Ubiquitin-specific protease 25 (USP25) is a key regulator of lipid metabolism and insulin-stimulated glucose transport. Nonetheless, its involvement in adipocyte maturation remains uncertain. In this study, we aimed to explore how the expression of USP25 contributes to obesity induced by a high-fat diet (HFD). Usp25-KO and WT mice, maintained on either a normal diet or an HFD, were evaluated for weight gain, insulin resistance status, adipose tissue development, energy metabolism, and systemic inflammation status. In vitro, 3T3-L1 cells were induced to mature adipocytes in a specific culture medium. We found that USP25 expression decreased in obese mice subjected to long-term HFD feeding and in mature adipocytes. Usp25-KO mice showed restrained adipose tissue development and improved insulin resistance, whereas USP25-deficient preadipocytes failed to differentiate. RNA sequencing analysis showed the downregulation of lipid synthesis-related pathways in Usp25-KO mice. Mechanistically, USP25 binds to and stabilizes poly (ADP-ribose) polymerase 1 through deubiquitination, whereas poly (ADP-ribose) polymerase 1 facilitates preadipocyte differentiation and maturation by regulating the elongation of very long-chain fatty acid protein 3. These findings show the essential role of USP25 in adipocyte differentiation and lipid metabolism, suggesting that targeting USP25 ablation in adipocytes could be a promising therapeutic strategy for obesity treatment.

Background:Pituitary stalk interruption syndrome (PSIS) is a clinical syndrome caused by the absence or thinning of the pituitary stalk. This syndrome mainly impairs the transport of hormones from the hypothalamus to the posterior pituitary gland and affects the action of relevant hormones on the anterior pituitary gland, thereby leading to common clinical manifestations such as diabetes insipidus, growth retardation, gonadal dysplasia, hypothyroidism, and adrenocortical hypofunction. In PSIS, cases presenting with infantile cholestasis as the initial and prominent manifestation are relatively rare and prone to misdiagnosis. Case Description:A boy aged 2 months was admitted for cholestatic liver disease, presenting with poor response to routine choleretic therapy, non-elevated gamma-glutamyl transferase (GGT) level, hypothyroidism and recurrent hypoglycemia. Difficulties were encountered in identifying the etiology of common infantile cholestatic liver disease with non-elevated GGT. Subsequently, cranial magnetic resonance imaging (MRI) and genetic testing were completed focusing on the symptoms related to the endocrine axis, leading to a definitive diagnosis of PSIS. The infant achieved stable and favorable therapeutic outcomes after receiving combined treatment by endocrinologists and gastroenterologists during follow-up. Conclusions:The prominent feature of this case was infantile cholestatic liver disease accompanied by hypoglycemia and hypothyroidism. For infants, hypoglycemia and hypothyroidism should not be overlooked, and close monitoring is required. As pediatric gastroenterologists, when routine treatment fails for infantile cholestatic liver disease, we need to consider the possibility of cholestasis caused by hypothalamic-pituitary axis abnormality, and conduct relevant imaging examinations, hormone level tests and genetic tests when necessary. At this point, the joint diagnosis and treatment by gastroenterologists and endocrinologists is particularly important.

Objective Gram-negative bacterial (GNB) infections, particularly multidrug-resistant GNB (MDR-GNB), significantly affect survival after liver transplantation. This study analyzed the epidemiology, resistance profiles, and mortality risk factors for early postoperative GNB infections. Methods We retrospectively reviewed 1,115 patients undergoing liver transplantation (2015–2024); 110 developed GNB infections within 30 days. Pathogen distribution, resistance patterns, and risk factors for MDR-GNB and mortality were analyzed using logistic regression. Results The MDR-GNB infection rate was 68.2% (75/110). Among 182 isolates, Klebsiella pneumoniae (33.0%) and Acinetobacter baumannii (30.2%) predominated. Common infection sites were abdominal cavity (44.5%) and respiratory tract (37.9%). Carbapenem resistance was high (87.5%); tigecycline (21.2%) and minocycline (49.0%) showed higher susceptibility. Pre-transplant MELD score ≥ 30 independently predicted MDR-GNB infection (OR = 4.094, P = 0.040). The 30-day mortality rate was 14.5% (16/110). Independent mortality risk factors included septic shock (OR = 387.098, P < 0.001), serum creatinine ≥ 133 µmol/L (OR = 7.136, P = 0.005), lymphocyte count ≤ 0.3×10⁹/L (OR = 4.719, P = 0.026), and MELD score ≥ 30 (OR = 3.971, P = 0.041). MDR-GNB infection correlated with lower 30-day survival (Log-rank P = 0.020). Conclusion Early postoperative GNB infections were predominantly MDR with severe carbapenem resistance. Septic shock, renal dysfunction, lymphocytopenia, and high MELD score independently increased mortality, highlighting the need for enhanced infection control, tailored empiric therapy, and early intervention.

