The incidence of papillary thyroid carcinoma (PTC) has been increasing worldwide. PTC is the most common type of differentiated thyroid cancer and usually shows good prognosis. However, some PTC is driven to advanced stage by epithelial-mesenchymal transition (EMT)-mediated drug resistance, which is particularly noticeable in pediatric patients. There are limited options for systemic treatment, necessitating development of new clinical approaches. Here, we aimed to clarify genetic differences due to age of patients with PTC, and thereby aid in developing novel therapeutics. Patients with biochemically and histologically confirmed PTC were included in this study. PTC cells were acquired from young and older patients showing drug resistance, and were compared via microarray analysis. Cellular proliferation and other properties were determined after treatments with lenvatinib and sorafenib. In vivo, tumor volume and other properties were examined using a mouse xenograft model. Lenvatinib-treated group showed obvious suppression of markers of anti-apoptosis, EMT, and the FGFR signaling pathway, compared with control and Sorafenib-treated group. In the xenograft models, lenvatinib treatment induced significant tumor shrinkage and blocked the proto-oncogene Bcl-2 (B cell lymphoma/leukemia gene-2) and FGFR signaling pathway, along with reduced levels of EMT markers, compared with control and Sorafenib-treated group. Our findings clarify the age-dependent characteristics of pediatric PTC, giving insights into the relationship between young age and poor prognosis. Furthermore, it provides a basis for developing novel therapeutics tailored to the age at diagnosis.

The incidence of thyroid cancer has increased rapidly worldwide, although most patients can survive for a long time without developing symptoms. While most thyroid cancers are treated with thyroidectomy alone, some patients are given additional radioactive iodine (RAI) in the form of 131I to treat thyroid cancer metastasis. RAI is associated with acute and chronic complications. Secondary malignancies are the most important in long-term cancer survivors. While many studies have reported the occurrence of acute myeloid leukemia after high-dose RAI, there are few reports on chronic myeloid leukemia (CML) after low-dose RAI treatment. Moreover, previous cases of CML following thyroid cancer were reported before the tyrosine kinase inhibitor (TKI) era. Here, we describe two cases of CML following thyroid cancer that were successfully treated with second-generation TKIs. (Korean J Med 2016;91:70-74) Keywords: Chronic myeloid leukemia; Thyroid cancer; Protein-tyrosine kinase 서 론 갑상선암의 발생률은 급격하게 증가하고 있으며, 대부분 의 환자에서는 5년 생존율이 100%에 육박할 정도로 장기 생 존이 가능하다고 보고되고 있다[1]. 갑상선암 환자에서 생존 율을 높이고 삶의 질을 향상시키기 위해 잔여 암을 제거하는 것은 매우 중요한 치료 전략으로, 131 I 형태의 방사성요오드 는 잔여 갑상선의 절제, 보조 요법 또는 전이암의 조절에 널 리 사용되고 있다[2]. 하지만, 방사선요오드는 침샘염, 구내 염, 골수형성 부전증을 일으키고 이차성 암을 유발하는 등의