Prognosis analysis of patients with pancreatic neuroendocrine tumors after surgical resection and the application of enucleation.

OBJECTIVE: To investigate the prognostic factors of patients with pancreatic neuroendocrine tumor (pNETs) after surgical resection, and to analyze the value of enucleation for pNETs without distant metastasis that are well-differentiated (G1) and have a diameter ≤ 4 cm. METHODS: Data from pNET patients undergoing surgical resection between 2004 and 2017 were collected from the Surveillance, Epidemiology, and End Results (SEER) database. Kaplan-Meier analysis and log-rank testing were used for the survival comparisons. Adjusted HRs with 95% CIs were calculated using univariate and multivariate Cox regression models to estimate the prognostic factors. P < 0.05 was regarded as statistically significant. RESULTS: This study found that female, cases diagnosed after 2010, and pancreatic body/tail tumors were protective factors for good survival, while histological grade G3, a larger tumor size, distant metastasis, AJCC 8th stage III-IV and age over 60 were independent prognostic factors for a worse OS/CSS. For the pNETs that were well-differentiated (G1) and had a tumor diameter ≤ 4 cm, the type of surgery was an independent factor for the long-term prognosis of this group. Compared with pancreaticoduodenectomy and total pancreatectomy, patients who were accepted enucleation had better OS/CSS. CONCLUSION: For pNETs patients undergoing surgical resection, sex, year of diagnosis, tumor location, pathological grade, tumor size, distant metastasis, race, and age were independent prognostic factors associated with the OS/CSS of patients. For pNETs patients with G1 and a tumor diameter less than 4 cm, if the tumor was located over 3 mm from the pancreatic duct, enucleation may be a wise choice.

Statin use and risk of gallstone disease: A meta-analysis.

AIM: There is emerging evidence from animal and human studies that current statins can decrease the formation of gallbladder cholesterol gallstones and subsequently decrease the risk of gallstone disease, but consistent results have not been reported. We performed a meta-analysis to provide an overview of the relevant studies. METHODS: Relevant studies published between January 1980 and February 2014 were identified by searching Medline, Embase and the Cochrane Library. Studies were selected using a priori defined criteria. The strength of the relationship between statin use and risk of gallstone disease was assessed by adjusted odds ratio (OR). RESULTS: A total of 622 868 participants from six studies (four case-control studies, one cohort study and one cross-sectional study) were identified in this meta-analysis. The studies provided adjusted overall OR estimates for current statin use versus non-use, leading to a pooled OR of 0.86 (95% confidence interval [CI], 0.77-0.97; P < 0.001). The overall OR of population-based case-control studies and cholecystectomy due to gallstone disease were 0.83 (95% CI, 0.73-0.95; P = 0.0131) and 0.78 (95% CI, 0.74-0.82; P = 0.615), respectively. CONCLUSION: There is evidence that current statin use lowers the risk of gallstone disease compared with non-use, especially for cholecystectomy due to gallstone disease. Low statin use (1-4 prescriptions) did not decrease the risk of gallstone disease, but moderate and high statin use significantly decreased the risk. Further multicenter and better controlled studies are needed to confirm these findings.

TPX2 is a prognostic marker and contributes to growth and metastasis of human hepatocellular carcinoma.

Targeting protein for Xenopus kinesin-like protein 2 (TPX2), a microtubule-associated protein, impacts spindle assembly in human cells. Several studies have demonstrated that TPX2 is overexpressed in different types of human cancers and promotes tumor growth and metastasis. In this study, we found that the expression level of TPX2 was obviously higher in hepatocellular carcinoma (HCC) tissues than in matched nontumor tissues. Elevated expressions of TPX2 mRNA were observed in all HCC cell lines (HepG2, Hep3B, SMMC-7721, Bel-7402 and Huh7) as compared with that in a non-transformed hepatic cell line (LO2). Clinical analysis indicated that the positive expression of TPX2 was significantly correlated with venous infiltration, high Edmondson-Steiner grading and advanced TNM tumor stage in HCC. Furthermore, TPX2 was a novel prognostic marker for predicting 5-year overall survival (OS) and disease-free survival (DFS) of HCC patients. In vitro studies found that TPX2 knockdown significantly inhibited cell proliferation and viability in both Hep3B and HepG2 cells. Moreover, TPX2 knockdown obviously slowed down tumor growth in a nude mouse xenograft model. Otherwise, TPX2 knockdown prominently suppressed HCC cell invasion and migration. In conclusion, these results indicate that TPX2 may serve as a prognostic marker and promotes tumorigenesis and metastasis of HCC.

