Administration of multikinase inhibitor followed by radioiodine therapy for poorly differentiated thyroid cancer: a case description and systematic review

Sep 30, 2026

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Letter to the Editor discussing a clinical strategy for poorly differentiated thyroid cancer (PDTC) that combines multikinase inhibitor administration followed by radioiodine (RAI) therapy. The text reviews why PDTC typically shows variable and reduced RAI uptake, explains treatment limitations of standard approaches, and frames the report’s rationale around disease assessment and appropriate timing of RAI intervention, given risks of recurrence and RAI refractoriness. It also provides clinical context from a described patient case.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages8

Reading Time20 min

AccessFree to download

Introduction

Background on PDTC and treatment challenges

Case presentation

Clinical history and imaging findings

Letter to the Editor Administration of multikinase inhibitor followed by radioiodine therapy for poorly differentiated thyroid cancer: a case description and systematic review Yahong Long1, Yan-Xia Mi2, Na Li1, Chaomin Li1, Kunpeng Ji1, Wanchun Zhang1 1Department of Nuclear Medicine, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Third Hospital of Shanxi Medical University, Tongji Shanxi Hospital, Taiyuan, China; 2Department of Nuclear Medicine, Shanxi Province Cancer Hospital/Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences/Cancer Hospital Affiliated to Shanxi Medical University, Taiyuan, China Correspondence to: Wanchun Zhang, MD. Department of Nuclear Medicine, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Third Hospital of Shanxi Medical University, Tongji Shanxi Hospital, No. 99 Longcheng Street, Taiyuan 030032, China. Email: [zhangwanchun@sxbqeh.com.cn](zhangwanchun@sxbqeh.com.cn). Submitted Feb 15, 2025. Accepted for publication Oct 27, 2025. Published online Dec 31, 2025. doi: 10.21037/qims-2025-381 View this article at: [https://dx.doi.org/10.21037/qims-2025-381](https://dx.doi.org/10.21037/qims-2025-381) Introduction Poorly differentiated thyroid cancer (PDTC) accounts for fewer than 5% of all thyroid cancer cases . Its pathological characteristics and biological behavior result in a significantly worse prognosis than does differentiated thyroid cancer (DTC), but it is not as severe as anaplastic thyroid cancer. PDTC is the most common disease-specific cause of mortality among patients with thyroid cancer, while distant metastasis is the primary cause of death among patients with PDTC, accounting for up to 85% of disease-related deaths (1) . The overall 10-year survival rate of those with PDTC is approximately 50% . Unlike the treatment of DTCs, the treatment of PDTC has not been standardized due to the rarity of the disease and the heterogeneity of inclusion criteria. Therapeutic decisionson PDTC have thus been mainly extrapolated from the treatment experience in DTC. However, in contrast to lowrisk thyroid cancers, these tumors require a more aggressive treatment strategy (2) . Complete surgical resection, when feasible, is considered the optimal initial approach for PDTC and may involve the excision of invaded adjacent structures (e.g. , the trachea and recurrent laryngeal nerve) and regional lymph nodes. However, the aggressive behavior of PDTC often leads to extensive local invasion, complicating complete resection and elevating recurrence risk. Although various adjuvant therapies have been proposed, none consistently demonstrate high efficacy (2,3) . Radioiodine (RAI) uptake in PDTC is variable and generally reduced compared to that in well-differentiated thyroid cancer, due to dedifferentiation and loss of sodium-iodide symporter (NIS) expression. Consequently, RAI therapy is often ineffective, with supporting evidence largely limited to case reports (4) . A portion of patients may initially respond but develop RAI refractoriness over time. Poorly differentiated histology, advanced age, invasive growth, and mutations such as BRAF and TERT further diminish iodine avidity (5,6) . External beam radiotherapy can provide local control in unresectable disease but does not significantly improve survival. Similarly, chemotherapy has not shown substantial survival benefits (7) . Targeted therapy has emerged as a promising research direction; however, the molecular landscape of PDTC is heterogeneous, involving diverse alterations (e.g., in BRAF, RAS, TERT, and TP53), and no dominant targetable driver has been established. Most evidence has been derived from preclinical models or small case series with limited follow-up (2,7) . High intertumor heterogeneity at the genomic and proteomic levels contributes to variable treatment responses, and predictive biomarkers are currently lacking. Furthermore, the rarity of PDTC has impeded the compl

FAQs

Why is radioiodine therapy often less effective in poorly differentiated thyroid cancer?

PDTC usually has variable and generally reduced RAI uptake compared with well-differentiated thyroid cancer due to dedifferentiation and loss of sodium-iodide symporter (NIS) expression.

What factors can further reduce iodine avidity and contribute to RAI refractoriness?

Poorly differentiated histology, advanced age, invasive growth, and mutations such as BRAF and TERT can diminish iodine avidity, and some patients may initially respond before developing RAI refractoriness.

What does the case report emphasize about using RAI in PDTC?

The report highlights that although RAI has limited overall value in PDTC, the timing of RAI intervention may have important clinical implications when combined with other therapies and guided by disease assessment.

Sep 30, 2026

Uploaded by Cipher