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Hepatocellular carcinoma (HCC) is the most common primary liver cancer and the incidence and mortality rates are increasing. Given the limited treatments of HCC and promising application of immunotherapy for cancer, we aimed to identify an immune-related prognostic signature that can predict overall survival (OS) rates and immunotherapy response in HCC.The initial signature development was conducted using a training dataset from the Cancer Genome Atlas followed by independent internal and external validations from that resource and the Gene Expression Omnibus. A signature based nomogram was generated using multivariate Cox regression analysis. The associations of signature score with tumor immune phenotype and response to immunotherapy were analyzed using single-sample gene set enrichment analysis and tumor immune dysfunction and exclusion algorithm. A cohort from Zhongshan Hospital was employed to verify the predictive robustness of the signature regarding prognostic risk and immunotherapy response.The prognostic signature, IGSIGS

Krüppel-like factor 4 (KLF4), a zinc-finger transcription factor in klfs family, is known for its crucial role in regulating cell growth, proliferation, and differentiation. This research aimed to explore the prognostic significance of KLF4 in hepatocellular carcinoma's (HCC) patients after curative resection and the role of KLF4 in HCC progression. There were 185 HCC patients who had hepatectomy from July 2010 to July 2011 included in this study. KLF4 expression was detected by microarray immunohistochemical technique, western blot, and qRT-PCR. Then, the correlation between the prognosis of patients and KLF4 expression was evaluated based on patients' follow-up data. The research found KLF4 expression was significantly downregulated in HCC tissues compared to para-tumorous tissues. More importantly, the overall survival rate (OS) and recurrence-free survival rate (RFS) of HCC patients with low KLF4 expression were both significantly decreased compared to those with a high level of KLF4. Further function and mechanism analysis showed that KLF4 could inhibit the proliferation, migration, invasion and epithelial-mesenchymal transition of HCC cells. The study revealed that KLF4 was not only a tumor suppressor in HCC but also can be regarded as a valuable prognostic factor and potential biological target for diagnosis and treatment in HCC patients.

The growing role of precision medicine in hepatocellular carcinoma (HCC) is expected to ameliorate the poor prognosis and high mortality of this highly malignant disease; however, it is faced with challenges such as the low frequency of tissue biopsy. Hence, attention is turning to the circulating tumor DNA (ctDNA), an important component of liquid biopsy. Obtaining molecular information about cancer from blood provides a good prospect in precision oncology including molecular diagnosis, molecular classification, targeted therapy, personalized decision making, and detection of drug-resistance mutations. However, inherent constraints of HCC and ctDNA (like background chronic liver diseases (CLD) and low concentration of ctDNA) along with some technical issues should be well handled and solved before the potential of ctDNA in precision medicine of HCC can be truly realized. In this review, we will focus on the prospects and challenges of ctDNA in HCC precision medicine.

Hepatocellular carcinoma (HCC) remains one of the most refractory malignancies worldwide. Schlafen family member 11 (SLFN11) has been reported to play an important role in inhibiting the production of human immunodeficiency virus 1 (HIV-1). However, whether SLFN11 also inhibits hepatitis B virus (HBV), and affects HBV-induced HCC remain to be systematically investigated. Methods: qRT-PCR, western blot and immunohistochemical (IHC) staining were conducted to investigate the potential role and prognostic value of SLFN11 in HCC. Then SLFN11 was stably overexpressed or knocked down in HCC cell lines. To further explore the potential biological function of SLFN11 in HCC, cell counting kit-8 (CCK-8) assays, colony formation assays, wound healing assays and transwell cell migration and invasion assays were performed in vitro. Meanwhile, HCC subcutaneous xenograft tumor models were established for in vivo assays. Subsequently, immunoprecipitation (IP) and liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) analyses were applied to understand the molecular mechanisms of SLFN11 in HCC. Co-IP, immunofluorescence and IHC staining were used to analyze the relationship between ribosomal protein S4 X-linked (RPS4X) and SLFN11. Finally, the therapeutic potential of SLFN11 with mTOR pathway inhibitor INK128 on inhibiting HCC growth and metastasis was evaluated in vitro and in vivo orthotopic xenograft mouse models. Results: We demonstrate that SLFN11 expression is decreased in HCC, which is associated with shorter overall survival and higher recurrence rates in patients. In addition, we show that low SLFN11 expression is associated with aggressive clinicopathologic characteristics. Moreover, overexpression of SLFN11 inhibits HCC cell proliferation, migration, and invasion, facilitates apoptosis in vitro, and impedes HCC growth and metastasis in vivo, all of which are attenuated by SLFN11 knockdown. Mechanistically, SLFN11 physically associates with RPS4X and blocks the mTOR signaling pathway. In orthotopic mouse models, overexpression of SLFN11 or inhibition of mTOR pathway inhibitor by INK128 reverses HCC progression and metastasis. Conclusions: SLFN11 may serve as a powerful prognostic biomarker and putative tumor suppressor by suppressing the mTOR signaling pathway via RPS4X in HCC. Our study may therefore offer a novel therapeutic strategy for treating HCC patients with the mTOR pathway inhibitor INK128.