Lamin B1 is a potential therapeutic target and prognostic biomarker for hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is an aggressive malignancy. Previous studies have found that lamin B1 (LMNB1) contributes to the development of human cancers. However, the biological functions and prognostic values of LMNB1 in HCC have not been adequately elucidated. In our present research, the expression pattern of LMNB1 was analyzed. The prognostic values of LMNB1 were evaluated by Kaplan-Meier survival analysis and Cox proportional hazards regression analysis. The effects of LMNB1 on HCC progression were assessed by Cell Counting Kit-8 (CCK-8), colony formation, wound healing, Transwell and in vivo xenograft assays. The mechanisms of LMNB1 in HCC progression were elucidated by gene set enrichment analysis (GSEA) and loss-of-function assays. Besides, a nomogram for predicting overall survival (OS) was constructed. The results demonstrated that LMNB1 was overexpressed in HCC and that increased LMNB1 expression predicted a dismal prognosis. Further experiments showed that LMNB1 facilitated cell proliferation and metastasis in HCC. Functional enrichment analysis revealed that LMNB1 modulated metastasis-associated biological functions such as focal adhesion, extracellular matrix, cell junctions and cell adhesion. Mechanistically, we revealed that LMNB1 promoted HCC progression by regulating the phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways. Moreover, incorporating LMNB1, Ki67 and Barcelona Clinic Liver Cancer (BCLC) stage into a nomogram showed better predictive accuracy than the Tumor-Node-Metastasis (TNM) stage and BCLC stage. In conclusion, LMNB1 may serve as an effective therapeutic target as well as a reliable prognostic biomarker for HCC.

A Lamin Family-Based Signature Predicts Prognosis and Immunotherapy Response in Hepatocellular Carcinoma.

Background: Lamin family members play crucial roles in promoting oncogenesis and cancer development. The values of lamin family in predicting prognosis and immunotherapy response remain largely unclarified. Our research is aimed at comprehensively estimating the clinical significance of lamin family in hepatocellular carcinoma and constructing a novel lamin family-based signature to predict prognosis and guide the precise immunotherapy. Methods: The expression features and prognostic value of LMNA, LMNB1, and LMNB2 were explored in the TCGA and GEO databases. The biological functions of LMNB1 and LMNB2 were validated by in vitro assays. A lamin family-based signature was built using the TCGA training set. The TCGA test set, entire TCGA set, and GSE14520 set were used to validate its predictive power. Univariate and multivariate analyses were performed to evaluate the independence of the lamin family-based signature from other clinicopathological characteristics. A nomogram was constructed using the lamin family-based signature and TNM stage. The associations of this signature with molecular pathways, clinical characteristics, immune cell infiltration, and immunotherapy response were analyzed. Results: Lamin family members were upregulated in HCC. Upregulation of LMNB1 and LMNB2 promoted HCC proliferation, migration, and invasion. The predictive signature was initially established based on LMNB1 and LMNB2 which could effectively identify differences in overall survival, immune cell infiltration, and clinicopathological characteristics of high- and low-risk patients. The nomogram showed high prognostic predictive accuracy. Importantly, the lamin family-based signature was correlated with immune suppression and expression of immune checkpoint molecules. Conclusions: The lamin family-based signature is a robust biomarker to predict overall survival and immunotherapy response in HCC. High-risk score patients have a poorer overall survival and might be more sensitive to immunotherapy. This signature may contribute to improving individualized prognosis prediction and precision immunotherapy for HCC patients.

Roles and Clinical Significances of ATF6, EMC6, and APAF1 in Prognosis of Pancreatic Cancer.

