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| 1 | Current and future treatments for hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC) represents a unique challenge for physicians and patients.There is no definitively curative treatment.Rather,many treatment and management modalities exist with differing advantages and disadvantages.Both current guidelines and individual patient concerns must be taken into account in order to properly manage HCC.In addition,quality of life issues are particularly complex in patients with HCC and these concerns must also be factored into treatment strategies.Thus,considering all the options and their various pros and cons can quickly become complex for both clinicians and patients.In this review,we systematically discuss the current treatment modalities available for HCC,detailing relevant clinical data,risks and rewards and overall outcomes for each approach.Surgical options discussed include resection,transplantation and ablation.We also discuss the radiation modalities:conformal radiotherapy,yttrium 90 microspheres and proton and heavy ion radiotherapy.The biologic agent Sorafenib is discussed as a promising new approach,and recent clinical trials are reviewed.We then detail currently described molecular pathways implicated in the initiation and progression of HCC,and we explore the potential of each pathway as an avenue for drug exploitation.We hope this comprehensive and forward-looking review enables both clinicians and patients to understand various options and thereby make more informed decisions regarding this disease. | Alexander Schlachterman Willie W Craft Jr Eric Hilgenfeldt Avir Mitra Roniel Cabrera | 2015 | World Journal of Gastroenterology2015，21，28： | 76 |
| 2 | Insulin resistance and chronic liver disease显示文摘Increased insulin resistance is frequently associated with chronic liver disease and is a pathophysiological feature of hepatogenous diabetes.Distinctive factors including hepatic parenchymal cell damage,portalsystemic shunting and hepatitis C virus are responsible for the development of hepatogenous insulin resistance/diabetes.Although it remains unclear whether insulin secretion from pancreatic beta cells is impaired as it is in type 2 diabetes,retinopathic and cardiovascular risk is low and major causes of death in cirrhotic patients with diabetes are liver failure,hepatocellular carcinoma and gastrointestinal hemorrhage.Hemoglobin A1c is an inaccurate marker for the assessment and management of hepatogenous diabetes.Moreover,exogenous insulin or sulfonylureas may be harmful because these agents may promote hepatocarcinogenesis.Thus,pathogenesis,cause of death,assessment and therapeutic strategy for hepatogenous insulin resistance/diabetes differ from those for lifestyle-related type 2 diabetes.In this article,we review features of insulin resistance in relationship to chronic liver disease.We also discuss the impact of anti-diabetic agents on interferon treatment and hepatocarcinogenesis. | Takumi Kawaguchi Eitaro Taniguchi Minoru Itou Masahiro Sakata Shuji Sumie Michio Sata | 2011 | World Journal of Hepatology2011，3，5： | 25 |
| 3 | Effects of hypoxia-inducible factor-1α silencing on the proliferation of CBRH-7919 hepatoma cells显示文摘AIM:To study the effects of hypoxia-inducible factor1α(HIF-1α) silencing on the proliferation of hypoxic CBRH-7919 rat hepatoma cells.METHODS:The CBRH-7919 rat hepatoma cell line was used in this study and the hypoxic model was constructed using CoCl2.The HIF-1α-specific RNAi sequences were designed according to the gene coding sequence of rat HIF-1α obtained from GeneBank.The secondary structure of the HIF-1α gene sequence was analyzed using RNA draw software.The small interfering RNA(siRNA) transfection mixture was produced by mixing the siRNA and Lipofectamine2000TM,and transfected into the hypoxic hepatoma cells.Real time reverse transcription-polymerase chain reaction(RTPCR) and Western