Enterohepatic circulation is essential for maintaining a constant bile acid concentration. Diseases with enterohepatic circulation disturbances are usually difficult to diagnose definitively without the time-consuming and expensive genetic tests. This study analyzed and compared duodenal fluid in patients with biliary atresia (BA), familial intrahepatic cholestasis 2 (FIC2), and sodium taurocholate cotransporting polypeptide (NTCP) deficiency. This study aimed to assess the diagnostic value of duodenal fluid analysis in patients with enterohepatic circulation disturbance. This study retrospectively analyzed data from 18 patients with BA, 13 patients with FIC2, and 15 patients with NTCP deficiency. All patients completed the duodenal tube tests before receiving treatment for cholestasis. The patients were intubated through the right nasal cavity to the middle or lower duodenum, as confirmed by radiography. 3-5 mL of duodenal fluid was collected at last. Clinical presentations, laboratory data, genetic data, and so forth were collected for the analysis. Among the 3 types of diseases, levels of total bile acid (TBA), total bilirubin (TB), direct bilirubin (DB), and gamma-glutamyl transpeptidase (GGT) in duodenal fluid showed significant differences (P < .01). Compared with the same indications in duodenal fluid, levels of TBA and GGT in serum did not show significant differences between patients with FIC2 and NTCP deficiency (P > .05). Duodenal TBA/serum TBA ratio, duodenal TB/serum TB ratio, duodenal DB/serum DB ratio, and duodenal GGT/serum GGT ratio also showed significant differences between patients with BA and NTCP deficiency, between patients with FIC2 and NTCP deficiency (P < .01). For diagnosis of BA, increased GGT and absent TB, DB, and TBAs had a sensitivity of 100%, 100%, 100%, and 100%, a specificity of 86.1%, 100%, 97.2%, and 97.2%. Duodenal tube tests have been used for the diagnosis of BA for over 10 years. Our findings support the duodenal fluid analysis as a tool for prompt timely diagnosis of BA. This study also indicates that the test is a useful diagnostic method with high accuracy for other diseases with enterohepatic circulation disturbance.

Due to the easier availability of transgenic mice and reagents, the mouse orthotopic liver transplantation model offers significant advantages in liver transplantation research. However, technical challenges have limited its broader application. The most challenging steps of the procedure include manual anastomosis of the suprahepatic vena cava, cuff anastomosis of the portal vein, and maintaining the anhepatic phase within 20 minutes. This study aims to provide detailed solutions to overcome these bottlenecks and introduces a modified magnetic device to facilitate safer and more efficient cuff anastomosis. We also describe the learning curve for beginners to achieve a 30-day survival rate exceeding 90% in mouse orthotopic liver transplantation. We demonstrate that mouse orthotopic liver transplantation can be mastered within 8 months of continuous practice, with 7-day and 30-day survival rates improving from 0% to 96.7% and 0% to 93.3%, respectively. The entire procedure can be completed within 80 minutes. We believe these technical improvements will provide more practical guidance for mouse liver transplantation.