Background: Pancreatic cancer (PC) is prevalent among malignant tumors with poor prognosis and lacks efficient therapeutic strategies. Endoplasmic reticulum (ER) stress and apoptosis are associated with chronic inflammation and cancer progression. However, the prognostic value of ER stress-related, and apoptosis-related genes in PC remains to be further elucidated. Our study aimed at confirming the prognostic values of the ER stress-related genes, ATF6, EMC6, XBP1, and CHOP, and the apoptosis-related gene, APAF1, in PC patients. Methods: Gene Expression Profiling Interactive Analysis 2 (GEPIA2) was used to evaluate prognosis value of ATF6, EMC6, XBP1, CHOP, and APAF1 in PC. Clinical data from 69 PC patients were retrospectively analyzed. Immunohistochemistry, Western blotting, and qRT-PCR were used for the assessment of gene or protein expression. The cell counting kit-8 (CCK-8) and the Transwell invasion assays were, respectively, used for the assessment of the proliferative and invasive abilities of PC cells. The prognostic values of ATF6, XBP1, CHOP, EMC6, and APAF1 in PC patients were evaluated using Kaplan-Meier and Cox regression analyses. Results: XBP1 and CHOP expressions were not associated with PC recurrence-free survival (RFS), overall survival (OS) and disease-specific survival (DSS). ATF6 upregulation and EMC6 and APAF1 downregulations significantly correlated with the poor RFS, OS, and DSS of PC patients. ATF6 promoted PC cell proliferation and invasion, while EMC6 and APAF1 inhibited these events. Conclusion: ATF6 upregulation and EMC6 and APAF1 downregulations may be valid indicators of poor prognosis of PC patients. Moreover, ATF6, EMC6, and APAF1 may constitute potential therapeutic targets in PC patients.

Parecoxib Improves the Outcomes of Acute Mild and Moderate Pancreatitis: A 3-Year Matched Cohort Study Based on a Prospective Database.

OBJECTIVES: The aim of this study was to evaluate the role of parecoxib in patients with different severities of acute pancreatitis (AP). METHODS: A total of 772 eligible patients with AP were divided into 4 groups: mild and moderately AP (MAP) treated with parecoxib (group A, n = 236), MAP without parecoxib treatment (group B, n = 453), severe AP (SAP) treated with parecoxib (group C, n = 28), and SAP without parecoxib treatment (group D, n = 55). Patients in group A were exactly matched with patients in group B by propensity score matching, similar to the matching between group C and group D. RESULTS: The morbidity of abdominal infection in group A was significantly lower as compared with that in group B (P < 0.050). The progression of MAP to SAP significantly decreased in group A than group B (P < 0.050). No significant differences were observed between group C and group D. The risk factors independently related to the progression of MAP included alcoholic/high-fat dietary (P = 0.028) and parecoxib administration (P = 0.011). CONCLUSIONS: Early administration of parecoxib could reduce the morbidity of complications among patients with MAP. Parecoxib may prevent the progression of MAP to SAP and improve its outcomes.

Role of TGFß3-Smads-Sp1 axis in DcR3-mediated immune escape of hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is a leading cause of tumour-associated mortality worldwide, but no significant improvement in treating HCC has been reported with currently available systemic therapies. Immunotherapy represents a new frontier in tumour therapy. Therefore, the immunobiology of hepatocarcinoma has been under intensive investigation. Decoy receptor 3 (DcR3), a member of the tumour necrosis factor receptor (TNFR) superfamily, is an immune suppressor associated with tumourigenesis and cancer metastasis. However, little is known about the role of DcR3 in the immunobiology of hepatocarcinoma. In this study, we found that overexpression of DcR3 in HCC is mediated by the TGFß3-Smad-Sp1 signalling pathway, which directly targets DcR3 promoter regions. Moreover, overexpression of DcR3 in HCC tissues is associated with tumour invasion and metastasis and significantly promotes the differentiation and secretion of Th2 and Treg cells while inhibiting the differentiation and secretion of Th1 cells. Conversely, knockdown of DcR3 expression in HCC significantly restored the immunity of CD4+ T cells. Inhibition of DcR3 expression may provide a novel immunotherapeutic approach to restoring immunity in HCC patients.

High-affinity human programmed death-1 ligand-1 variant promotes redirected T cells to kill tumor cells.

Tumor cells can escape immune surveillance through the programmed cell death protein 1 (PD-1) axis suppressing T cells. However, we recently demonstrated that high-affinity variants of soluble human programmed death-ligand 1 (shPD-L1) could diminish the suppression. We propose that in comparison to the wild-type shPD-L1, the further affinity enhancement will confer the molecule with opposite characteristics that augment T-cell activation and immunotherapeutic drug potential. In this study, a new shPD-L1 variant, L3C7c, has been generated to demonstrate ∼167 fold greater affinity than wild-type hPD-L1. The L3C7c-Fc fusion protein demonstrated completely opposite effects of conventional PD-1 axis by promoting redirected T-cell proliferation, activation and cytotoxicity in vitro, as being slightly better than that of anti-PD1-Ab (Pembrolizumab). Moreover, L3C7c-Fc was more effective than Pembrolizumab in enhancing redirected T cells' ability to suppress Mel624 melanoma growth in vivo. As a downsized L3C7c-Fc variant, L3C7v-Fc improved the anti-tumor efficacy in vivo when combined with dendritic cell vaccines. In conclusion, our studies demonstrate that high-affinity hPD-L1 variants could be developed as the next generation reagents for tumor immunotherapy based on the blockade of the PD-1 axis.