blotting assay were used to detect the expression levels of mRNA and protein.HIF-1α and vascular endothelial growth factor(VEGF) mRNA was determined using real time RT-PCR;the protein expression levels of AKT,p-AKT,p21 and cyclinD1 were determined using Western blotting.The proliferation of hepatoma cells was observed using the methyl thiazolyl tetrazolium(MTT) assay and the bromodeoxyuridine(BrdU) incorporation cell proliferation assay.RESULTS:Under induced hypoxia,the viability of the hepatoma cells reached a minimum at 800 μmol/L CoCl2;the viability of the cells was relatively high at CoCl2 concentrations between 100 μmol/L and 200 μmol/L.Under hypoxia,the mRNA and protein expression levels of HIF-1α and VEGF were significantly higher than that of hepatoma cells that were cultured in normaxia.HIF-1α-specific RNAi sequences were successfully transfected into hepatoma cells.The transfection of specific siRNAs significantly inhibited the mRNA and protein expression levels of HIF-1α and VEGF,along with the protein expression levels of p-AKT and cyclinD1;the protein expression of p21 was significantly increased,and there was no significant difference in the expression of AKT.The MTT assay showed that the amount of hepatoma cells in S phase in the siRNA transfection group was obviously smaller than that in the control group;in the siRNA transfection group,the amount of hepatoma cells in G1 phase was more than that in the control group.The BrdU incorporation assay showed that the number of BrdU positive hepatoma cells in the siRNA transfection group was less than that in the control group.The data of the MTT assay and BrdU incorporation assay suggested that HIF-1α silencing using siRNAs significantly inhibited the proliferation of hepatoma cells.CONCLUSION:Hypoxia increases the expression of HIF-1α,and HIF-1α silencing significantly inhibits the proliferation of hypoxic CBRH-7919 rat hepatoma cells. | Lin-Feng Xu Jia-Yan Ni Hong-Liang Sun Yao-Ting Chen Yu-Dan Wu | 2013 | World Journal of Gastroenterology2013，19，11： | 18 |
| 4 | The cloning of 3'-truncated preS/S gene from HBV genomic DNA and its expression in transgenic mice显示文摘INTRODUCTIONHepatitis B virus (HBV) is regarded as one of themain etiologic factors involved in the developmentof human hepatocellular carcinoma (HCC).The open reading frame (orf)of X gene of HBVencoded a transactivating factor is the evidence thatstrongly supported the notion that the X gene ofHBV DNA integrated in HCC genomic DNA couldcontribute to the carcinogenesis of liver cells byactivation of some related cellular genes | Yi Ping Hu~1 Yu Cheng Yao~1 Jian Xiu Li~1 Xin Min Wang~1 Hong Li~2 Zhong Hua Wang~1 Zhang Heng Lei~3 1 Department of Cell Biology,Second Military Medical University,Shanghai 200433,China 2 Department of Biology,Department of Basic Medicine,West-China University of Medical Sciences,Chengdu 610041,China 3 Department of Biology,North Sichuan Medical College,Nanchong 637007,China | 2000 | World Journal of Gastroenterology2000，6，5： | 18 |
| 5 | Abnormal expression of hepatoma- derived γ-glutamyltransferase subtyping and its early alteration for carcinogenesis of hepatocytes显示文摘BACKGROUND: Although the hepatoma-specific band of gamma-glutamyltransferase ( GGT ) is a highly sensitive marker in diagnosis of hepatocellular carcinoma, the kine- tic expression and the early alterations of GGT in the deve- lopment of hepatoma remain unclear. In this study, we in- vestigated the expression and the alterations of GGT multi- ple molecular forms in hepatotumorigenesis. METHODS: The expression of GGT in a chemically in- duced hepatocarcinogenesis model was examined by giving 0. 