Young Joo Park South Korea

Professor Young Joo Park is Professor of Medicine at Seoul National University College of Medicine and Staff Endocrinologist at Seoul National University Hospital. She is Editor-in-Chief of Endocrinology and Metabolism, official journal of the Korean Endocrine Society. She is also a member of the National Academy of Medicine of Korea and serves on the council of the Asia and Oceanic Thyroid Association. Her research focuses on the biology of thyroid disease using multi-omics approaches, including genomics, proteomics, and metabolomics. She has investigated genetic and environmental risk factors for thyroid disorders through genome-wide association studies and chemical exposure analyses. A major area of her work is the molecular characterization of thyroid nodules and cancers using next-generation sequencing to clarify mechanisms of thyroid cancer progression and to improve diagnosis and prognosis prediction. She has led several large-scale clinical and epidemiologic studies. These include MAeSTro, a prospective multicenter cohort study of papillary thyroid microcarcinoma designed to define its natural history, which expanded internationally as MAeSTro-EXP. She also directs the MASTER trial, a multicenter randomized controlled study evaluating the role of thyroid-stimulating hormone suppression after lobectomy in patients with low- to intermediate-risk thyroid cancer. Through these efforts, Professor Park is working to advance the understanding of thyroid tumor biology and to optimize individualized management strategies.

20 MARCH

Time	Session

10:30 12:00	Oral Presentation 1: Thyroid Excellence: From Autoimmunity to Neoplasia Saeed Ahmed MaharPakistan Moderator Young Joo ParkSouth Korea Moderator 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. 103

Time

Session

10:30

12:00

Oral Presentation 1: Thyroid Excellence: From Autoimmunity to Neoplasia

Saeed Ahmed MaharPakistan Moderator

Young Joo ParkSouth Korea Moderator 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.

103

22 MARCH

Time	Session

11:00 12:30	[Symposium] Thyroid (5) Novel Treatment and Diagnostic Approaches for Thyroid Cancer in Post-NGS Era Angela M. LeungUnited States Moderator Key Highlights of the American Thyroid Association Thyroid and Pregnancy GuidelinesThis session will present the key highlights of the American Thyroid Association 2026 guidelines for thyroid disease in preconception, pregnancy, and postpartum that have been published by a multidisciplinary group of experts with global perspective. The discussion will provide an overview of the methodology used to prepare these updated guidelines in partnership with and endorsed by several other collaborating societies. The presentation will cover the most notable changes and new recommendations surrounding thyroid function testing, iodine nutrition, infertility and assisted reproductive techniques, hypothyroidism, hyperthyroidism (including Graves’ disease), thyroid nodules, and thyroid cancers for women planning pregnancy, are pregnant, or seen for postpartum care.Thyroid Risks of Iodine ExcessIodine is a micronutrient that is required for the production of thyroid hormone. Iodine is commonly obtained from consuming an iodine-rich diet or iodine-fortified foods, amiodarone use, iodine-containing supplements, and iodinated contrast media. This session will review the potential forms of thyroid dysfunction arising from an acute iodine load, due to the failure to escape from the Wolff-Chaikoff effect and to the Jod-Basedow phenomenon. The risks of iodine excess in vulnerable populations, and current guidelines regarding the screening and monitoring of iodinated contrast-induced thyroid dysfunction, will be summarized. Pei-Lung ChenTaiwan Moderator Gender-Affirming Hormone Therapy in Taiwan 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. Translating the Genetic Landscape of Thyroid Cancer to Precision Diagnosis and Therapy 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 TaiwanBackground: Patients with BRAF p.V600E-mutated radioactive iodine-refractory differentiated thyroid cancer (RAIR-DTC) face a poor prognosis. While MAPK pathway inhibition can restore radioiodine (RAI) avidity, standard full-dose protocols (e.g., MERAIODE) are often associated with significant toxicity (Grade 3/4 adverse events >20%). This study investigates the efficacy and safety of a novel low-dose, pulsed redifferentiation strategy in a real-world Asian cohort. Methods: We conducted a retrospective cohort study of 24 patients with metastatic BRAF p.V600E RAIR-PTC. Patients received a 60-day induction regimen of Dabrafenib (75 mg BID) and Trametinib (2 mg QOD, every other day). A "Treat-All" strategy was employed, omitting diagnostic scanning to avoid stunning effects, followed by a fixed therapeutic dose of 131-I (150-200 mCi). Primary endpoints included RAI uptake restoration, objective response rate (ORR), disease control rate (DCR), and safety profile. Results: RAI avidity was restored in 83.3% of patients. The regimen demonstrated an exceptional safety profile without Grade 3/4 adverse events. While the ORR was 16.7%, the DCR reached 83.3% at 6 months. Age <55 years was identified as the most significant predictor for objective tumor regression (p=0.007). Furthermore, the study highlights the clinical value of "TKI-Free Survival," with 88.9% of prior TKI users achieving a sustained drug holiday. Conclusion: The low-dose, pulsed BRAF/MEK inhibition protocol offers a highly tolerable and effective redifferentiation strategy. While tumor shrinkage is less pronounced than with full-dose regimens, the high rate of disease control and excellent safety profile make it a viable option for stabilizing disease and improving quality of life, particularly for younger patients (<55) or those intolerant to standard TKI therapy. 201BC

