, even with histological observation. Even with histological observation, it is difficult to confirm the relationship between them.
(4) Chronic lymphocytic thyroiditis (HT): In recent years, there are more and more reports of thyroid cancer found in HT, with an incidence of 4.3% to 24%, which varies widely, and the actual incidence of HT is difficult to estimate because it does not require surgical treatment. On the other hand, focal HT may also be an immune response to thyroid cancer, which may lead to destruction of thyroid follicular cells, hypothyroidism, reduction of thyroid hormone secretion, and feedback to increase TSH. It is also thought 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 thyroid nodules already exist, and most of them are treated with medication. Therefore, we should pay attention to the clinical situation of hyperthyroidism combined with thyroid cancer, and we should be more alert to the existence of thyroid cancer.
Thyroid cancer can be seen in various causes of hyperthyroidism, including Graves’ disease, while hyperthyroidism caused by the tumor itself secreting thyroid hormones is rare. Whether it is Graves’ disease or toxic nodular goiter, the tumor lesions are small or insidious, the metastasis rate is low, and the prognosis is good, similar to that of non-hyperthyroid patients with thyroid cancer.
7. Family factors and thyroid cancer
Thyroid cancer is rarely 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, and 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, which is an autosomal dominant disorder. It is 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, and can become cancerous in a minority of individuals when stimulated by TSH. Thyroid cancer.