05% of 2-fluoenylacetamide in diet for 12 weeks. The ex- pression levels of total RNA and GGT, and the changes of liver pathology, GGT multiple molecular forms and sugar- chain heterogeneity were investigated at the different stages of rat hepatoma development. RESULTS: Pathological examination and biochemical ana- lysis found that liver GGT was over-expressed and secreted into blood during canceration. Serum total GGT and liver GGT specific activities (IU/g) including soluble and mem- brane-combined GGT were significantly higher (P <0.05) in experimental groups than those in control group, respec- tively. A highly positive correlation was found between to- tal GGT activities and total RNA levels (r =0.90, P <0.05) of the liver. Both were higher six weeks later than before. Con A-non-reactive-GGT was increased consistantly dur- ing the development of rat hepatoma. GGT multiple mo- lecular forms in the liver and sera of experimental rats showed that fetal liver-type GGT bands were associated with the development of hepatoma. CONCLUSIONS: Fetal liver-type GGT in sera and the liver of rats is closely related to hepatotumorigenesis. It can be used as a sensitive enzymatic marker for the early diagnosis of liver cancer. | Deng-Fu Yao, Zhi-Zhen Dong, Deng-Bing Yao, Xin-Hua Wu, Wei Wu, Li-Wei Qiu, Hong-Mei Wang and Xian-Yong Meng Nantong, China Research Center of Clinical Molecular Biology, Affilia- ted Hospital of Nantong University, Nantong 226001 , China Insti- tute of Neuroscicnces, Nantong University, Nantong 226001 , China | 2004 | Hepatobiliary & Pancreatic Diseases International2004，3，4： | 17 |
| 6 | Establishment of a human hepatoma multidrug resistant cell line in vitro显示文摘AIM:To establish a multidrug-resistant hepatoma cell line(SK-Hep-1),and to investigate its biological characteristics.METHODS:A highly invasive SK-Hep-1 cell line of human hepatocellular carcinoma,also known as malignant hepatoma was incubated with a high concentration of cisplatin(CDDP) to establish a CDDP-resistant cell subline(SK-Hep-1/CDDP).The 50% inhibitory dose(IC50) values and the resistance indexes [(IC50 SK-Hep-1/CDDP)/(IC50 SK-Hep-1)] for other chemotherapeutic agents and the growth curve of cells were all evaluated using cell counting kit-8 assays.The distribution of the cell cycles were detected by flow cytometry.Expression of acquired multidrug resistance P-glycoprotein(MDR1,ABCB1) and multidrug resistance-associated protein 1(MRP1,ABCC1) was compared with that in parent cells by Western blotting and immunofluorescence combined with laser scanning confocal microscopy.RESULTS:The SK-Hep-1/CDDP cells(IC50 = 70.61 ± 1.06 μg/mL) was 13.76 times more resistant to CDDP than the SK-Hep-1 cells(IC50 = 5.13 ± 0.09 μg/mL),and CDDP-resistant cells also demonstrated cross-resistance to many anti-tumor agents such as doxorubicin,5-fluorouracil and vincristine.Similar morphologies were determined in both SK-Hep-1 and SK-Hep-1/CDDP groups.The cell cycle distribution of the SK-Hep-1/CDDP cell line exhibited a significantly increased percentage of cells in S(42.2% ± 2.65% vs 27.91% ± 2.16%,P < 0.01) and G2/M(20.67% ± 5.69% vs 12.14% ± 3.36%,P < 0.01) phases in comparison with SK-Hep-1 cells,while the percentage of cells in the G0/G1 phase decreased(37.5% ± 5.05% vs 59.83% ± 3.28%,P < 0.01).The levels of MDR1 and MRP1 were overexpressed in the SK-Hep-1/CDDP cells exhibiting the MDR phenotype.CONCLUSION:Multiple drug resistance of multiple drugs in the human hepatoma cell line SK-Hep-1/CDDP was closely related to the overexpression of MDR1 and MRP1. | Zhou, Yuan Ling, Xian-Long Li, Shi-Wei Li, Xin-Qiang Yan, Bin | 2010 | World Journal of Gastroenterology2010，16，18： | 17 |
