The thyroid gland is one of the most sensitive organs to the carcinogenic effects of ionizing radiation. Although radiation-induced thyroid cancer is a frequently reported SMN, it is rarely fatal. Thyroid SMNs range from well-differentiated, highly curable papillary and follicular carcinomas to poorly differentiated, rapidly fatal anaplastic carcinoma, with the former being the most common . Papillary carcinoma accounts for 75-90% of all radiation-induced thyroid SMNs in survivors of childhood cancer. There is a striking increased risk for young children exposed to ionizing radiation, as shown by both the atomic bomb experience and in studies of children who were less than five years of age at the time of exposure. In general, children younger than 10 years are at the greatest risk [53,59]. This has been attributed to the known age-related changes in cell proliferation with the thyroid gland. The younger the child at the time of exposure, the more actively dividing are the thyroid cells and the greater the potential for an active growth phase following therapy. Females in the general population are three times more likely to develop a primary thyroid cancer; a gender difference that has also been shown in those previously exposed to radiation. Thyroid SMNs following radiation therapy have been shown to increase linearly with increasing doses of radiation, with a flattening of the curve at doses greater than 30Gy . This finding may result from inhibition of cellular prolif eration after high-dose radiation that prevents the development of an expanded malignant clone.
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