LncRNA CDKN2B-AS1 promotes tumor growth and metastasis of human hepatocellular carcinoma by targeting let-7c-5p/NAP1L1 axis.

Long non-coding RNAs (lncRNAs) show great potential as therapeutic targets in many diseases including hepatocellular carcinoma (HCC). Here, we aimed to investigate the clinical significance and function of lncRNA CDKN2B antisense RNA 1 (CDKN2B-AS1) in HCC. Here, we identified a novel oncogenic lncRNA CDKN2B-AS1, which was highly expressed in HCC and positively associated with large tumor size, microvascular invasion, high tumor grade, advanced tumor stage and reduced survival of HCC patients. CDKN2B-AS1 knockdown inhibited cell proliferation, migration and invasion, and induced G1 arrest and apoptosis of HCC cells in vitro, and CDKN2B-AS1 silencing suppressed tumor growth and metastasis of HCC in vivo. In accordance, CDKN2B-AS1 overexpression accelerated HCC cell growth and metastasis. Mechanistically, CDKN2B-AS1 promoted nucleosome assembly protein 1 like 1 (NAP1L1) expression by sponging let-7c-5p, thereby activated PI3K/AKT/mTOR signaling in HCC cells. Notably, NAP1L1 restoration abolished the effects of CDKN2B-AS1 silencing on HCC cell growth and metastasis. CDKN2B-AS1, an oncogenic lncRNA of HCC, promoted NAP1L1-mediated PI3K/AKT/mTOR signaling by acting as a molecular sponge of let-7c-5p. Our findings indicate that CDKN2B-AS1 may be a potential prognostic biomarker and a candidate target for HCC therapy.

microRNA-489 Plays an Anti-Metastatic Role in Human Hepatocellular Carcinoma by Targeting Matrix Metalloproteinase-7.

Dysregulation of microRNAs (miRNAs) is actively involved in the pathogenesis and tumorigenicity of hepatocellular carcinoma (HCC). miR-489 was found to play either oncogenic or tumor suppressive roles in human cancers. Recent study reported that the levels of miR-489 in late recurrent HCC patients were evidently higher than that in early recurrent cases, suggesting that miR-489 may function as a tumor suppressive miRNA in HCC. Yet, the clinical value and biological function of miR-489 remain rarely known in HCC. Here, we presented that miR-489 level in HCC tissues was notably reduced compared to matched non-cancerous specimens. Its decreased level was evidently correlated with adverse clinical parameters and poor prognosis of HCC patients. Accordingly, the levels of miR-489 were obviously down-regulated in HCC cells. Ectopic expression of miR-489 in HCCLM3 and MHCC97H cells prominently inhibits the migration and invasion of tumor cells and reduced lung metastases in vivo, while miR-489 knockdown increased these behaviors of HepG2 and MHCC97L cells. Mechanically, miR-489 negatively regulated matrix metalloproteinase-7 (MMP7) abundance in HCC cells. Herein, MMP7 was found to be a downstream molecule of miR-489 in HCC. An inversely correlation between miR-489 and MMP7 was confirmed in HCC specimens. MMP7 knockdown prohibited cell migration and invasion while MMP7 overexpression showed opposite effects on HCC cells. Furthermore, restoration of MMP7 expression could abrogate the anti-metastatic effects of miR-489 on HCCLM3 cells with enhanced cell migration and invasion. Altogether, miR-489 potentially acts as a prognostic predictor and a drug-target for HCC patients.

Zinc finger protein ZBTB20 is an independent prognostic marker and promotes tumor growth of human hepatocellular carcinoma by repressing FoxO1.

