RECIST 1.1 and serum thyroglobulin measurements in the evaluation of responses to sorafenib in patients with radioactive iodine-refractory differentiated thyroid carcinoma

Abstract

The present study was designed to investigate the association between response evaluation criteria in solid tumors (RECIST) 1.1 and 1.0, and to explore the utility of thyroglobulin (Tg) measurements in assessing tumor responses to sorafenib in patients with radioactive iodine (RAI)-refractory differentiated thyroid carcinoma (DTC). In total, 23 patients with RAI-refractory DTC were enrolled. A comparison of RECIST 1.1 and 1.0 was performed in all patients with measurable disease. Following the exclusion of patients who were positive for anti-Tg antibody, the correlation between RECIST 1.1 and Tg was investigated in patients with measurable disease, and the concordance of the change in Tg between these patients and the patients with non-measurable disease only was analyzed over time. Tumor responses, assessed by RECIST 1.1 and 1.0, were concordant in 96% of the 23 records. However, the number of target lesions, according to RECIST 1.1, was significantly lower than when using RECIST 1.0. Progressive disease (PD) was identified in one of the five patients who underwent fluorodeoxyglucose-positron emission tomography (FDG-PET)/computed tomography (CT) scanning. A correlation between the Tg levels and the sum of the diameters of the target lesions was verified, with the percentage decrease in Tg levels significantly greater than that in the radiograph, demonstrating shrinkage. Furthermore, the percentage change in Tg levels was consistent between the patients with measurable disease and the subjects with non-measurable disease only. In conclusion, in patients with RAI-refractory DTC, RECIST 1.1 is highly concordant with RECIST 1.0 in the assessment of responses to sorafenib treatment, with the advantage of simplified procedures and the complementary use of FDG-PET. Tg measurements, in concordance with RECIST 1.1, are valuable in the evaluation of tumor responses.