Manar Atyah,1,* Chenhao Zhou,1,* Qiang Zhou,1 Wanyong Chen,1 Jialei Weng,1 Pengcheng Wang,1 Yi Shi,2 Qiongzhu Dong,3,4 Ning Ren1,3 1Department of Liver Surgery, Liver Cancer Institute, Zhongshan Hospital, and Key Laboratory of Carcinogenesis and Cancer Invasion (Ministry of Education), Fudan University, Shanghai, 200032, People’s Republic of China; 2Biomedical Research Centre, Zhongshan Hospital, Fudan University, Shanghai, 200032, People’s Republic of China; 3Institute of Fudan Minhang Academic Health System, and Key Laboratory of Whole-period Monitoring and Precise Intervention of Digestive Cancer (SMHC), Minhang Hospital & AHS, Fudan University, Shanghai, 201199, People’s Republic of China; 4Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, People’s Republic of China*These authors contributed equally to this workCorrespondence: Ning Ren,Department of Liver Surgery, Liver Cancer Institute, Zhongshan Hospital, and Key Laboratory of Carcinogenesis and Cancer Invasion (Ministry of Education), Fudan University, Shanghai, 200032, People’s Republic of China, Tel +86-21-64041990, Email ren.ning@zs-hospital.sh.cn;Qiongzhu Dong,Institute of Fudan Minhang Academic Health System, and Key Laboratory of Whole-period Monitoring and Precise Intervention of Digestive Cancer (SMHC), Minhang Hospital & AHS, Fudan University, Shanghai, 201199, People’s Republic of China, Tel +86-21- 64923400, Email qzhdong@fudan.edu.cnBackground: Nuclear factor (erythroid-derived 2)-like 2 (NRF2) functions decline with age; however, cancer cells can hijack its pathways to ensure survival and aggressiveness. Yet, the role of NRF2 in hepatocellular carcinoma (HCC) is rarely investigated in an age-specific manner. This study investigates the expression of NRF2 and its activator (MAPK10) in different age groups of HCC patients, in addition to the age-specific features of NRF2 and MAPK10 interaction and their clinical significance.Methods: Tumor and near-tumor tissue samples of 181 HCC patients were used to complete a protein expression analysis of NRF2 and MAPK10. Patients’ survival and clinical data were collected for clinical analysis. Global databases (TCGA, ICGC) were used to collect MAPK10 genetic mutation and mRNA expression data in patients with HCC, colorectal, stomach, and pancreatic cancers.Results: Our findings revealed an increase in NRF2 protein expression but only in younger HCC patients, along with a decline in MAPK10 ability to activate NRF2 in older patients. We also found an increased MAPK10 genetic mutation rate and decreased mRNA expression in older patients. Low MAPK10 and NRF2 expression levels were associated with shorter survival and poorer prognosis due to positive correlation with microvascular invasion, tumor thrombus, elevated AFP levels, and larger tumor size.Conclusion: NRF2 expression and oxidative stress mechanism in HCC patients are influenced by age. This magnifies the need to consider patients’ age in treatment strategies and guidelines and re-evaluates the application of studies’ age-standardized findings in older patients who are usually excluded from relevant research.Keywords: NRF2, MAPK10, hepatocellular carcinoma, oxidative stress, aging

