Won Gu KimProf. South Korea

Won Gu KimProf.
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.

21 MARCH

Time Session
08:30
10:00
[Symposium] Thyroid (3)
New Development in Thyroid Cancer Management
Guodong FuCanada Moderator Preoperative Molecular Testing for Thyroid NodulesTitle: Preoperative Quantitative Molecular Testing for a Definitive Cancer Diagnosis among Patients with Thyroid Nodules Objective: Molecular testing is increasingly used in the assessment of thyroid nodules. Tumors harboring the same genomic variant may not behave the same because a gene variant is not expressed equally in tumor cells among patients. This study is to delineate interpatient variabilities in genomic variants in thyroid tumors and assess their diagnostic significance in definitive thyroid cancer diagnosis. Methods: Interpatient differences in BRAF V600E, TERT promoter, and RAS variants (ie, NRAS, HRAS, and KRAS) were analyzed in residual thyroid fine-needle aspiration (FNA) biopsies and compared with surgical histopathologic diagnoses. Malignancy rates, sensitivity, specificity, positive predictive values (PPV), and negative predictive values (NPV) were calculated. Results: This retrospective study enrolled 620 patients (470 [75.8%] female; mean [SD] age, 50.7 [15.9] years), including 438 surgically resected thyroid tumors and 249 thyroid nodule FNA biopsies. Of 438 tumors, 178 (40.6%) and 58 (13.2%) carcinomas were detected with interpatient variabilities of BRAF V600E and TERT promoter variants (C228T and C250T), with variant allele fraction (VAF) levels ranging from 0.03% to 48.56% and 0.13% to 54.74%, respectively. Furthermore, 89 (20.3%) were identified with the presence of RAS variants, including 51 (11.6%) with NRAS, 29 (6.6%) with HRAS, and 9 (2.1%) with KRAS, with VAF levels ranging from 0.15% to 51.53%. VAF assays of 249 residual FNA specimens identified 50 specimens (20.1%) with BRAF V600E, 25 FNAs (10.0%) with TERT promoter variants, and 36 specimens (14.5%) with RAS variants with interpatient variabilities (including 23 FNAs [9.2%] with NRAS, 10 FNAs [4.0%] with HRAS, and 3 FNAs [1.2%] with KRAS). Interpatient differences in the 5 gene variants (NRAS, HRAS, KRAS, BRAF, and TERT) were detected in 54 of 126 indeterminate FNAs (42.9%) and 18 of 76 ND FNAs (23.7%). Compared with the 5 gene variants detected in the matched surgical specimens, VAF assays on residual FNA biopsies exhibited a high agreement (κ = 0.80; P < .001) and demonstrated a sensitivity of 87.1% (95% CI, 69.2%-95.8%), specificity of 92.5% (95% CI, 78.5%-98.0%), PPV of 90.0% (95% CI, 72.3%-97.4%), and NPV of 90.2% (95% CI, 75.9%-96.8%). Conclusions: This diagnostic study delineated that quantitative discrimination of interpatient variabilities in genomic variants could facilitate cytology examinations in preoperative precision malignancy diagnosis among patients with thyroid nodules.
Won Gu KimSouth Korea Moderator 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.
  • Long-Term Changes of Urinary Exosomal Peptide Levels after Thyroidectomy in Patients with Thyroid Cancer: A Prospective Observational Study
    Chih-Yuan WangTaiwan Speaker Obesity 2026 updateObesity remains one of the most critical and rapidly evolving global health challenges entering 2026, characterized by persistently rising prevalence, expanding clinical consequences, and profound societal and economic impacts. Over the past three decades, the prevalence of overweight and obesity has more than doubled among adults and increased nearly threefold among children and adolescents worldwide, driven by complex interactions between genetic susceptibility, obesogenic environments, sedentary lifestyles, dietary transitions toward energy-dense ultra-processed foods, and broader socio-economic determinants. Projections indicate that, if current trends continue, more than half of the global adult population and a substantial proportion of children will be living with obesity within the next two decades, with particularly rapid increases occurring in low- and middle-income countries undergoing nutritional and urban transitions. This epidemiologic shift has translated into a marked escalation in obesity-related non-communicable diseases, including type 2 diabetes, cardiovascular disease, chronic kidney disease, non-alcoholic fatty liver disease, osteoarthritis, and several obesity-associated malignancies, positioning excess adiposity as a leading contributor to global morbidity, mortality, and disability-adjusted life years. Alongside the growing disease burden, the conceptual framework of obesity has undergone important refinement. While body mass index remains a pragmatic population-level screening tool, its limitations in capturing adiposity distribution and metabolic risk have prompted international efforts to redefine obesity as a chronic, relapsing disease characterized by excess or dysfunctional adipose tissue with heterogeneous clinical expression. Emerging diagnostic paradigms increasingly emphasize waist-based measures, ectopic fat accumulation, and the presence of obesity-related complications, distinguishing pre-clinical obesity from clinically manifest disease and enabling more precise risk stratification and individualized management. Therapeutically, the obesity landscape has been transformed by advances in incretin-based pharmacotherapy, particularly glucagon-like peptide-1 receptor agonists and dual or multi-agonist agents, which have demonstrated unprecedented and sustained weight reduction alongside meaningful improvements in cardiometabolic outcomes. The recent development of effective oral formulations further expands treatment accessibility and has the potential to improve long-term adherence, although challenges related to cost, equity, and health-system implementation remain substantial. Importantly, pharmacotherapy alone is insufficient to address the obesity epidemic, and contemporary management strategies emphasize multimodal, life-course approaches integrating nutritional therapy, physical activity promotion, behavioral and psychological interventions, digital health technologies, and, when