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  • Painless swelling in region of thyroid.

  • Thyroid function tests are usually normal.

  • Possible history of childhood irradiation to head and neck region.

  • Positive thyroid FNA cytology.


The incidence of thyroid cancer in the United States is 53,000/year and increasing annually, probably as a result of the wider use of ultrasound, CT, MRI, and PET that may detect small thyroid malignancies. Thyroid cancer mortality has been stable, accounting for about 2000 deaths in the United States annually. The incidence of differentiated (papillary and follicular) thyroid carcinomas increases with age (Table 26–7) with a 3:1 female:male ratio. In routine autopsy series, thyroid papillary microcarcinoma (10 mm or smaller) is found with the surprising frequency of 11.5%. Most thyroid cancers remain microscopic and indolent. However, larger thyroid cancers (palpable or 1 cm or larger) are more malignant and require treatment.

Table 26–7.Some characteristics of thyroid cancer.

Pure papillary (and mixed papillary-follicular) carcinoma comprises 80% of all thyroid cancers. It usually presents as a single thyroid nodule but can arise out of a multinodular goiter. Papillary thyroid carcinoma is commonly multifocal, with other foci usually arising de novo rather than a result of intraglandular metastases. The tumor involves both lobes in 30% of patients.

Papillary thyroid carcinoma is the least aggressive thyroid malignancy. It tends to grow slowly and often remains confined to the thyroid and regional lymph nodes for years. In about 80% of patients, there are microscopic metastases to cervical lymph nodes. The malignancy may become more aggressive in patients over age 45 years and most particularly in older adults. The cancer may invade the trachea and local muscles and spread to the lungs. Papillary thyroid carcinoma is caused by genetic mutations or translocations. Activating mutations of the Ras oncogene can cause benign thyroid adenomas or nodular goiter. Additional activating mutations in BRAF or TRK genes can lead to papillary carcinoma. About 45% of papillary thyroid carcinomas are caused by over expression of the ret protooncogene (RET) by the translocation of certain gene promoters to it, producing retPTC-1, retPTC-2, or retPTC-3. Radiation treatments to the head and neck region tend to cause retPTC-1. Nuclear fallout exposure tends to cause retPTC-3, resulting in more aggressive papillary thyroid carcinomas. Additional loss of the p53 tumor suppressor gene can cause progression of papillary thyroid carcinoma to anaplastic thyroid carcinoma.


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