| 7 | Overexpression of insulin-like growth factor-Ⅰ receptor as a pertinent biomarker for hepatocytes malignant transformation显示文摘AIM:To investigate the dynamic features of insulinlike growth factor-Ⅰreceptor(IGF-ⅠR)expression in rat hepatocarcinogenesis,and the relationship between IGF-ⅠR and hepatocytes malignant transformation at mRNA or protein level.METHODS:Hepatoma models were made by inducing with 2-fluorenylacetamide(2-FAA)on male SpragueDawley rats.Morphological changes of hepatocytes were observed by pathological Hematoxylin and eosin staining,the dynamic expressions of liver and serum IGF-ⅠR were quantitatively analyzed by an enzymelinked immunosorbent assay.The distribution of hepatic IGF-ⅠR was located by immunohistochemistry.The fragments of IGF-ⅠR gene were amplified by reverse transcription-polymerase chain reaction,and confirmed by sequencing.RESULTS:Rat hepatocytes after induced by 2-FAA were changed dynamically from granule-like degeneration,precancerous to hepatoma formation with the progressing increasing of hepatic mRNA or IGF-ⅠR expression.The incidences of liver IGF-ⅠR,IGF-ⅠR mRNA,specific IGF-ⅠR concentration(ng/mg wet liver),and serum IGF-ⅠR level(ng/mL)were 0.0%,0.0%,0.63±0.17,and 1.33±0.47 in the control;50.0%,61.1%,0.65±0.2,and 1.51±0.46 in the degeneration;88.9%,100%,0.66±0.14,and 1.92±0.29 in the precancerosis;and 100%,100%,0.96±0.09,and2.43±0.57 in the cancerous group,respectively.IGF-ⅠR expression in the cancerous group was significantly higher(P<0.01)than that in any of other groups at mRNA or protein level.The closely positive IGF-ⅠR relationship was found between livers and sera(r=0.91,t=14.222,P<0.01),respectively.CONCLUSION:IGF-ⅠR expression may participate in rat hepatocarcinogenesis and its abnormality should be an early marker for hepatocytes malignant transformation. | Xiao-Di Yan Min Yao Li Wang Hai-Jian Zhang Mei-Juan Yan Xing Gu Yun Shi Jie Chen Zhi-Zhen Dong Deng-Fu Yao | 2013 | World Journal of Gastroenterology2013，19，36： | 16 |
| 8 | Efficacy of intra- tumor injection of Kang-Lai-Te in treating transplanted hepatoma in rats显示文摘BACKGROUND: Non-operative therapy takes an impor- tant position in comprehensive therapy of liver cancer. De- spite some effects by using ethanol, acetic acid and heat sa- line for intra-tumor injection in the treatment of liver canc- er, it is difficult to attain a complete cure but bring about injury to the liver to some extent. Hence, searching for other drugs for the local treatment of liver tumor is an im- portant option. This study was designed to set up rat mo- dels of transplanted liver cancer, intra-tumor injection of Kang-Lai-Te (KLT), and negative control (saline) and positive control (ethanol). The effect of intra-tumor injec- tion of KLT in treating transplanted hepatoma in rats and its advantages and disadvantages were assessed and the pos- sibility of its use in treating patients with liver cancer was evaluated. METHODS: Forty rats were divided into 4 groups ( G1, G2, G3 and G4, 10 rats in each group). Different drugs were injected into their implanted hepatoma (G1 with 0.2 ml saline as control, G2 with 10 mg KLT, G3 with 20 mg KLT, G4 with 0.2 ml ethanol). After 3 and 8 days, the hepa- toma volume (HV), the serum levels of albumin, alanine aminotransferase(ALT), aspartate aminotransferase alkaline phosphatase( ALP) and creatinine, as well as the expression of proliferation cell nuclear antigen (PCNA) in hepatoma were detected. RESULTS: After 3 days, the HVs were smaller in G3 and G4 than in G1 (P <0.05), the serum levels of albumin were higher in G2 and G3 than in Gl and G4 (P <0.05), the se- rum levels of ALT and AST were lower in G2 and G3 than in G4 (P<0.05), the serum levels of ALP was lower in G2 and G3 than in Gl and G4 (P <0. 05), the PCNA labeling indexes (PCNA LI) were lower in G2 and G3 than in Gl and GA (P <0.05). After 8 days, the HVs were smaller in G2, G3 and G4 than in Gl (P <0.05), and the differences of HVs among G2, G3 and G4 were not significant. The serum levels of ALP were lower in G1, G2 and G3 than in G4 (P <0.05), and the PCNA LI were lower in G3 than in Gl andG4 (P<0.05). CONCLUSION: Intra-tumor injection of KLT into implan- ted hepatoma is evidently effective, but it is less effective than ethanol. The effect of KLT on liver function is markedly lower than that of ethanol. | Li-Qun Wu, Yun Lu, Hua-Jun Lu, Zong-Gang Zhao and Meng Yang Qingdao, China Department of Hepato-biliary-vascular Surgery, Qing- dao University Medical College, Qingdao 266003 , China | 2004 | Hepatobiliary & Pancreatic Diseases International2004，3，4： | 12 |
