Revised: July 17, 2026
Accepted: August 28, 2026
Published online: September 27, 2026
Processing time: 108 Days and 4.9 Hours
Conversion therapy has increased the proportion of patients with initially unrese
To evaluate RECIST 1.1 and mRECIST for predicting pathological complete response and radiologic-pathologic discordance after HCC conversion therapy surgery.
We retrospectively analysed 66 patients with initially unresectable HCC under
According to mRECIST, 55 patients were classified as having PR and 11 as having stable disease (SD), whereas RECIST 1.1 categorised 37 patients as having PR and 29 as having SD. Overall, 20 patients (30.3%) achieved pCR. Under the mRECIST criteria, all patients with pCR were classified as having PR, yielding a sensitivity of 100% but a low specificity of 23.9% and a PPV of 36.4%. For RECIST 1.1, the sensitivity and specificity were 60.0% and 45.7%, respectively. Agreement between radiologic PR and pCR was poor for both criteria (Cohen’s κ = 0.16 for mRECIST and 0.046 for RECIST 1.1). These findings indicate substantial discordance between radiologic PR and pathological response.
Radiologic PR does not reliably predict pCR after HCC conversion therapy. Imaging alone should not guide surgical timing; integrating clinical and biological markers may improve preoperative response assessment.
Core Tip: Radiologic response is widely used to assess treatment efficacy in hepatocellular carcinoma after conversion therapy, yet its correlation with pathological response remains uncertain. In this study, radiologic partial response assessed by both Response Evaluation Criteria in Solid Tumours (RECIST) version 1.1 and modified RECIST showed poor concordance with pathologic complete response (pCR). Although all patients achieving pCR were classified as responders by modified RECIST, most radiologic responders still had residual viable tumor. These findings underscore the limitations of imaging-based response assessment and support the integration of additional biomarkers to improve preoperative evaluation and treatment planning.
- Citation: Xu C, Liang QY, Sun JP, Zhou K, Pan J, Zhao HT. Radiologic partial response poorly predicts pathologic complete response in hepatocellular carcinoma after conversion therapy. World J Hepatol 2026; 18(9): 123924
- URL: https://www.wjgnet.com/1948-5182/full/v18/i9/123924.htm
- DOI: https://dx.doi.org/10.4254/wjh.123924
Hepatocellular carcinoma (HCC) is the most common subtype of primary liver malignancy, accounting for approximately 75%-85% of cases[1,2]. Based on data from the Global Cancer Observatory, liver cancer is the sixth most commonly diagnosed malignancy worldwide and the third leading cause of cancer-related death. In 2021, approximately 739299 new liver cancer cases were estimated globally [95% confidence interval (CI): 673114-821948][3]. Curative treatments, including surgical resection and liver transplantation, remain the cornerstone of long-term survival. However, a substantial proportion of patients present with intermediate- or advanced-stage disease that is initially unresectable[4-6]. Recently, conversion therapy, which includes locoregional or systemic treatments, has enabled tumour downstaging to facilitate potentially curative surgery[4,7,8]. Advances in transarterial chemoembolization (TACE), hepatic arterial infusion chemotherapy (HAIC), tyrosine kinase inhibitors, and immune checkpoint inhibitors (ICIs) have substantially improved tumour response rates, allowing selected patients to proceed to resection following favourable radiologic responses[8-11].
Despite these advances, a critical challenge remains in the preoperative assessment of treatment efficacy. Clinicians primarily rely on the Response Evaluation Criteria in Solid Tumours (RECIST) version 1.1 and the modified RECIST (mRECIST) to monitor tumour response. While RECIST 1.1 measures overall tumour shrinkage, mRECIST focuses on the reduction of arterial enhancement as a surrogate for tumour viability[12,13]. However, radiologic response is itself a surrogate marker of tumour viability and may not accurately reflect histopathological outcomes. Several previous radiologic-pathological correlation studies have shown only modest concordance between imaging-defined response and histological necrosis. Radiologic complete response or partial response (PR) may both overestimate and underestimate the presence of residual viable tumour in explant or resection specimens[14-16].