Jialei Weng,1,* Chenhao Zhou,1,2,* Qiang Zhou,1 Wanyong Chen,1,3 Yirui Yin,1 Manar Atyah,1 Qiongzhu Dong,2– 4 Yi Shi,5 Ning Ren1,3 1Department of Liver Surgery, Liver Cancer Institute, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion (Ministry of Education), Fudan University, Shanghai, People’s Republic of China; 2Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; 3Institute of Fudan Minhang Academic Health System, Minhang Hospital, Key Laboratory of Shanghai Municipal Health Commission, Fudan University, Shanghai, People’s Republic of China; 4Institutes of Biomedical Sciences, Fudan University, Shanghai, People’s Republic of China; 5Biomedical Research Centre, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China*These authors contributed equally to this workCorrespondence: Ning RenDepartment of Liver Surgery, Liver Cancer Institute, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion (Ministry of Education), Fudan University, 180 Fenglin Road, Shanghai, 200032, People’s Republic of ChinaTel +86-21-64041990Email ren.ning@zs-hospital.sh.cnYi ShiBiomedical Research Centre, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People’s Republic of ChinaTel +86-21-64041990Email shi.yi@zs-hospital.sh.cnBackground: Hepatocellular carcinoma (HCC) is a malignant tumor with great variation in prognosis among individuals. Changes in metabolism influence disease progression and clinical outcomes. The objective of this study was to determine the overall survival (OS) risk of HCC patients from a metabolic perspective.Patients and Methods: The model was constructed using the least absolute shrinkage and selection operator (LASSO) COX regression based on The Cancer Genome Atlas (TCGA, n=342) dataset. The International Cancer Genome Consortium (ICGC, n=232), GSE14520 (n=242) datasets, and a clinical cohort (n=64) were then used to assess the prognostic value of the signature.Results: A 10 metabolic gene-based signature was constructed and verified as a robust and independent prognostic classifier in public and real-world validation cohorts. Meanwhile, the signature enabled the identification of HCC molecular subtypes, yielding an AUC value of 0.678 [95% CI: 0.592– 0.763]. Besides, the signature was associated with metabolic processes like glycolysis, supported by a clear correlation between the risk score and expression of rate-limiting enzymes. Furthermore, high-risk tumor was likely to have a high tumor infiltration status of immunosuppressive cells, as well as elevated expression of some immune checkpoint molecules. For final clinical translation, a nomogram integrating the signature and tumor stage was established, and showed improved predictive accuracy of 3- and 5-year OS and brought more net benefit to patients.Conclusion: We developed a prognostic signature based on 10 metabolic genes, which has proven to be an independent and reliable prognostic predictor for HCC and reflects the metabolic and immune characteristics of tumors.Keywords: hepatocellular carcinoma, metabolism-related gene, signature, prognosis

Despite the use of immune checkpoint blockade (ICB) therapy for hepatocellular carcinoma (HCC), developing more effective immunotherapy and predicting HCC’s response to ICB therapy remain top priorities. Ribosomal protein S3A (RPS3A) is a multifunctional molecule, but its association with tumor immune cell infiltration and prognosis in HCC patients is unknown. Thus, we aimed to investigate the correlation of RPS3A with HCC immune cell infiltration and prognosis to explore novel therapeutic strategies and prognostic biomarkers for this disease. Here, we showed that RPS3A expression levels were higher in HCC cell lines and samples than in normal hepatocytes and adjacent tumor-free tissues, respectively, and patients with high RPS3A expression had worse overall and recurrence-free survival durations than did patients with low expression. Moreover, single-sample gene set enrichment analysis (ssGSEA) and immunohistochemistry demonstrated a strongly negative correlation between RPS3A expression and tumor immune cell infiltration. Meanwhile, RPS3A was revealed to be positively correlated with that of most examined immune checkpoint molecules. GSEA also suggested that high RPS3A expression promoted the biological processes related to tumorigenesis, metastasis, and immunosuppression. Finally, RPS3A-based nomograms were constructed and exhibited better predictive accuracy for HCC prognosis and more net clinical benefits when compared with traditional prognosis-prediction staging systems. In short, these findings suggest that high RPS3A expression correlates with low tumor immune cell infiltration and poor prognosis in HCC patients. Furthermore, RPS3A-based nomograms are robust HCC prognostic predictors. RPS3A therefore may serve as a therapeutic target in and predict the efficacy of ICB therapy for HCC.