| 9 | IMMUNOHISTOCHEMICAL OBSERVATION OF MACROPHAGE COLONY STIMULATING FACTOR AND ITS RECEPTOR IN BREAST CANCER AND HEPATOMA TISSUES显示文摘Objective: To study the potential role of cellular macrophage colony-stimulating factor (cM-CSF) and cellular macrophage colony-stimulating factor receptor (cM-CSF-R) with breast cancer and hepatoma and search the way for clinical application. Methods: Frozen surgical specimens from 48 breast cancer patients, including 29 cases of histological grade II and 19 eases of grade III, and 16 hepatoma patients were investigated by Avidin Biotin Complex (ABC) immunohistochemical assay with anti-M-CSF monoclonal antibody (Mab) and anti-M-CSF-R Mab. Pathohistological examination was performed as well. Results: cM-CSF and cM-CSF-R were detected in tested specimens. The expression levels of cM-CSF and cM-CSF-R in grade III group were higher than in grade II group and more higher than control group hyperplasia of breast. Hepatoma tissues also showed higher expression level of cM-CSF and cM-CSF-R than normal adult and fetal liver. Conclusion: Breast cancer and hepatoma tissues presented higher expression levels of cM-CSF and cM-CSF-R than control and expression level might be related with tumor’s process. | 宋玉华 林永敏 吴克复 杨文清 李戈 郑德先 | 2001 | Chinese Journal of Cancer Research2001，13，1： | 8 |
| 10 | Effect of arsenic trioxide on human hepatoma cell line BEL-7402 cultured in vitro显示文摘AIM To study the effect of a varyingconcentrations of arsenic trioxide on humanhepatoma cell line BEL-?402 cultured in vitro andits mechanism of action.METHODS The BEL-7402 cells were treatedwith arsenic trioxide(at the concentrations of0.5,1,2 μmol/L,respectively)for 4 successivedays.The cell growth and proliferation wereobserved by cell counting and cell-growth curve.Morphologic changes were studied withelectronmicroscopy.Flow cytometry was usedto assay celI-DNA distribution and the proteinexpression of Bcl-2 and Bax detected byimmunocytochemical method.RESULTS The cell growth was significantlyinhibited by varying concentrations of arsenictrioxide as revealed by cell counting and cell-growth curve,which was dose- and time-dependent.Arsenic trioxide treatment at 0.5,1and 2 μmol/L resulted in a sub-G1 cell peak,theapoptosis rate of the control group was 9.31%and that of 0.5 μmol/L arsenic trioxide 15.53%,no significant difference was seen between thetwo.The apoptosis rates of 1,2 μmol/L arsenictrioxide were 19.10% and 21.87% respectively,which were much higher(both P<0.05).Decrease of G0/G1 phase cells and increase of Sphase cells were observed by flow cytometry,suggesting the inhibition effect of 0.5,1,2 μmol/L arsenic trioxide on BEL-7402 cell lay in the G0/G1 phase.Morphologic changes such asintact cell membrane,nucleic condensation,apoptotic body formation were seen undertransmission electronmicrescopy,whereas the0.5 mol/L arsenic trioxide-treated BEL-7402cells showed decrease of nucleocytoplasmicratio,round nucleus,well-differentiatedorganelles in the cytoplasm.The processes andmicrovilli on the cell surface of the experimentalgroups under scanning electron microscopy weresignificantly decreased.High expressions ofBcl-2 and Bax were detected in 1 and 2 μmol/Larsenic trioxide-treated cells,these were 46%,87.33% and 83.08%,95.83% respectively,among which that of Bax was more significant.Arsenic trioxide treatment at 0.5 μmol/Lresulted in a higher expression level of Bcl-2 andlower expression level of Bax,which were8.81% and 3.83% respectively,as comparedwith that of the control group(15.33%)(P1<0.01,P2<0.01).CONCLUSION Arsenic trioxide not onlyinhibited proliferation but also induced apoptosisof human hepatoma cell line BEL-7402.Theinduced-apoptosis effect of 1,2 μmol/L arsenictrioxide was related to the expression level ofBcl-2 and Bax. | Hong Yu Xu You Lin Yang Yuan Yuan Gao Qiao Li Wu Guang Qiang Gao | 2000 | World Journal of Gastroenterology2000，6，5： | 8 |