This distinction has important implications for conversion therapy. If radiologic PR is considered equivalent to pathologic complete response (pCR), clinicians may prematurely conclude that the disease has been eradicated, thereby influencing decisions regarding the indication for or timing of resection or overstating treatment efficacy in trials that use imaging-based endpoints. Conversely, an overly conservative interpretation of imaging findings could delay potentially curative surgery in patients who actually have minimal residual disease. Therefore, clarifying the concordance between radiologic PR, as assessed by mRECIST and RECIST 1.1, and pCR is essential for guiding surgical decision-making and interpreting conversion therapy outcomes[17,18].
Despite the growing literature on conversion therapy regimens and multiple reports correlating imaging findings with histopathological outcomes after locoregional therapy, relatively few studies have specifically quantified how well radiologic PR predicts true pCR in cohorts treated with systemic and locoregional therapies. Therefore, this single-centre retrospective cohort study aimed to evaluate whether radiologic PR, as assessed by mRECIST and RECIST after conversion therapy, can accurately predict pCR in patients with HCC undergoing subsequent surgical resection. By systematically comparing preoperative imaging findings with postoperative histopathological results, we aimed to quantify the degree of concordance between radiologic and pathological responses. A clearer understanding of this relationship may help optimise preoperative assessment strategies and inform therapeutic decision-making in the multidisciplinary management of HCC.
This was a single-centre retrospective cohort study. We included patients with HCC who were initially considered unres
Inclusion criteria: (1) Patients with HCC diagnosed histopathologically or clinically according to the Chinese Guidelines for Diagnosis and Treatment of Primary Liver Cancer (2024 edition)[19]; (2) Age between 18 years and 85 years; (3) Patients who underwent surgical resection after completing at least two cycles of ICI-based combination therapy and at least one cycle of locoregional treatment; (4) Eastern Cooperative Oncology Group performance status of 0 or 1 and Child-Pugh class A or B liver function; (5) Tumours assessed as unresectable by the multidisciplinary team (MDT) or surgical evaluation, or cases in which surgical resection was not expected to provide better outcomes than non-surgical treatment; (6) No evidence of distant metastases; and (7) Voluntary participation, with the ability to undergo the required examinations and follow-up according to the study protocol, and provision of written informed consent.
Exclusion criteria: (1) Patients with severe systemic diseases, including significant hepatic, renal, cardiac, or pulmonary dysfunction; (2) Coagulation disorders, defined as a severe bleeding tendency (platelet count < 50 × 109/L, international normalized ratio > 1.5, or prothrombin time > 18 seconds); (3) Known allergy to contrast agents that would preclude pre- and post-treatment contrast-enhanced dynamic computed tomography (CT) or magnetic resonance imaging (MRI); (4) Active acute infections or acute exacerbations of chronic infections; (5) Mental illness or a psychiatric history that impairs the ability to comply independently with the study procedures; (6) Pregnancy; and (7) Any other condition that, in the opinion of the investigative team, would make the patient unsuitable for participation in the study.
All patients received a multimodal conversion therapy regimen consisting of locoregional therapy combined with systemic ICIs and anti-angiogenic targeted agents. All eligible participants received an intravenous programmed cell death protein 1 or programmed death-ligand 1 inhibitor every 21 days, including pembrolizumab, camrelizumab, sintilimab, tislelizumab (200 mg), toripalimab (240 mg), atezolizumab (1200 mg), nivolumab, and cadonilimab (15 mg/kg). Additionally, patients received either a tyrosine kinase inhibitor or an anti-vascular endothelial growth factor agent. These agents included lenvatinib (12 mg/day for patients with a body weight ≥ 60 kg or 8 mg/day for those weighing < 60 kg), apatinib (250 mg orally once daily), regorafenib (160 mg orally once daily during the first 3 weeks of each 4-week cycle), and bevacizumab (15 mg/kg administered intravenously on day 1 of each 21-day cycle). The selection of the specific ICI regimen was based on patient preference and clinical circumstances. Furthermore, all patients received locoregional interventions, including TACE, HAIC, or combined TACE and HAIC. These treatment strategies were determined through MDT discussion and patient preference.