Zinc finger and BTB domain-containing 20 (ZBTB20) is a new BTB/POZ-domain gene and a member of the POK family of transcriptional repressors. Notably, the role of ZBTB20 and its underlying mechanisms involved in hepatocarcinogenesis are poorly investigated. In this study, the expression of ZBTB20 was significantly overexpressed in hepatocellular carcinoma (HCC) tissues. The positive expression of ZBTB20 was associated with large tumor size, high Edmondson-Steiner grading and advanced tumor-node-metastasis (TNM) tumor stage. Additionally, HCC patients with positive expression of ZBTB20 had a poorer 5-year survival. Multivariate analyses revealed that ZBTB20 overexpression was an independent prognostic factor for HCC. Gain- and loss-of-function experiments demonstrated that ZBTB20 promoted HCC cell viability, proliferation, tumorigenicity, and cell cycle progression. Mechanistically, Cyclin D1 and Cyclin E were increased, while p21 and p27 were decreased by ZBTB20 in HCC cells. FoxO1 was inversely correlated with ZBTB20 protein expression in the same cohort of HCC specimens. We further revealed that FoxO1 was transcriptionally repressed by ZBTB20 in HCC. Moreover, restoration of FoxO1 expression partially abrogated ZBTB20-induced HCC cell proliferation and growth entry in vitro and in vivo. Collectively, these results indicate that ZBTB20 may serve as a prognostic marker and promotes tumor growth of HCC via transcriptionally repressing FoxO1.

DcR3 induces epithelial-mesenchymal transition through activation of the TGF-ß3/SMAD signaling pathway in CRC.

Decoy receptor 3 (DcR3), a novel member of the tumor necrosis factor receptor (TNFR) family, was recently reported to be associated with tumorigenesis and metastasis. However, the role of DcR3 in human colorectal cancer (CRC) has not been fully elucidated. In this study, we found that DcR3 expression was significantly higher in human colorectal cancer tissues than in paired normal tissues, and that DcR3 expression was strongly correlated with tumor invasion, lymph node metastases and poor prognoses. Moreover, DcR3 overexpression significantly enhanced CRC cell proliferation and migration in vitro and tumorigenesis in vivo. Conversely, DcR3 knockdown significantly repressed CRC cell proliferation and migration in vitro, and DcR3 deficiency also attenuated CRC tumorigenesis and metastasis in vivo. Functionally, DcR3 was essential for TGF-ß3/SMAD-mediated epithelial-mesenchymal transition (EMT) of CRC cells. Importantly, cooperation between DcR3 and TGF-ß3/SMAD-EMT signaling-related protein expression was correlated with survival and survival time in CRC patients. In conclusion, our results demonstrate that DcR3 may be a prognostic biomarker for CRC and that this receptor facilitates CRC development and metastasis by participating in TGF-ß3/SMAD-mediated EMT of CRC cells.

Long non-coding RNA MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation in colorectal cancer cells.

Our earlier findings indicate that the long non-coding RNA MALAT1 promotes colorectal cancer (CRC) cell proliferation, invasion and metastasis in vitro and in vivo by increasing expression of AKAP-9. In the present study, we investigated the molecular mechanism by which MALAT1 enhances AKAP9 expression in CRC SW480 cells. We found that MALAT1 interacts with both SRPK1 and SRSF1. MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation. Following MALAT1 knockdown, overexpression of SRPK1 was sufficient to restore SRSF1 phosphorylation and AKAP-9 expression to a level that promoted cell proliferation, invasion and migration in vitro. Conversely, SRPK1 knockdown after overexpression of MALAT1 in SW480 cells diminished SRSF1 phosphorylation and AKAP-9 expression and suppressed cell proliferation, invasion and migration in vitro. These findings suggest MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation in CRC cells. These results reveal a novel molecular mechanism by which MALAT1 regulates AKAP-9 expression in CRC cells.

MicroRNA-520g induces epithelial-mesenchymal transition and promotes metastasis of hepatocellular carcinoma by targeting SMAD7.

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. Aberrant expression of miRNAs contributes to HCC development. Here, we observed elevated miR-520g expression in tumor samples from HCC patients with relapse and metastasis, and this high miR-520g expression was correlated with poor survival. Through gain- and loss-of-function studies, miR-520g was demonstrated to facilitate HCC cell migration, invasion and epithelial-mesenchymal transition (EMT). SMAD7 was identified as a direct target of miR-520g. Accordingly, we conclude that high miR-520g expression promotes HCC cell mobility and EMT by targeting SMAD7, and this is correlated with reduced survival in HCC patients.

Null genotypes of GSTM1 and GSTT1 contribute to male factor infertility risk: a meta-analysis.