appropriate, metabolic and bariatric surgery, tailored to individual risk profiles and comorbidity burdens. At the population level, global policy initiatives increasingly recognize that obesity is not solely an individual responsibility but a systems-driven condition requiring coordinated action across healthcare, education, food systems, urban planning, and regulatory environments to create supportive contexts for healthy living. Concurrently, ongoing research continues to elucidate the complex pathophysiology of obesity, including the roles of genetics, epigenetics, gut microbiota, neuroendocrine regulation, and adipose tissue inflammation, while implementation science seeks to bridge gaps between evidence and real-world practice. Collectively, the 2026 obesity update portrays a paradoxical landscape of escalating global burden alongside unprecedented scientific and therapeutic progress, underscoring that meaningful and sustainable impact will depend on integrating biomedical innovation with structural policy reform, equitable access to care, and sustained public health commitment to reverse current trajectories and improve outcomes across the lifespan.Long-Term Changes of Urinary Exosomal Peptide Levels after Thyroidectomy in Patients with Thyroid Cancer: A Prospective Observational StudyIn this prospective observational study, we investigated whether longitudinal changes in urinary exosomal peptide profiles after thyroidectomy could predict recurrence risk in patients with papillary thyroid cancer, a disease with reported recurrence rates of up to 30%. Adults older than 20 years with newly diagnosed papillary thyroid cancer who had undergone thyroidectomy were enrolled, and urine samples were collected at 12 months after study entry and again one year later for exosomal peptide identification and comparison. Seventy patients were included and stratified according to the interval between surgery and enrollment (<5 years, 5–10 years, and >10 years). During the two-year follow-up after enrollment, no recurrences were observed. Across groups and time intervals, there were no significant differences in serum protein levels or urinary exosomal peptide concentrations, and established high-risk clinical factors showed only weak correlations with these biomarkers. Collectively, these findings delineate the long-term basal fluctuation ranges of serum proteins and urinary exosomal peptides in post-thyroidectomy thyroid cancer survivors, suggesting that biomarker levels remaining within these ranges may be indicative of a lower long-term risk of recurrence in high-risk patients following thyroidectomy.
  • Salvage Radiofrequency Ablation Followed by External Beam Radiotherapy for Inoperable Recurrent Differentiated Thyroid Cancer
    Chen-Kai ChouTaiwan Speaker Salvage Radiofrequency Ablation Followed by External Beam Radiotherapy for Inoperable Recurrent Differentiated Thyroid Cancer
  • Re-Differentiation Therapy in RAI-Refractory Thyroid Cancer
    Samantha Peiling YangSingapore Speaker Harnessing Molecular Diagnostics in Cytologically-Indeterminate Thyroid NodulesRe-Differentiation Therapy in RAI-Refractory Thyroid Cancer
201BC
16:50
17:30
Plenary 7
Won Gu KimSouth Korea Moderator 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.
  • Genomic Alterations in Thyroid Cancer: Biological and Clinical Insights
    Maria E. CabanillasUnited States Speaker Genomic Alterations in Thyroid Cancer: Biological and Clinical InsightsGenomic alterations play a central role in the initiation, progression, and clinical behavior of thyroid cancers, offering critical insights into their underlying biology and therapeutic vulnerabilities. Follicular cell derived thyroid tumors commonly harbor driver mutations that constitutively activate the MAPK signaling pathway, most notably BRAFV600E and RAS mutations. These early events define major molecular subtypes and strongly influence differentiation status, tumor phenotype, and response to therapy. Progression toward aggressive or dedifferentiated forms, such as poorly differentiated and anaplastic thyroid carcinomas, is driven by additional alterations in key genes regulating chromatin remodeling, cell cycle control, and genomic stability, including TERT promoter mutations, TP53, PIK3CA, and EIF1AX. Actionable genomic alterations are increasingly leveraged to personalize treatment strategies in thyroid cancer and underscore the importance of genomic characterization in improving outcomes in thyroid cancer. Anaplastic Thyroid CancerAnaplastic thyroid cancer (ATC) is one of the most aggressive human malignancies, characterized by rapid local invasion, early metastasis, and near‑universal disease‑specific mortality and is considered a medical emergency. Current treatment strategies prioritize rapid assessment of resectability, with surgery pursued only when complete or near‑complete tumor removal is feasible, as partial debulking offers limited benefit. For unresectable disease, localized disease, combined modality therapy—typically external‑beam radiation with concurrent systemic therapy—remains the cornerstone of local control. Recent advances in molecular profiling have transformed systemic management, enabling targeted therapies for tumors harboring BRAFV600E mutations. These agents have demonstrated meaningful responses and, in select cases, have converted unresectable tumors to operable ones, expanding the role of surgery in modern care. However, due to the high risk of relapses, immunotherapy has been added to the treatment strategy. Patients with distant metastatic disease without a BRAFV600E mutation have a more complicated treatment regimen which is still under investigation but require systemic therapy combination strategies involving immunotherapy. These evolving strategies reflect a shift toward precision‑based, time‑critical management aimed at improving outcomes in this highly lethal cancer.
101

22 MARCH

Time Session
11:00
12:30
[Symposium] Thyroid (5)
Novel Treatment and Diagnostic Approaches for Thyroid Cancer in Post-NGS Era
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