Clinical variables extracted from the institutional database included age, sex, hepatitis status, cirrhosis, Barcelona Clinic Liver Cancer (BCLC) stage, the presence of macrovascular invasion or extrahepatic disease, baseline largest tumour diameter, serum alpha-fetoprotein (AFP) level, treatment regimen, and the number of treatment cycles before surgery. The last available contrast-enhanced CT or MRI scan before surgery was used to determine the radiologic response.
Contrast-enhanced CT or MRI was performed at baseline and every six to eight weeks thereafter. Two independent radiologists, blinded to the pathological results, evaluated treatment response according to the following criteria: RECIST 1.1: Response was evaluated based on the change in the sum of the longest diameters of the target lesions. mRECIST: Response was evaluated based on the change in the sum of the diameters of the viable (arterially enhancing) tumour components. Response was categorised as complete response, PR, stable disease (SD), or progressive disease.
Surgical resection was performed at least one week after the last treatment cycle once the MDT had determined that the tumour was resectable. Resected specimens were examined to determine the percentage of tumour necrosis. pCR was defined as 100% tumour necrosis with no viable tumour cells identified in any treated nodule. Any amount of residual viable tumour cells was classified as non-pCR.
Continuous variables were summarised as means ± SDs or medians with interquartile ranges (IQRs), depending on the data distribution. Categorical variables were presented as n (%) with 95%CIs. Between-group comparisons were performed using Student’s t-test or the Mann-Whitney U test for continuous variables and the χ2 test or Fisher’s exact test for categorical variables. The association between radiologic response and pCR was assessed using contingency tables and Fisher’s exact test. The predictive performance of radiologic PR for pCR was evaluated using sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and overall accuracy. Agreement between radiologic PR and pCR was assessed using Cohen’s kappa coefficient. Additionally, baseline serum AFP levels were compared between the pCR and non-pCR groups using the Mann-Whitney U test. AFP was further categorized as ≤ 20 ng/mL or > 20 ng/mL, and the proportions between groups were compared using the χ2 test or Fisher’s exact test, as appropriate. A two-sided P value < 0.05 was considered statistically significant. All data were analysed using Stata statistical software (version 18.0 BE; StataCorp LLC, College Station, TX, United States)[20].
A total of 66 patients were included in the study (Figure 1), with a median age of 53 years (IQR: 47-62), and 90.91% of them were male. The majority had hepatitis B virus infection (87.88%), whereas 15.15% had metabolic dysfunction-associated steatotic liver disease. Most patients presented with advanced disease, with 65.15% classified as BCLC stage C, 24.24% having portal vein tumour thrombus, and 66.67% having extrahepatic metastasis. In addition, 92.42% of patients were classified as Child-Pugh class A. The median number of systemic therapy cycles was 4 (IQR: 3-6). The median largest tumour diameter decreased from 8.6 cm (range: 1.6-18.6 cm) before treatment to 6.1 cm (range: 1.1-15.4 cm) after treatment. Baseline serum AFP data were available for 59 patients. The median AFP level was 280 ng/mL (IQR: 12.8-4200). At the time of analysis, the median overall survival had not been reached, and the median progression-free survival was 33.27 months (95%CI: 19.3-40.63) (Table 1).