Time

Session

11:00

12:30

[Symposium] Thyroid (5)

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

Angela M. LeungUnited States Moderator Key Highlights of the American Thyroid Association Thyroid and Pregnancy GuidelinesThis session will present the key highlights of the American Thyroid Association 2026 guidelines for thyroid disease in preconception, pregnancy, and postpartum that have been published by a multidisciplinary group of experts with global perspective. The discussion will provide an overview of the methodology used to prepare these updated guidelines in partnership with and endorsed by several other collaborating societies. The presentation will cover the most notable changes and new recommendations surrounding thyroid function testing, iodine nutrition, infertility and assisted reproductive techniques, hypothyroidism, hyperthyroidism (including Graves’ disease), thyroid nodules, and thyroid cancers for women planning pregnancy, are pregnant, or seen for postpartum care.Thyroid Risks of Iodine ExcessIodine is a micronutrient that is required for the production of thyroid hormone. Iodine is commonly obtained from consuming an iodine-rich diet or iodine-fortified foods, amiodarone use, iodine-containing supplements, and iodinated contrast media. This session will review the potential forms of thyroid dysfunction arising from an acute iodine load, due to the failure to escape from the Wolff-Chaikoff effect and to the Jod-Basedow phenomenon. The risks of iodine excess in vulnerable populations, and current guidelines regarding the screening and monitoring of iodinated contrast-induced thyroid dysfunction, will be summarized.

Pei-Lung ChenTaiwan Moderator Gender-Affirming Hormone Therapy in Taiwan

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.
Translating the Genetic Landscape of Thyroid Cancer to Precision Diagnosis and Therapy

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 TaiwanBackground: Patients with BRAF p.V600E-mutated radioactive iodine-refractory differentiated thyroid cancer (RAIR-DTC) face a poor prognosis. While MAPK pathway inhibition can restore radioiodine (RAI) avidity, standard full-dose protocols (e.g., MERAIODE) are often associated with significant toxicity (Grade 3/4 adverse events >20%). This study investigates the efficacy and safety of a novel low-dose, pulsed redifferentiation strategy in a real-world Asian cohort. Methods: We conducted a retrospective cohort study of 24 patients with metastatic BRAF p.V600E RAIR-PTC. Patients received a 60-day induction regimen of Dabrafenib (75 mg BID) and Trametinib (2 mg QOD, every other day). A "Treat-All" strategy was employed, omitting diagnostic scanning to avoid stunning effects, followed by a fixed therapeutic dose of 131-I (150-200 mCi). Primary endpoints included RAI uptake restoration, objective response rate (ORR), disease control rate (DCR), and safety profile. Results: RAI avidity was restored in 83.3% of patients. The regimen demonstrated an exceptional safety profile without Grade 3/4 adverse events. While the ORR was 16.7%, the DCR reached 83.3% at 6 months. Age <55 years was identified as the most significant predictor for objective tumor regression (p=0.007). Furthermore, the study highlights the clinical value of "TKI-Free Survival," with 88.9% of prior TKI users achieving a sustained drug holiday. Conclusion: The low-dose, pulsed BRAF/MEK inhibition protocol offers a highly tolerable and effective redifferentiation strategy. While tumor shrinkage is less pronounced than with full-dose regimens, the high rate of disease control and excellent safety profile make it a viable option for stabilizing disease and improving quality of life, particularly for younger patients (<55) or those intolerant to standard TKI therapy.

201BC