OBJECTIVES:Accurate and timely assessment of liver graft function is of great significance for the survival of liver grafts and liver transplant recipients. This study aimed to investigate the correlation between the functional automated whole-liver score (FAWLS) system derived from gadoxetic acid-enhanced magnetic resonance imaging (MRI) and quantitative measurements of liver graft function. Additionally, it sought to determine the utility of FAWLS in evaluating the severity of liver graft injury and monitoring treatment response following therapy, through an association analysis with liver biopsy findings to validate its effectiveness as a non-invasive diagnostic tool. METHODS:Between July 2021 and September 2023, 172 liver transplant recipients underwent liver MRI at a 3 T system, which included T1 mapping and high-speed T2-corrected multi-echo magnetic resonance spectroscopy in this prospective cohort study. The Albumin-Bilirubin (ALBI) score was utilized to quantitatively evaluate liver graft function. T1 maps were obtained before and 20 minutes after the injection of gadoxetic acid (0.025 mmol/kg). This study assessed the relationship between the ALBI score and various MRI parameters, including pre- and post-contrast liver T1 values, FAWLS, liver volume, and functional liver imaging score (FLIS). Diagnostic performance of the FAWLS in identifying patients with an ALBI score greater than -2.6. Utilized the areas under the receiver operating characteristic curve to compare across other parameters. RESULTS:FAWLS exhibited a negative correlation with ALBI ( r = -0.72; P < 0.001). Participants with ALBI scores of -2.6 or lower showed significant differences in FAWLS, post-contrast T1 liver , and ΔT1 liver compared to those with ALBI scores greater than -2.6. FAWLS demonstrated superior performance in detecting ALBI of greater than -2.6 compared to liver volume (0.83 vs 0.59; P < 0.0001), ΔT1 liver (0.83 vs 0.76; P = 0.03), and FLIS (0.83 vs 0.65; P = 0.01). Significant alterations in FAWLS were observed between pre-treatment and post-treatment measurements. CONCLUSION:FAWLS is negatively correlated with liver function based on ALBI scores and provide good diagnostic accuracy in identifying patients with ALBI of greater than -2.6. Additionally, FAWLS is valuable for monitoring treatment response after therapy in these individuals.

BACKGROUND:The impact of resection margin width on surgical outcomes in hepatocellular carcinoma (HCC) patients with microvascular invasion (MVI) remains controversial. This study explores whether MVI sub-classification influences prognosis after curative resection for solitary HCC. METHODS:We analyzed 601 solitary HCC patients who underwent hepatectomy between May 2018 and December 2019, classifying them into no vascular invasion (NVI), microvessel invasion (MI), and microscopic portal vein invasion (MPVI) groups. The effects of resection margin width on progression-free survival (PFS) and overall survival (OS) were evaluated. RESULTS:MVI was identified in 133 patients (22.1 %). The 3-year OS rates for patients with NVI, MI, and MPVI were 87.4 %, 70.2 %, and 53.9 %, while PFS rates were 59.5 %, 47.7 %, and 29.9 %, respectively (p < 0.0001). A wide margin (≥1 cm) improved OS and PFS in MI patients (80.7 % vs. 50.0 %; 64.5 % vs. 23.7 %; p < 0.05) but not in NVI or MPVI groups. Multivariate analysis indicated that tumor size, MI and MPVI were the independent risk factors affecting RFS and OS after curative liver resection. CONCLUSION:MPVI was associated with a worse prognosis after resection compared to MI and NVI. A wide resection margin improved survival in MI patients but had no benefit in NVI or MPVI cases.