| Characteristics1 | Total (n = 66) |
| Age (years) | 53 (47, 62) |
| Sex | |
| Female | 6 (9.09) |
| Male | 60 (90.91) |
| HBV infection | |
| Yes | 58 (87.88) |
| No | 8 (12.12) |
| MASLD | |
| Yes | 10 (15.15) |
| No | 56 (84.85) |
| BCLC stage | |
| B | 23 (34.85) |
| C | 43 (65.15) |
| Child-Pugh class | |
| A | 61 (92.42) |
| B | 5 (7.58) |
| PVTT | |
| Yes | 16 (24.24) |
| No | 50 (75.76) |
| Extrahepatic metastasis | |
| Yes | 22 (66.67) |
| No | 44 (33.33) |
| Number of systemic therapy cycles | 4 (3, 6) |
| Pre-treatment largest tumour diameter (cm), median (range) | 8.6 (1.6, 18.6) |
| Post-treatment largest tumour diameter (cm)2, median (range) | 6.1 (1.1, 15.4) |
| Baseline AFP level | 280 (120.8, 4200) |
| Tumour response by mRECIST | |
| PR | 55 (83.33) |
| SD | 11 (16.67) |
| Tumour response by RECIST 1.1 | |
| PR | 37 (56.06) |
| SD | 29 (43.94) |
| pCR | |
| Yes | 20 (30.30) |
| No | 46 (69.70) |
| OS (months), median (95%CI) | Not reached |
| PFS (months), median (95%CI) | 33.27 (19.3-40.63) |
According to mRECIST, 55 of the 66 patients (83.3%) were classified as having PR and 11 (16.7%) as having SD. According to RECIST 1.1, 37 patients (56.1%) were classified as having PR and 29 (43.9%) as having SD. On final pathological examination, 20 patients (30.3%) achieved pCR, whereas 46 (69.7%) had residual viable tumour (Table 2).
| Radiologic response | pCR | Non-pCR | Total |
| mRECIST | |||
| PR | 20 | 35 | 55 |
| SD | 0 | 11 | 11 |
| Total | 20 | 46 | 66 |
| RECIST 1.1 | |||
| PR | 12 | 25 | 37 |
| SD | 8 | 21 | 29 |
| Total | 20 | 46 | 66 |
Among the 55 patients with mRECIST PR, 20 achieved pCR, whereas 35 had residual viable tumour. None of the 11 patients with mRECIST SD achieved pCR. The contingency table comparing mRECIST response with pCR yielded a Fisher’s exact test P value of 0.026. When mRECIST PR was used as a positive test for pCR, the performance metrics were as follows: Sensitivity, 100.0%; specificity, 23.9%; PPV, 36.4%; NPV, 100.0%; and accuracy, 47.0%. Cohen’s kappa coefficient for agreement between mRECIST PR and pCR was 0.160, indicating only slight agreement beyond chance (Tables 3 and 4). Among the 37 patients with RECIST 1.1 PR, 12 achieved pCR, whereas 25 did not. Among the 29 patients with RECIST 1.1 SD, 8 achieved pCR, whereas 21 did not. When RECIST 1.1 PR was used as a positive test for pCR, the performance metrics were as follows: Sensitivity, 60.0%; specificity, 45.7%; PPV, 32.4%; NPV, 72.4%; and accuracy, 50.0%. Cohen’s kappa coefficient was 0.046, indicating minimal agreement beyond chance.
| Metric | mRECIST | RECIST 1.1 |
| Sensitivity (%) | 100.0 | 60.0 |
| Specificity (%) | 23.9 | 45.7 |
| Positive predictive value (%) | 36.4 | 32.4 |
| Negative predictive value (%) | 100.0 | 72.4 |
| Accuracy (%) | 47.0 | 50.0 |
| Cohen’s kappa coefficient (κ) | 0.160 | 0.046 |
| Classification | mRECIST | RECIST 1.1 |
| PR + pCR (true positive) | 20 | 12 |
| PR + non-pCR (false positive) | 35 | 25 |
| SD + pCR (false negative) | 0 | 8 |
| SD + non-pCR (true negative) | 11 | 21 |
Baseline serum AFP levels were comparable between the pCR and non-pCR groups, with median (IQR) values of 591.35 (10.4, 1984) ng/mL and 238 (29.6, 9362) ng/mL, respectively (P value = 0.44). The proportion of patients with positive baseline AFP (> 20 ng/mL) did not differ significantly between the pCR and non-pCR groups (67.39% vs 80.00%, P value = 0.30).
