Prof.Won GuKim - AOCE 2026

Won Gu Kim, MD, PhD Professor, Department of Endocrinology and Metabolism, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea Prof. Kim is an endocrinologist whose research focuses on thyroid diseases, particularly thyroid cancer. His major interests include molecular biomarkers, tumor biology, and precision medicine. He has published more than 200 papers on thyroid research, encompassing both clinical and translational studies. He currently serves as the General Secretary of the Asia & Oceania Thyroid Association (AOTA) and has been actively involved in international collaborations in thyroid research. He also serves on the review boards of several leading journals, including Thyroid, European Thyroid Journal, Clinical Endocrinology, and Endocrinology & Metabolism.

22 MARCH

Time	Session

11:00 12:30	[Symposium] Thyroid (5) Novel Treatment and Diagnostic Approaches for Thyroid Cancer in Post-NGS Era Advances in the Treatment of Radioactive Iodine-Refractory Differentiated Thyroid Cancer: Multikinase Inhibitors and Beyond – An Asian Perspective Won Gu KimSouth Korea Speaker Advances in the Treatment of Radioactive Iodine-Refractory Differentiated Thyroid Cancer: Multikinase Inhibitors and Beyond – An Asian PerspectiveDifferentiated thyroid cancer (DTC) arising from follicular cells generally has a good prognosis; however, about 5-10% of patients experience recurrence or distant metastasis. High-dose radioactive iodine (RAI) therapy is the mainstay of treatment for metastatic DTC, but its efficacy depends on the iodine avidity of the tumor. Iodine uptake of metastatic lesions tends to decline over time, and ultimately, around 60-70% of metastatic cases become refractory to RAI therapy. Patients whose metastases remain RAI-avid have a median survival approaching 10 years, whereas those with RAI-refractory disease have a roughly 10% of 10 10-year survival. Because the clinical course of RAI-refractory DTC is variable, it is critical to determine which patients should receive systemic therapy with a tyrosine kinase inhibitor (TKI) and how to integrate local treatment before and during systemic therapy. TKIs such as sorafenib and lenvatinib, which primarily inhibit tumor angiogenesis, have been approved. The DECISION trial reported that sorafenib achieved a median progression-free survival (PFS) of 10.8 months compared with 5.8 months in the control group. The SELECT trial showed that lenvatinib achieved a median PFS of 18.3 months versus 3.6 months in controls. Based on these results, sorafenib and lenvatnib are now widely used as the first-line treatments for patients with RAI-refractory DTC who have progressive or symptomatic metastatic disease. A recent multi-center real-world study in Korea suggested that lenvatinib provides better efficacy and longer PFS (median 35.3 months) than sorafenib (median 13.3 months, p<0.001). However, lenvatinib is also associated with higher rates of adverse events such as hypertension (95%) and proteinuria (80%). These TKIs show activity irrespective of the underlying genetic alterations that drive thyroid cancer. Recently, selective NTRK and RET inhibitors have been developed for solid tumors harboring NTRK or RET gene fusions, and their efficacy has been confirmed in clinical trials. In addition, genetic testing to identify actionable mutations is increasingly being incorporated into practice, and personalized treatment approaches are reflected in current clinical guidelines. A recent Korean multicenter study found that approximately 31% of patients with RAI-refractory thyroid cancer who had wild-type BRAF carried targetable gene fusions. The choice and sequencing of TKI, the optimal timing of their use, strategies to prevent and manage adverse events, and individualized treatment plans based on patient characteristics will be crucial for improving clinical outcomes in patients with RAI-refractory thyroid cancer. The Genetic Landscape of Thyroid Cancer Young Joo ParkSouth Korea Speaker Translating the Genetic Landscape of Thyroid Cancer to Precision Diagnosis and TherapyThyroid cancer is characterized by a relatively low mutational burden compared with other solid tumors, with recurrent alterations mainly involving BRAF, RAS, and various fusion genes. Several novel driver candidates have also been identified through next-generation sequencing studies. The frequency and pattern of these genomic alterations differ across thyroid cancer subtypes and are often associated with distinct histopathological phenotypes, providing valuable clues for differential diagnosis. Moreover, molecular subtypes defined by driver mutations are closely linked to tumor biology and clinical behavior, allowing more accurate prediction of disease aggressiveness and prognosis. Most differentiated thyroid cancers (DTCs) harbor a single dominant driver alteration; however, acquisition of additional mutations such as TERT promoter, tumor suppressor genes, or PI3K–AKT pathway alterations may lead to dedifferentiation and progression to aggressive or metastatic disease. Advances in our understanding of these genetic alterations have refined the pathological classification of thyroid cancer and enabled improved prognostication, treatment selection, and follow-up strategies. Importantly, the identification of actionable genetic alterations—including RET and NTRK fusions, as well as BRAF mutations—has revolutionized therapeutic approaches. Targeted agents such as selpercatinib, pralsetinib, larotrectinib, and entrectinib demonstrate substantial clinical efficacy with fewer adverse events than multikinase inhibitors, while dabrafenib plus trametinib has shown marked benefit in anaplastic thyroid cancer. With multiple targetable mutations being uncovered, incorporating comprehensive genomic testing into the diagnostic workflow is essential to guide precision therapy for patients with thyroid cancer. Redifferentiation Strategies in Refractory Thyroid Cancer: First Insights from Taiwan He-Jiun JiangTaiwan Speaker Redifferentiation Strategies in Refractory Thyroid Cancer: First Insights from Taiwan 201BC