Glutamate-cysteine ligase catalytic subunit (GCLC) has been reported to overexpress in a variety types of cancer and be related with tumor progression and drug resistance. However, little has been known about GCLC's prognostic significance and biological roles in hepatocellular carcinoma (HCC). In the present study, we evaluated GCLC expression level using immunohistochemical staining (IHC) in tissue microarray (TMA) containing paired tumor and peritumoral liver tissues from 168 patients with HCC who received curative resection. GCLC levels in tumor tissues were significantly higher than in peritumoral liver tissues, and tumor GCLC level was associated with overall survival (OS) and disease-free survival (DFS). Five-year OS and DFS rates were 41.15% and 25.88% for the group with high tumor GCLC level, compared with 68.09% and 47.51% for the group with low tumor GCLC level (P

Pancreatic ductal adenocarcinoma (PDAC) is one of the most fatal malignancies worldwide. PDAC prognostic and diagnostic biomarkers are still being explored. The aim of this study is to establish a robust molecular signature that can improve the ability to predict PDAC prognosis. 155 overlapping differentially expressed genes between tumor and non-tumor tissues from three Gene Expression Omnibus (GEO) datasets were explored. A least absolute shrinkage and selection operator method (LASSO) Cox regression model was employed for selecting prognostic genes. We developed a 6-mRNA signature that can distinguish high PDAC risk patients from low risk patients with significant differences in overall survival (OS). We further validated this signature prognostic value in three independent cohorts (GEO batch, P < 0.0001; ICGC, P = 0.0036; Fudan, P = 0.029). Furthermore, we found that our signature remained significant in patients with different histologic grade, TNM stage, locations of tumor entity, age and gender. Multivariate cox regression analysis showed that 6-mRNA signature can be an independent prognostic marker in each of the cohorts. Receiver operating characteristic curve (ROC) analysis also showed that our signature possessed a better predictive role of PDAC prognosis. Moreover, the gene set enrichment analysis (GSEA) analysis showed that several tumorigenesis and metastasis related pathways were indeed associated with higher scores of risk. In conclusion, identifying the 6-mRNA signature could provide a valuable classification method to evaluate clinical prognosis and facilitate personalized treatment for PDAC patients. New therapeutic targets may be developed upon the functional analysis of the classifier genes and their related pathways.

Despite the rapid growing and aging of populations worldwide, our knowledge on hepatocellular carcinoma (HCC) is still age-standardized rather than age-specific, with only few studies exploring the topic from a genetic point of view. Here, we analyze clinical and genetic aspects of HCC in patients of different age groups with the major attention directed to children (≤20 y) and elderly groups (≥80 y). A number of significant differences were found in elderly patients compared to children group, including smaller tumor size (P=0.001) and improved survival rates (P=0.002). Differences in gene mutations, copy number variants, and mRNA expressions were identified between the groups, with alteration rates for some genes like AKR1B10 increasing significantly with the age of patients. Immunohistochemistry testing of AKR1B10 showed a significant difference in expression levels at the age of 40 (30.77% high expression rate in patients younger than 40 compared to 51.57% in older patients) (P=0.043). Expression levels also differed between HCC tissues (49.64%) and near-tumor tissues (6.58%) (P

Introduction: The WW domain-containing oxidoreductase (WWOX), widely expressed in human tissues, is considered as a tumor suppressor gene and plays an important role in the incidence and progression of human cancer, HCC included. This study was to investigate the correlation between single nucleotide polymorphisms (SNPs) of the WWOX gene and the prognosis of hepatocellular carcinoma (HCC) patients. Materials and Methods: After a total of 152 HCC patients were recruited, 8 cases with tumor recurrence within 2-years after operation and 8 cases without recurrence were selected randomly for SNP genotyping and screening using Affymetrix Array 6.0. And then we confirmed candidate SNPs in the remaining 136 patients by time-of-flight mass spectrometry (TOF-MS). Results: In total, 32 SNPs were screened and identified as candidate SNPs with one SNP in particular, (rs9926344), being further verified to be valuable. We found that AA+AG genotype and A allele of WWOX rs9926344 were significantly associated with recurrent risk of HCC (p=0.002 and p=0.001, respectively). The Kaplan-Meier curve showed that patients carrying rs9926344 AA +AG genotype had poor RFS (P=0.004) and OS (P=0.005) compared to those carrying GG genotypes. The multivariate COX regression analysis showed that the AA+AG genotype were an independent prognostic factor for tumor recurrence (HR 1.787, 95% CI 1.042-3.064, P=0.035). Furthermore, IHC analysis showed that the WWOX protein down-regulation is more frequent in patients with AG genotype compared to those with GG genotype (P=0.023). Conclusion: Our findings indicate that WWOX rs9926344 polymorphism is positively correlated with tumor recurrence and can be used as an independent prognostic marker for HCC patients after operation.

