# Preoperative contrast-enhanced CT prediction of distinct vascular patterns in solitary early-stage hepatocellular carcinoma and its prognostic value

**Authors:** Wanli Zhang, Wen Lv, Yi Long, Jiaxin Lin, Jiamin Li, Chuanxian Zhang, Yandong Zhao, Jie Zhan, Shengsheng Lai, Mingyong Gao, Xinqing Jiang, Ruimeng Yang

PMC · DOI: 10.1186/s13244-026-02224-5 · Insights into Imaging · 2026-02-16

## TL;DR

This study uses CT scans to predict vascular patterns in early liver cancer, helping identify patients at higher risk of cancer recurrence.

## Contribution

A combined model using clinical and CT features effectively identifies vascular patterns and predicts recurrence in early-stage hepatocellular carcinoma.

## Key findings

- The combined model achieved an AUC of 0.784 in training and 0.794 in external validation for predicting V/M+ status.
- A V/M+ score ≥34 and tumor size ≥60 mm were significant predictors of HCC recurrence.
- The model helps stratify patients into high- and low-risk groups for 2-year recurrence-free survival.

## Abstract

To investigate the value of qualitative and quantitative contrast-enhanced CT (CECT) features for noninvasive identification of two distinct vascular patterns, vessels that encapsulate tumor clusters (VETC) and/or microvascular invasion (MVI), in solitary early-stage (BCLC 0-A) hepatocellular carcinoma (HCC) and assess their prognostic implications.

We retrospectively included 347 patients with solitary early-stage HCC who underwent preoperative CECT and subsequent resection at two centers. Patients were divided into V/M+ (MVI and/or VETC positive, n = 174) and VM− (both MVI and VETC negative, n = 173) groups based on histopathology. Four predictive models (clinical, CT quantitative, CT qualitative, and combined) integrating clinical and CECT features were developed and validated for identifying V/M+ status. The optimal model was further applied to predict 2-year recurrence-free survival (RFS). Sensitivity analysis was performed using propensity score matching (PSM). Models’ performance was evaluated and compared using AUC analyses and DeLong tests.

The combined model [serum AFP ≥ 200 ng/mL, non-smooth tumor margin, internal arteries, and lower tumor-to-liver density ratio in the portal venous phase (P-TLR)] achieved optimal predictive performance for V/M + HCC, with training AUC of 0.784 and 0.782 pre- and post-PSM, and external validating AUC of 0.794. A derived V/M+ score stratified patients, with higher scores associated with significantly shorter 2-year RFS. V/M+ score ≥ 34 and tumor size ≥ 60 mm were significant predictors of HCC recurrence (p < 0.05).

The combined model integrating clinical and CECT-based features, enables non-invasive assessment of V/M status in early-stage solitary HCC and effectively stratifies patients according to recurrence risk.

Specific CT-based qualitative and quantitative features are associated with a distinct vascular pattern of BCLC stage 0-A HCC. The developed combined model and derived V/M+ score offer a reliable tool for clinicians to predict V/M + HCC and patients’ 2-year RFS.

Specific CECT-based qualitative and quantitative features are associated with V/M + HCC at the BCLC stage 0-A.The developed combined model offers a reliable tool for clinicians to identify V/M + HCC.The derived V/M+ score helps stratify HCC patients into high- and low-risk groups for 2-year RFS, facilitating personalized management of HCC.

Specific CECT-based qualitative and quantitative features are associated with V/M + HCC at the BCLC stage 0-A.

The developed combined model offers a reliable tool for clinicians to identify V/M + HCC.

The derived V/M+ score helps stratify HCC patients into high- and low-risk groups for 2-year RFS, facilitating personalized management of HCC.

## Linked entities

- **Diseases:** hepatocellular carcinoma (MONDO:0007256), HCC (MONDO:0007256)

## Full-text entities

- **Genes:** LOC102724197 (inactive glutathione hydrolase 2) [NCBI Gene 102724197] {aka GGT2}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, CD34 (CD34 molecule) [NCBI Gene 947], GGTLC5P (gamma-glutamyltransferase light chain 5 pseudogene) [NCBI Gene 653590] {aka GGT}, PDCD1 (programmed cell death 1) [NCBI Gene 5133] {aka ADMIO4, AIMTBS, CD279, PD-1, PD1, SLEB2}, KRT19 (keratin 19) [NCBI Gene 3880] {aka CK19, K19, K1CS}, GLRA2 (glycine receptor alpha 2) [NCBI Gene 2742] {aka GLR, MRXSP}, RBM8A (RNA binding motif protein 8A) [NCBI Gene 9939] {aka BOV-1A, BOV-1B, BOV-1C, C1DELq21.1, DEL1q21.1, MDS014}, STAR (steroidogenic acute regulatory protein) [NCBI Gene 6770] {aka STARD1}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, AFP (alpha fetoprotein) [NCBI Gene 174] {aka AFPD, FETA, HPAFP}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}
- **Diseases:** VETC (MESH:D009383), ischemia (MESH:D007511), cirrhosis (MESH:D005355), NLR (MESH:D015467), Tumor (MESH:D009369), CECT (MESH:C564835), hepatic B or C infection (MESH:D006509), ES (OMIM:605130), necrosis (MESH:D009336), BCLC (MESH:D006528), venous invasion (MESH:D009361), TLR (MESH:D008113), metastases (MESH:D009362), MVI (MESH:D017566), SEN (MESH:D003807), MTM (MESH:D014202), death (MESH:D003643)
- **Chemicals:** tyrosine (MESH:D014443), Sorafenib (MESH:D000077157), DP (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12909690/full.md

## References

4 references — full list in the complete paper: https://tomesphere.com/paper/PMC12909690/full.md

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Source: https://tomesphere.com/paper/PMC12909690