CLDN18.2 is a promising target for GI cancer therapy, with various modalities under clinical evaluation. However, these therapies face challenges due to the heterogeneous expression of CLDN18.2, leading to inconsistent efficacy and the need of patient stratification, as observed with Zolbetuximab, AZD0901 and IBI343. Besides, these treatments may induce drug resistance by downregulating CLDN18.2. Recently, CDH17 (Cadherin 17) has emerged as a novel target for biologics, often overexpressed in GI cancers. But in normal tissues, it remains inaccessible as it is hidden within the tight junctions of intestinal epithelial cells, which makes it a favorable target for cancer therapy. More importantly, systematic analysis of expression data reveals high co-expression or complementary expression of CDH17 with CLDN18.2 in GI cancers, with no co-expression in other major organs. This discovery presents an opportunity for a bispecific anti-CDH17/CLDN18.2 therapy, potentially addressing the limitation of targeting CLDN18.2 alone. VBC108 is a bispecific ADC designed to target both CDH17 and CLDN18.2 with TOPO1i payload. The unique design maximizes efficacy while minimizing safety risks. VBC108 distinguishes itself from other CLDN18.2-targeting therapies through the following features. VBC108 targets both CDH17 and CLDN18.2, potentially overcoming tumor heterogeneity and covering over 80% of gastric and 50% of pancreatic cancers without CLDN18.2 IHC selection. It has high affinity to CDH17 and CLDN18.2, enhanced binding avidity, internalization and cytotoxicity. Moreover, it has a strong bystander effect to help further overcome the heterogeneity of tumor antigen expression. In CDH17 single-positive CDX models, which represent clinical scenarios lacking targeted therapies, VBC108 exhibited strong efficacy, whereas AZD0901 did not inhibit tumor growth at all. In CDH17/CLDN18.2 double-positive CDX models, representing clinical scenarios with target expression heterogeneity, VBC108 further showed its superiority. In CLDN18.2 single-positive CDX models, reflecting clinical scenarios with available CLDN18.2-targeted therapies, VBC108 demonstrated comparable efficacy with different payload mechanisms. In the PDX (GC, PADC, CRC) studies, especially in the GC model with low to medium expression of CDH17/CLDN18.2, it achieved a 100% CR. Furthermore, preliminary toxicity studies in Cyno-monkeys showed good tolerability with repeated doses. VBC108 also exhibited excellent developability in a comprehensive developability assessment (DA) test, making it a strong candidate for further CMC development. In summary, VBC108, with its unique design, shows the potential as a first-in-class ADC for GI cancer and supports the advancement to clinical trials. Wei (Vivian) Wang, Lingyu Guan, Man Xu, Qun Yin, Chen Dong, Jing Li. VBC108: a first-in-class CDH17/CLDN18.2 targeted bispecific antibody drug conjugate (ADC) to overcome tumor heterogeneity of gastrointestinal cancers (GC, PADC, CRC, etc.) [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 341.

BACKGROUND:The current study aimed to understand the genetic landscape and investigate the diagnostic and prognostic biomarkers of primary hepatocellular carcinoma (HCC). METHODS:A cohort of 36 Chinese HCC samples with hepatitis B virus (HBV) infection was examined by whole-exome sequencing (WES). Prognosis-related alterations were identified and further verified in the TCGA database and GSE65372 profiles in the GEO database. A Chinese replication cohort of 180 HCC samples with HBV infection was collected to evaluate the candidate genes by immunohistochemical analysis. A receiver operating characteristic (ROC) curve analysis evaluated the prognostic power of candidate genes. Finally, EdU and transwell invasion assay were performed to detect the function of candidate genes. RESULTS:A total of 11 novel genes showed a significant association with HCC in the discovery cohort. The data were verified using the GEO and TCGA databases, and the expression of ARID1A, CSMD1, and SENP was evaluated in the replication cohort. Furthermore, ARID1A, CSMD1, and SENP3 are effective prognostic biomarkers for HCC patients in the replication population. CONCLUSIONS:Molecular heterogeneity was detected in HCC patients, and ARID1A, CSMD1, and SENP3 were identified as effective HCC prognosis biomarkers. CSMD1 prevents HCC by suppressing cell invasion.

BACKGROUND:Arsenic trioxide (ATO) is indicated as a broad-spectrum medicine for a variety of diseases, including cancer and cardiac disease. While the role of ATO in hepatic ischemia/reperfusion injury (HIRI) has not been reported. Thus, the purpose of this study was to identify the effects of ATO on HIRI. METHODS:In the present study, we established a 70% hepatic warm I/R injury and partial hepatectomy (30% resection) animal models in vivo and hepatocytes anoxia/reoxygenation (A/R) models in vitro with ATO pretreatment and further assessed liver function by histopathologic changes, enzyme-linked immunosorbent assay, cell counting kit-8, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. Small interfering RNA (siRNA) for extracellular signal-regulated kinase (ERK) 1/2 was transfected to evaluate the role of ERK1/2 pathway during HIRI, followed by ATO pretreatment. The dynamic process of autophagic flux and numbers of autophagosomes were detected by green fluorescent protein-monomeric red fluorescent protein-LC3 (GFP-mRFP-LC3) staining and transmission electron microscopy. RESULTS:A low dose of ATO (0.75 μmol/L in vitro and 1 mg/kg in vivo ) significantly reduced tissue necrosis, inflammatory infiltration, and hepatocyte apoptosis during the process of hepatic I/R. Meanwhile, ATO obviously promoted the ability of cell proliferation and liver regeneration. Mechanistically, in vitro  studies have shown that nontoxic concentrations of ATO can activate both ERK and phosphoinositide 3-kinase-serine/threonine kinase (PI3K-AKT) pathways and further induce autophagy. The hepatoprotective mechanism of ATO, at least in part, relies on the effects of ATO on the activation of autophagy, which is ERK-dependent. CONCLUSION:Low, non-toxic doses of ATO can activate ERK/PI3K-AKT pathways and induce ERK-dependent autophagy in hepatocytes, protecting liver against I/R injury and accelerating hepatocyte regeneration after partial hepatectomy.

