Abstract
Thyroid squamous cell carcinoma is very rare. At present, it is limited to case reports. Since the thyroid follicular epithelium is the non-squamous epithelium, how primary squamous cell carcinoma (SCC) of the thyroid occurs is still a controversial issue. Hashimoto’s thyroiditis (HT) is considered to be an independent risk factor for thyroid cancer, under the basis of HT, how tumor cells evolve and develop to papillary thyroid carcinoma (PTC), and particularly to de-differentiate into SCC is elusive. We report a 72-year-old female patient who developed multiple subtypes of PTC on a basis of HT, and finally to de-differentiate into SCC within the local foci of lymph node metastasis. We found that there was a variety of sub-types of PTC in this patient in the background of HT. SCC was found within local lymph node metastasis. Pathomorphology, immunohistochemistry, and molecular pathology have confirmed that the SCC was derived from PTC, and then developed into poorly differentiated SCC and/or anaplastic carcinoma. We also conducted a comprehensive literature review.
Highlights
More and more evidence shows that the thyroid is an autoimmune organ, which can occur in a variety of autoimmunerelated inflammatory diseases, such as Hashimoto’s thyroiditis (HT), chronic lymphocytic thyroiditis (CLT), and so on [2]
On the left side of the thyroid, hematoxylin and eosin (H&E) slides showed hyperplasia of thyroid follicular epithelial under the background of HT (Figure 1(a)), and the follicular epithelium in the focal area of HT was transformed into papillary thyroid carcinoma (PTC) (Figure 1(b))
The case we provided here showed that the atypical hyperplasia and canceration of the focal thyroid follicular epithelium were commonly noted in the background of HT
Summary
Papillary thyroid carcinoma (PTC) is a relatively well-differentiated malignant tumor of the thyroid gland, accounting for more than 85% of all types of thyroid cancer [1]. The relationship between immunity and inflammation has been concerned by scientists for a long time. More and more evidence shows that the thyroid is an autoimmune organ, which can occur in a variety of autoimmunerelated inflammatory diseases, such as Hashimoto’s thyroiditis (HT), chronic lymphocytic thyroiditis (CLT), and so on [2]. When HT occurs, in addition to a large number of interstitial lymphocyte infiltration and the formation of lymphoid follicles, fibrosis and calcification can be appeared, especially the proliferation of thyroid follicular epithelium, and even form neoplastic hyperplasia. On the basis of immune inflammation, thyroid cancer, especially PTC could be induced [3] [4] [5] [6]. The association between thyroid cancer and concomitant autoimmune thyroiditis is controversial [4] [7]
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