OBJECTIVE: To study the null of GSTM1, GSTT1, or GSTT1-GSTM1 and the risk of male factor infertility. DESIGN: Meta-analysis using electronic databases (Pubmed, Medline, Embase, and China National Knowledge Infrastructure) up to August 22, 2011. SETTING: The strength of the relationship between the null of GSTM1, GSTT1, and GSTT1-GSTM1 and the risk of male factor infertility was assessed by odds ratios (ORs). A total of 16 studies were identified in this meta-analysis. Among the 16 studies, 15 studies reported GSTM1null, 10 reported GSTT1, and five reported GSTM1-GSTT1. PATIENT(S): Male infertility patients and a fertile control group. INTERVENTION(S): Meta-analyses by means of random-effects models and fixed-effects models. MAIN OUTCOME MEASURE(S): Ratio of male factor infertility. RESULT(S): The studies provided overall OR estimates for GSTM1, GSTT1, and GSTM1-GSTT1, leading to a pooled OR of 1.41 (95% confidence interval [CI], 1.10-1.81), 1.15 (95% CI, 0.95-1.39), and 2.99 (95% CI, 2.14-4.18), respectively. CONCLUSION(S): There was evidence that the null of GSTM1 and GSTM1-GSTM1 increased the risk of male factor infertility, but the null genotype of GSTT1 was not associated with an increased infertility risk. We still need further multicenter and better controlled studies to confirm these findings.

Meta-analysis of alcohol consumption and risk of extrahepatic bile system cancer.

AIM: Alcohol consumption increases the risk of liver cancer. However, there is still controversy regarding alcohol consumption and the risk of extrahepatic bile system cancer (EBSC). We performed a meta-analysis to provide an overview of the relevant studies and gain more robust estimates of the relationship between alcohol consumption and risk of EBSC. METHODS: Relevant studies published between January 1966 and October 2010 were identified by searching Medline, Embase and the Cochrane Library. Studies were selected using a priori defined criteria. The strength of the relationship between alcohol consumption and risk of EBSC was assessed by adjusted odds ratio (OR). RESULTS: A total of 113 767 participants from 10 studies (nine case-control studies and one cohort study) were identified in this meta-analysis. The studies provided adjusted overall OR estimates for drinkers versus non-/low drinkers, leading to a pooled adjusted OR of 0.82 (95% confidence interval [CI] = 0.72-0.94, P for heterogeneity = 0.194, I(2) = 27.2%). The overall adjusted OR of hospital-based studies and population-based studies were 0.80 (95% CI = 0.65-0.99, P = 0.260) and 0.79 (95% CI = 0.64-0.98, P = 0.119), respectively. For the heavy drinkers, the adjusted OR significance increased to 1.58 (95% CI = 0.97-2.57, P for heterogeneity = 0.055, I(2) = 65.4%), but it had no statistical significance. CONCLUSION: There is evidence that moderate alcohol consumption lowers the risk of EBSC compared with non-/low alcohol consumption, but not heavy alcohol consumption. Further multicenter and better controlled studies are required to confirm these findings.

[Adult-to-adult living-related donor liver transplantation: report of 2 cases].

OBJECTIVE: To investigate the feasibility and safety of adult-to-adult living-related donor liver transplantation using a right lobe graft. METHODS: The clinical data of 2 cases of living-related donor liver transplantation performed between July, 2010 and November, 2010 were analyzed. RESULTS: Liver transplantation was performed using a right lobe graft including the middle hepatic vein in one case and a right lobe graft without the middle hepatic vein in the other. The ratio of graft volume to standard liver volume was 46.2% and 47.3% in the two cases, with GR/WR of 0.83 and 0.80, and donor residue liver of 42.1% and 39.5%, respectively. The donor operation lasted for 6.5 h and 5 h in the two cases with blood loss of about 200-250 ml without blood transfusion. The donors recovered uneventfully without any surgical complications, whose liver function was normal 7 days after the operation, and were discharged 14 days and 16 days after the surgery, respectively. The recipient operation lasted for 8 h and 7 h with blood loss of about 800-1000 ml. The right hepatic vein, hepatic artery, portal vein and bile duct reconstruction were performed by end-to-end anastomoses in the 2 recipients. Bile duct anastomosis stricture occurred in the first recipient 2 months after transplantation and was treated with percutaneous transhepatic cholangiography and drainage. The second recipient recovered smoothly without any complications. The recipients have so far survived 9 months and 5 months, respectively. CONCLUSION: Adult-to-adult living-related donor liver transplantation is a safe and effective option for treatment of end-stage liver diseases in the context of cadaveric liver graft shortage.