BACKGROUND & AIMS:Hepatic ischemia-reperfusion injury (HIRI) is a critical complication of liver surgery and transplantation that contributes significantly to severe organ failure. GRINA, a calcium-regulating endoplasmic reticulum (ER) protein, plays an essential role in controlling the unfolded protein response; however, its role in HIRI remains unclear. The aim of this study was to investigate the function of GRINA in HIRI and explore its potential as a therapeutic target. METHODS:Liver tissues from patients undergoing hepatectomy, alongside a mouse model of partial HIRI, were used to assess GRINA expression levels. Hepatocyte-specific Grina knockout and transgenic mouse models were generated to explore the effects of GRINA on HIRI. Key markers of inflammation, apoptosis, ER stress, and autophagy were evaluated via real-time PCR, Western blotting, immunohistochemistry, immunofluorescence, and ELISA. RNA sequencing, mass spectrometry, coimmunoprecipitation and ubiquitination assays were used to elucidate the underlying molecular mechanisms. RESULTS:GRINA expression was markedly reduced in hepatocytes from both patients and mice with HIRI, and its expression was inversely correlated with the severity of liver damage. Hepatocyte-specific Grina overexpression mitigated liver injury, the inflammatory response, and hepatocyte apoptosis following HIRI, whereas GRINA deficiency exacerbated these outcomes. Mechanistically, GRINA interacted directly with ATF6 and recruited HRD1 to form a multiprotein complex that catalyzed ATF6 polyubiquitination, thereby promoting its degradation. This process suppressed ER autophagy (ER-phagy), providing cellular protection following HIRI. The inhibition of ATF6 degradation attenuated the protective effects of GRINA in HIRI. CONCLUSIONS:Our study highlights the critical role of the GRINA-HRD1-ATF6 complex in regulating ER stress and autophagy during HIRI. These findings provide new insights into therapeutic strategies to alleviate HIRI. IMPACT AND IMPLICATIONS:Hepatic ischemia-reperfusion injury (HIRI) represents a multifaceted pathophysiological challenge commonly encountered during liver surgeries, yet its underlying molecular mechanisms remain inadequately understood. In this study, we revealed a significant negative correlation between GRINA levels and the severity of liver damage in patients with HIRI. Our findings demonstrate that GRINA alleviates endoplasmic reticulum stress by enhancing HRD1-mediated ubiquitination of ATF6, thereby maintaining calcium homeostasis and inhibiting ER-phagy. This study provides novel insights into the role of GRINA in protecting liver cells under HIRI, offering fresh perspectives for clinical prevention and management strategies for HIRI.

One of the challenges of laparoscopic liver resection (LLR) is the exposure of the surgical field. We propose a new surgical approach to better expose the right liver, stretching of the ligamentum teres hepatis (SLTH), and we evaluated its clinical feasibility and limitations through a study analyzing relevant cases. Clinicopathologic data on patients who underwent laparoscopic right partial hepatectomy (LRPH) at our center were retrospectively collected, and subjects were 276 patients with liver space-occupying lesions who met the selection criteria and who underwent the new surgical approach (SLTH) or the conventional surgical approach (no stretching of the ligamentum teres hepatis, or NSLTH). After 1:1 propensity score matching (PSM), 102 patients in each cohort were selected for further analysis. There were no significant differences in the operating time or the duration of postoperative hospitalization between the SLTH cohort and the NSLTH cohort. The duration of detachment of the hepatic parenchyma and the duration of hepatic portal occlusion were significantly shorter in the SLTH cohort than in the NSLTH cohort. The intraoperative blood loss in the SLTH cohort was significantly less than that in the NSLTH cohort. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were significantly lower in the SLTH cohort than in the NSLTH cohort on day 5 postoperatively. Results confirmed that SLTH is a simple, safe, effective, and highly reproducible technique for the treatment of LRPH. SLTH may help to perform LRPH by increasing the level of laparoscopic exposure of the right liver and reducing bleeding and operating time.