To improve minimally invasive outcomes, we designed a new procedure, lower abdominal laparoscopic cholecystectomy (LALC). This study was conducted to evaluate the effects of LALC versus classical (CLC) and single-incision (SILC) laparoscopic cholecystectomy on reducing systemic acute inflammatory response, improving cosmesis, and postoperative pain relief.Beginning from July 2014, 105 patients meeting the inclusion criteria were randomly assigned to three groups: LALC, CLC, and SILC. The primary endpoint was the determination of systemic inflammatory response to the surgery. Other outcome measures included cosmesis, postoperative pain, and perioperative indices.Each of the three groups consisted of 35 patients. The duration of the operation was significantly longer in the SILC group (p= .005). The rates of adverse events were similar. Changes in interleukin-6 (p = .001) and tumor-necrosis factor-α (p = .016) measured before and after surgery differed significantly; patients who underwent LALC had the smallest change in inflammatory response. Cosmesis scores at one (p = .002) and 12 (p = .004) weeks after surgery favored LALC and SILC. Significant differences in pain scores at four (p = .011) and 12 h (p = .024) postoperatively were also observed.In selected patients, LALC shows more advantages in terms of lower systemic inflammatory response, improved cosmesis, and a favorable postoperative pain profile when compared with CLC and SILC.

Background: Microvascular invasion (MVI) is a significant hazard factor which influences the recurrence and survival of hepatocellular carcinoma (HCC) patients after hepatectomy. We aimed to develop and validate a nomogram that combines hematological and imaging features of hepatocellular carcinoma patients for preoperative prediction of microvascular invasion. Methods: The study included a total of 709 HCC patients who underwent liver resection at the Liver Cancer Institute of Zhongshan Hospital, Fudan University (FDZS) between June 1,2015 and December 30,2016 (496 as training validation cohort and 213 as validation cohort). Blood biochemistry parameters and radiological features of dynamic contrast‑enhanced MRI were extracted. Lasso regression model and multivariable logistic regression were used for data dimension reduction, variable selection and development of the predicting model. The model was presented as a nomogram and its performance was assessed in terms of discrimination, calibration and clinical usefulness. Results: In the training cohort, 218 of 496 patients (43.9%) had histopathologically identified MVI compared to 88 of 213 patients (41.3%) in the validation cohort. Independent prognostic factors including alkaline phosphatase (ALP, >125 U/L), alpha-fetoprotein (AFP, within 20 - 400 or >400 ng/mL), protein induced by vitamin K absence-II (PVIKA-II, within 40 – 400 or >400 mAU/mL), tumor number, diameter, pseudo-capsule, tumor growth pattern and intratumor hemorrhage were incorporated in our nomogram. The model showed good discrimination and calibration , with a concordance indexes (C-index,0.82[ 95% CI: 0.7822-0.857]) in the training cohort and C-index (0.80, [95% CI: 0.772-0.837]) in the validation cohort. Decision curve analysis (DCA) also showed that this model was clinically useful. Interpretation: This study presents an optimal model that addresses and combines hematological and radiological features. By predicting the incidence of MVI preoperatively , this model could help surgeons choose the best treatment options for HCC patients before and after the operation. Funding Statement: This work was funded by grants from the Shanghai International Science and Technology Collaboration Program (18410721900), the National Natural Science Foundation of China (81472672), and Shanghai Municipal Key Clinical Specialty Declaration of Interests: All authors declare no potential conflicts of interest. Ethics Approval Statement: The study was approved by Ethics Committee of Zhongshan Hospital, Fudan University. Informed consent of clinical data used in this study was obtained from all patients without financial compensation.