Time

Session

11:00

12:30

[Symposium] Thyroid (5)

Novel Treatment and Diagnostic Approaches for Thyroid Cancer in Post-NGS Era

Advances in the Treatment of Radioactive Iodine-Refractory Differentiated Thyroid Cancer: Multikinase Inhibitors and Beyond – An Asian Perspective

Won Gu KimSouth Korea Speaker Advances in the Treatment of Radioactive Iodine-Refractory Differentiated Thyroid Cancer: Multikinase Inhibitors and Beyond – An Asian PerspectiveDifferentiated thyroid cancer (DTC) arising from follicular cells generally has a good prognosis; however, about 5-10% of patients experience recurrence or distant metastasis. High-dose radioactive iodine (RAI) therapy is the mainstay of treatment for metastatic DTC, but its efficacy depends on the iodine avidity of the tumor. Iodine uptake of metastatic lesions tends to decline over time, and ultimately, around 60-70% of metastatic cases become refractory to RAI therapy. Patients whose metastases remain RAI-avid have a median survival approaching 10 years, whereas those with RAI-refractory disease have a roughly 10% of 10 10-year survival. Because the clinical course of RAI-refractory DTC is variable, it is critical to determine which patients should receive systemic therapy with a tyrosine kinase inhibitor (TKI) and how to integrate local treatment before and during systemic therapy. TKIs such as sorafenib and lenvatinib, which primarily inhibit tumor angiogenesis, have been approved. The DECISION trial reported that sorafenib achieved a median progression-free survival (PFS) of 10.8 months compared with 5.8 months in the control group. The SELECT trial showed that lenvatinib achieved a median PFS of 18.3 months versus 3.6 months in controls. Based on these results, sorafenib and lenvatnib are now widely used as the first-line treatments for patients with RAI-refractory DTC who have progressive or symptomatic metastatic disease. A recent multi-center real-world study in Korea suggested that lenvatinib provides better efficacy and longer PFS (median 35.3 months) than sorafenib (median 13.3 months, p<0.001). However, lenvatinib is also associated with higher rates of adverse events such as hypertension (95%) and proteinuria (80%). These TKIs show activity irrespective of the underlying genetic alterations that drive thyroid cancer. Recently, selective NTRK and RET inhibitors have been developed for solid tumors harboring NTRK or RET gene fusions, and their efficacy has been confirmed in clinical trials. In addition, genetic testing to identify actionable mutations is increasingly being incorporated into practice, and personalized treatment approaches are reflected in current clinical guidelines. A recent Korean multicenter study found that approximately 31% of patients with RAI-refractory thyroid cancer who had wild-type BRAF carried targetable gene fusions. The choice and sequencing of TKI, the optimal timing of their use, strategies to prevent and manage adverse events, and individualized treatment plans based on patient characteristics will be crucial for improving clinical outcomes in patients with RAI-refractory thyroid cancer.
The Genetic Landscape of Thyroid Cancer

Young Joo ParkSouth Korea Speaker Translating the Genetic Landscape of Thyroid Cancer to Precision Diagnosis and TherapyThyroid cancer is characterized by a relatively low mutational burden compared with other solid tumors, with recurrent alterations mainly involving BRAF, RAS, and various fusion genes. Several novel driver candidates have also been identified through next-generation sequencing studies. The frequency and pattern of these genomic alterations differ across thyroid cancer subtypes and are often associated with distinct histopathological phenotypes, providing valuable clues for differential diagnosis. Moreover, molecular subtypes defined by driver mutations are closely linked to tumor biology and clinical behavior, allowing more accurate prediction of disease aggressiveness and prognosis. Most differentiated thyroid cancers (DTCs) harbor a single dominant driver alteration; however, acquisition of additional mutations such as TERT promoter, tumor suppressor genes, or PI3K–AKT pathway alterations may lead to dedifferentiation and progression to aggressive or metastatic disease. Advances in our understanding of these genetic alterations have refined the pathological classification of thyroid cancer and enabled improved prognostication, treatment selection, and follow-up strategies. Importantly, the identification of actionable genetic alterations—including RET and NTRK fusions, as well as BRAF mutations—has revolutionized therapeutic approaches. Targeted agents such as selpercatinib, pralsetinib, larotrectinib, and entrectinib demonstrate substantial clinical efficacy with fewer adverse events than multikinase inhibitors, while dabrafenib plus trametinib has shown marked benefit in anaplastic thyroid cancer. With multiple targetable mutations being uncovered, incorporating comprehensive genomic testing into the diagnostic workflow is essential to guide precision therapy for patients with thyroid cancer.
Redifferentiation Strategies in Refractory Thyroid Cancer: First Insights from Taiwan

He-Jiun JiangTaiwan Speaker Redifferentiation Strategies in Refractory Thyroid Cancer: First Insights from Taiwan

201BC

Prof.Won GuKim South Korea

22 MARCH