| 11 | Non-cirrhotic hepatocellular carcinoma in chronic viral hepatitis: Current insights and advancements显示文摘Primary liver cancers carry significant morbidity and mortality.Hepatocellular carcinoma(HCC)develops within the hepatic parenchyma and is the most common malignancy originating from the liver.Although 80%of HCCs develop within background cirrhosis,20%may arise in a non-cirrhotic milieu and are referred to non-cirrhotic-HCC(NCHCC).NCHCC is often diagnosed late due to lack of surveillance.In addition,the rising prevalence of non-alcoholic fatty liver disease and diabetes mellitus have increased the risk of developing HCC on noncirrhotic patients.Viral infections such as chronic Hepatitis B and less often chronic hepatitis C with advance fibrosis are associated with NCHCC.NCHCC individuals may have Hepatitis B core antibodies and occult HBV infection,signifying the role of Hepatitis B infection in NCHCC.Given the effectiveness of current antiviral therapies,surgical techniques and locoregional treatment options,nowadays such patients have more options and potential for cure.However,these lesions need early identification with diagnostic models and multiple surveillance strategies to improve overall outcomes.Better understanding of the NCHCC risk factors,tumorigenesis,diagnostic tools and treatment options are critical to improving prognosis and overall outcomes on these patients.In this review,we aim to discuss NCHCC epidemiology,risk factors,and pathogenesis,and elaborate on NCHCC diagnosis and treatment strategies. | Abhilash Perisetti Hemant Goyal Rachana Yendala Ragesh B Thandassery Emmanouil Giorgakis | 2021 | World Journal of Gastroenterology2021，27，24： | 6 |
| 12 | Inhibition of apoptosis by oncogenic hepatitis B virus X protein: Implications for the treatment of hepatocellular carcinoma显示文摘Hepatitis B virus X protein(HBx) plays an important role in the development of hepatocellular carcinoma(HCC). In addition, hepatoma upregulated protein(HURP) is a cellular oncogene that is upregulated in a majority of HCC cases. We highlight here recent findings demonstrating a link between HBx, HURP and anti-apoptosis effects observed in cisplatin-treated HCC cells. We observed that Hep3B cells overexpressing HBx display increased HURP mRNA and protein levels, and show resistance to cisplatin-induced apoptosis. Knockdown of HURP in HBx-expressing cells reverses this effect, and sensitizes cells to cisplatin. The anti-apoptotic effect of HBx requires activation of the p38/MAPK pathway as well as expression of SATB1, survivin and HURP. Furthermore, silencing of HURP using short-hairpin RNA promotes accumulation of p53 and reduces cell proliferation in SK-Hep-1 cells(p53^(+/–)), whereas these effects are not observed in p53-mutant Mahlavu cells. Similarly, HURP silencing does not affect the proliferation of H1299 lung carcinoma cells or Hep3 B HCC cells which lack p53. Silencing of HURP sensitizes SK-Hep-1 cells to cisplatin. While HURP overexpression promotes p53 ubiquitination and degradation by the proteasome, HURP silencing reverses these effects. Inoculation of SK-Hep-1 cancer cells in which HURP has been silenced produces smaller tumors than control in nude mice. Besides, gankyrin, a positive regulator of the E3 ubiquitin ligase MDM2, is upregulated following HURP expression, and silencing of gankyrin reduces HURP-mediated downregulation of p53. In addition, we observed a positive correlation between HURP and gankyrin protein levels in HCC patients(r^2 = 0.778; n = 9). These findings suggest a role for the viral protein HBx and the host protein HURP in preventing p53-mediated apoptosis during cancer progression and establishment of chemoresistance. | Chuck C K Chao | 2016 | World Journal of Hepatology2016，8，25： | 5 |