Background Ribosomal protein S11 (RPS11), a member of ribosomal protein family, is reported to overexpress in diverse malignancies and correlates with tumor recurrence. However, our current knowledge on RPS11 in hepatocellular carcinoma (HCC) remains limited. In this study, we are going to explore the potential prognostic value of RPS11 in HCC patients after curative resection. Methods Immunohistochemistry (IHC) was performed to evaluate RPS11 expression on tissue microarrays in training cohort comprising 182 HCC patients and validation cohort enrolling 90 HCC patients in Zhongshan Hospital, Fudan University. Western blot and quantitative reverse transcription PCR (qRT-PCR) were also used to determine the expression level of RPS11 in liver cell lines. Two nomograms, calibration curves and decision curve analysis (DCA) were further performed to assess the performance of RPS11 level in predicting clinical outcomes of HCC patients. Additionally, single-sample gene-set enrichment analysis (ssGSEA) was conducted in TCGA liver cancer database to investigate the potential biological pathways involved in RPS11. Results Both increased mRNA and protein levels of RPS11 were observed in most HCC cell lines when compared to the normal hepatocytes, and high tumor RPS11 level was associated with shorter overall survival (OS) and recurrence-free survival (RFS) of HCC patients after curative resection. Univariate and multivariate analysis indicated that RPS11 was an independent prognostic factor in HCC. Two nomograms, calibration and DCA curves were further established and displayed a superior prognostic accuracy of OS and RFS, and showed more clinical benefits than traditional staging systems in HCC. Furthermore, several pathways and molecules related to tumor resistance, survival and recurrence were enriched in high RPS11 expression by ssGSEA. Conclusions Tumorous RPS11 acts as a potential prognostic biomarker for HCC patients who received curative resection.

Hepatocellular carcinoma (HCC) is one of the top three cancer killers worldwide. To identify CNV-driven differentially expressed genes (DEGs) in HBV related HCC, this study integrated analysis of copy number variations (CNVs) and gene expression profiling. Significant genes in regions of CNVs were overlapped with those obtained from the expression profiling. 93 CNV-driven genes exhibiting increased expression in the duplicated regions and 45 showing decreased expression in the deleted regions were obtained, which duplications and deletions were mainly documented at chromosome 1 and 4. Functional and pathway enrichment analyses were performed using DAVID and KOBAS, respectively. They were mainly enriched in metabolic process and cell cycle. Protein-protein interaction (PPI) network was constructed by Cytoscape, then four hub genes were identified. Following, survival analyses indicated that only high NPM1 expression was significantly and independently associated with worse survival and increased recurrence in HCC patients. Moreover, this correlation remained significant in patients with early stage of HCC. In addition, we showed that NPM1 was overexpressed in HCC cells and in HCC versus adjacent non-tumor tissues. In conclusion, these results showed that integrated analysis of genomic and expression profiling might provide a powerful potential for identifying CNV-driven genes in HBV related HCC pathogenesis.

Background Tumor invasion or adherence to the portal vein–superior mesenteric vein (PV/SMV) may be encountered during pancreatic surgery. In such cases, venous resection and reconstruction might be required for complete resection of the tumor. We report an innovative technique in which the graft for PV/SMV reconstruction was made with the falciform ligament. Methods Between May 2011 and July 2016, PV/SMV reconstruction with a falciform ligament graft was performed in 10 cases during pancreatectomy. Among these cases, including six cases with a patch graft and four cases with a conduit graft. Retrospective reviews of medical records and radiologic studies were performed. Results Ten patients with pancreatobiliary cancer underwent en bloc tumor resection with concurrent PV/SMV resection and reconstruction with a falciform ligament graft. There were six males and four females, and the mean age was 65.3 ± 9.4 (48-80) y. Using Doppler ultrasound examination, all 10 grafts were shown to be patent at postoperative 2 wk. However, occlusion was found in one case with conduit graft and stenosis in the other three cases with conduit graft using enhanced computed tomography at postoperative 2 mo. Complete patency was shown in three of six cases with patch graft and stenosis in the other three cases at 2 mo after the operation. Although occlusion or stenosis of the grafts was observed, no severe adverse events occurred, and normal liver function was discovered in all 10 cases at postoperative 2 mo. Conclusions Falciform ligament grafts might be considered for reconstruction of PV/SMV in the absence of appropriate vascular grafts.