Related Experiment Video
Updated: May 2, 2026

Y-90 Radioembolization and PD-1 Inhibitor as Neoadjuvant Treatment in Hepatocellular Carcinoma
Published on: May 24, 2024
Radiologic Response Assessment With RECIST 1.1 and mRECIST in Patients With Hepatocellular Carcinoma Treated With
Boryeong Jeong1, Hyo Jung Park2, Won-Mook Choi3
1Department of Radiology and Research Institute of Radiological Science, Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Objective:
Evidence remains limited regarding whether Response Evaluation Criteria in Solid Tumors version 1.1 (RECIST 1.1) or modified RECIST (mRECIST) more reliably assesses treatment response in patients with hepatocellular carcinoma (HCC) receiving atezolizumab plus bevacizumab (Atezo/Bev). This study aimed to evaluate response patterns based on RECIST 1.1 and mRECIST, analyze inter-reader agreement, and assess their prognostic value for overall survival (OS) in patients with HCC receiving first-line Atezo/Bev.
Materials And Methods:
This retrospective study included patients with HCC treated with first-line Atezo/Bev between June 2020 and December 2022 at a tertiary center. Patients with at least one hypervascular hepatic target lesion were eligible. Two radiologists independently assessed treatment responses using RECIST 1.1 and mRECIST. Inter-reader agreement was evaluated using Cohen's kappa coefficient. Time-dependent Cox regression analysis was performed, with radiologic response and progression treated as time-varying covariates. Prognostic discrimination was evaluated using Harrell's concordance index (C-index).
Results:
A total of 207 patients were included (171 men; median age, 63 years; median follow-up, 10.7 months [range, 0.8-46.4 months]; median OS, 10.7 months [95% confidence interval, 9.2-12.8 months]). mRECIST identified more responders than RECIST 1.1 (54.6% vs. 16.9%). RECIST 1.1 demonstrated excellent inter-reader agreement, whereas mRECIST showed substantial agreement (weighted kappa, 0.89 vs. 0.79). A significantly higher rate of dissociated responses was observed with mRECIST than with RECIST 1.1 (14.0% vs. 4.3%, P < 0.001). Both RECIST 1.1- and mRECIST-based responses and progression were independently associated with OS. Models incorporating RECIST 1.1 demonstrated slightly higher C-index values than those incorporating mRECIST (RECIST 1.1: 0.68 for response and 0.75 for progression; mRECIST: 0.65 and 0.70, respectively).
Conclusion:
RECIST 1.1 is more reproducible and prognostically valuable for guiding treatment decisions in patients with HCC receiving first-line Atezo/Bev. However, this does not invalidate the use of mRECIST as a biological tumor response marker.