In this single-centre retrospective cohort of 66 patients who underwent surgery after conversion therapy for HCC, we observed a discrepancy between radiologic PR and pCR. All patients who achieved pCR were classified into the mRECIST PR group, yielding a sensitivity of 100%; however, only 36.4% of patients with mRECIST PR achieved pCR on final histopathological examination. Therefore, mRECIST identified patients who may have achieved pCR, but most radiologic PRs did not correspond to complete pathological tumour eradication. These findings indicate that mRECIST PR should not be used as a surrogate for pCR when making definitive decisions regarding surgery or prognostic assessments.
The differential performance of mRECIST and RECIST 1.1 observed in the present study is consistent with the concep
Clinically, this imaging-pathology mismatch has two immediate implications. First, using radiologic PR alone to determine resectability or to conclude that the tumour has been eradicated carries a risk of misclassification. Patients with mRECIST PR may still have substantial residual viable tumour, with implications for the extent of resection, lymphadenectomy planning, and the intensity of postoperative surveillance. Second, clinical trials or reports that use radiologic PR as a primary endpoint to claim profound or curative responses should interpret these endpoints cautiously. Radiologic PR does not equate to histological cure and may therefore overestimate treatment efficacy unless supported by pathological findings or long-term outcome data[24,25].
Consequently, imaging remains essential. The high sensitivity of mRECIST PR for identifying patients who achieved pCR indicates that imaging remains clinically valuable; patients without mRECIST PR are very unlikely to have achieved pCR and may therefore require continued therapy or alternative treatment strategies. For patients with mRECIST PR, multidisciplinary evaluation should integrate imaging findings with clinical markers (e.g., dynamic AFP trends), functional imaging where available (e.g., diffusion-weighted MRI and contrast-enhanced sequences), and careful consideration of the interval between completion of therapy and surgery to maximise the likelihood of complete resection while avoiding premature conclusions of tumour eradication[15,21].
The literature supports the prognostic relevance of pCR in certain contexts, such as improved outcomes after bridging therapies and in transplant cohorts; however, the findings are heterogeneous and are substantially confounded by baseline tumour biology and patient selection criteria[25,26]. Several studies evaluating locoregional therapy as a bridge to transplantation or resection have shown that radiologic response correlates with, but does not accurately predict, histological necrosis. Furthermore, major pathological response appears to be associated with improved recurrence-free or overall survival in some studies, whereas others have shown that baseline risk factors remain the dominant predictors of outcome even after the achievement of a pathological response. These observations underline that pCR is informative but should not be considered a stand-alone surrogate for favourable long-term outcomes unless adjusted for pre-treatment risk[16,23,25].
This study has several limitations. First, this was a retrospective, single-centre study, which is inherently subject to selection bias. In addition, the sample size was relatively small. More importantly, only patients who ultimately underwent surgical resection after conversion therapy were included because pathological assessment of treatment response was available only from resected specimens. Consequently, patients who experienced disease progression, remained unresectable, or were otherwise unable to undergo surgery after conversion therapy were excluded, which may have introduced selection bias and limited the generalisability of our findings to the broader population of patients receiving conversion therapy. Furthermore, the interval between the last treatment cycle and surgery was not fully standardised, which may have influenced the extent of tumour necrosis observed in the surgical specimens. In addition, patients received heterogeneous conversion therapy regimens, including different locoregional treatments (TACE with or without HAIC), ICIs, and targeted agents. These treatment strategies may induce distinct patterns of tumour necrosis and potentially influence the relationship between radiologic and pathological responses. However, because the number of patients within the individual treatment subgroups was limited, adequately powered stratified analyses could not be performed. Therefore, whether the radiology-pathology correlation differs among specific conversion therapy regimens remains uncertain. Future multicentre prospective studies with larger sample sizes, standardised treatment protocols, inclusion of both surgical and non-surgical patients, and longitudinal follow-up are needed to validate our findings and improve their generalisability.
Despite these limitations, our study demonstrates the imperfect correlation between radiologic response and patho
Radiologic PR assessed using conventional imaging criteria does not necessarily correspond to pCR in patients with HCC undergoing conversion therapy. These findings emphasise the need for cautious interpretation of imaging responses and highlight the importance of developing more accurate imaging and biological markers to guide clinical decision-making in the era of multimodal HCC treatment.
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