Clinical data on oral fecal microbiota transplantation (FMT), a promising therapy for Crohn’s disease (CD), are limited. Herein, we determined the short-term safety and feasibility of FMT for pediatric patients with active CD. In this open-label, parallel-group, single-center prospective trial, patients with active CD were treated with oral FMT capsules combined with partial enteral nutrition (PEN) (80

BACKGROUND:The incidence of carbapenem-resistant Klebsiella pneumoniae (CRKP) infection following liver transplantation (LT) has been increasing. The primary objective of this study was to investigate the utility of rectal swab screening for CRKP in this patient population. METHODS:We retrospectively collected rectal swab screening data from 472 liver transplant recipients between June 2018 and December 2023. Subsequently, we analyzed the risk factors associated with CRKP bloodstream infections (BSIs) and assessed the incidence of CRKP BSIs following an intervention involving a combination therapy of tigecycline and polymyxin. RESULTS:Among the 472 liver transplant recipients, 38 (8.1%) tested positive for CRKP in rectal swab screening. Univariate analysis identified severe hepatitis (P = 0.008), delayed recovery of transplanted liver function (P = 0.006), and the use of anti-human thymocyte immunoglobulin (P = 0.020) as significant risk factors for CRKP BSIs. The incidence of bloodstream infection was significantly lower in recipients who received the intervention treatment compared to those who did not (P = 0.021). CONCLUSIONS:Rectal swab screening in liver transplant recipients provides early warning for the development of CRKP BSIs. Early intervention in high-risk patients with positive rectal swab results may effectively reduce the incidence of CRKP BSIs.

BACKGROUND:The Notch signaling pathway plays a crucial role in intrahepatic bile duct development. Here, we aimed to investigate the effect of the Notch receptor, NOTCH2, on intrahepatic bile duct development to better understand congenital intrahepatic bile duct dysplasia. RESULTS:Estradiol increased NOTCH2 and its downstream proteins expression, which promoted the differentiation of hepatoblasts into intrahepatic cholangiocytes and the development of intrahepatic bile ducts by upregulating the Notch signaling pathway. NOTCH2 siRNA inhibited the above processes (P < 0.05). There was no significant difference between estradiol and estradiol + non-targeting siRNA groups (P > 0.1). CONCLUSIONS:In conclusion, the activation of the Notch signaling pathway leads to increased NOTCH2 expression, which promotes the differentiation of hepatoblasts into intrahepatic cholangiocytes and the development of intrahepatic bile ducts during embryonic stages in C57BL/6CrSlc mice. The results of this study may provide a theoretical basis for infantile intrahepatic cholestasis treatment.

Background and Aims Tumor recurrence significantly affects the prognostic outcomes for liver cancer patients following liver transplantation. However, existing predictive models often neglect the inclusion of body composition indicators. Hence, this research aimed to investigate the significance of the psoas muscle index (PMI) in evaluating the post-transplant prognosis of liver cancer. Methods A retrospective analysis was conducted on liver cancer patients who underwent liver transplantation surgery. Imaging analysis was performed using CT data to calculate PMI based on the left and right psoas muscle areas. Subsequently, the patients were categorized into PMI-Low and PMI-High groups using the established cut-off values. Univariate and multivariate analyses were performed using Cox proportional hazards regression to assess the correlation between PMI and clinical outcomes, and a nomogram was constructed accordingly. Results Among the 225 patients included in the analysis, the PMI-High group exhibited significantly improved overall survival (P<0.001) and disease-free survival (DFS, P<0.001) rates compared to the PMI-Low group. PMI exhibited a positive correlation with body mass index (R=0.25, P<0.001), but no significant correlations were observed. In the multivariate analysis, PMI (HR=4.596, P<0.001), MELD score (HR=1.591, P=0.038), and Hangzhou criteria (HR=2.557, P<0.001) emerged as significant predictors of DFS. The constructed nomogram, incorporating these predictors, demonstrated outstanding predictive performance. Decision curve analysis revealed the superiority of the nomogram over conventional methods. Conclusions PMI serves as a valuable prognostic factor for tumor recurrence in liver cancer patients after liver transplantation. The established nomogram is pivotal in delivering personalized predictions of DFS.