| 13 | Prognostic value of ^(18)F-FDG PET/CT in liver transplantation for hepatocarcinoma显示文摘AIM:To evaluate the prognostic value of pretreatment F D G p o s i t r o n e m i s s i o n t o m o g ra p h y c o m p u t e d tomography(PET-CT) in patients with hepatocarcinoma treated by liver transplantation(LT).METHODS:The authors retrospectively analyzed the data of 27 patients(mean age 58 ± 9 years) who underwent FDG PET-CT before LT for hepatocarcinoma.Mean follow-up was 26 ± 18 mo.The FDG PET/CT was performed according to a standard clinical protocol:4 MBq FDG/kg body weight,uptake 60 min,low-dose non-enhanced CT.The authors measured the SUVmax and SUVmean of the tumor and the normal liver.The tumor/liver activity ratios(RSUVmax and RSUVmean) were tested as prognostic factors and compared to the following conventional prognostic factors:MILAN,CLIP,OKUDA,TNM stage,alphafoetoprotein level,portal thrombosis,size of the largest nodule,tumor differentiation,microvascular invasion,underlying cirrhosis and liver function.RESULTS:Overall and recurrence free survivals were80.7%and 67.4%at 3 years,and 70.6%and 67.4%at 5 years,respectively.According to a multivariate Cox model,only FDG PET/CT RSUVmax predicted recurrence free survival.Even though the MILAN criteria alone were not predictive,it is worth noting that none of the patients outside the MILAN criteria and with RSUVmax<1.15 relapsed.CONCLUSION:FDG PET/CT with an RSUVmax cutoff value of 1.15 is a strong prognostic factor for recurrence and death in patients with HCC treated by LT in this retrospective series.Further prospectivestudies should test whether this metabolic index should be systematically included in the preoperative assessment. | Olivier Detry Laurence Govaerts Arnaud Deroover Morgan Vandermeulen Nicolas Meurisse Serge Malenga Noella Bletard Charles Mbendi Anne Lamproye Pierre Honoré Paul Meunier Jean Delwaide Roland Hustinx | 2015 | World Journal of Gastroenterology2015，21，10： | 5 |
| 14 | CO-EXPRESSION OF MACROPHAGE COLONY-STIMULATING FACTOR WITH ITS RECEPTOR IN HUMAN HEPATOMA CELLS AND ITS POTENTIAL ROLES显示文摘Objective: To investigate the potential role of macrophage colony-stimulating factor (M-CSF) and macrophage colony-stimulating factor receptor (M-CSFR) on the growth of human hepatoma cells. Methods:Specimens of different origin, including tissues of human hepatocellular carcinoma (HCC), human fetal liver (FL) and normal liver (NL), the hepatoma cell lines,as well as the peripheral blood mononuclear cells (PBMC) from patients with HCC or liver metastatic tumor (LMT), were used to detect the expression levels of M-CSF and M-CSF-R by ABC immunohistochemistry staining and reverse transcription polymerase chain reaction methods the expression levels of M-CSF and MCSF’R. Influence of monoclonal antibody against MCSF (BS) or M-CSF’R (RE2) on proliferation ability of hepatoma cell tilles in vitro was also studied. Results: The results showed that hepatoma tissues produced elevated levels of both M-CSF and M-CSF-R compared with those of fetal liver (P<0.001). The M-CSFIM’CSF-R expression levels of PBMC from hepatoma patients were higher than those of LMT patients (P<0.01, P<0.05) and the normal people (P<0.001). The hepatoma cell lines showed strong positive for M-CSF and M-CSF-R production. Both BS and REZ displayed a dosedependent inhibitory effect on the growth and proliferation of hepatoma cells. Conclusion: The study indicates a co-expression model for M-CSF-R in hepatoma cells, suggesting an involvement of M-CSFIMCSF-R in growth signaling of those malignant cells. The M-CSFIM-CSF-R seems to function through an autonomy mechanism in human hepatoma. | 杨文清 吴克复 宋玉华 赵明河 张陆松 宋乃国 张丽娜 | 1999 | Chinese Journal of Cancer Research1999，11，2： | 4 |
| 15 | Conversion of hepatoma cells to hepatocyte-like cells by defined hepatocyte nuclear factors显示文摘Normal cells become cancer cells after a malignant transformation,but whether cancer cells can be reversed to normal status remains elusive.Here,we report that the combination of hepatocyte nuclear factor IA (HNFIA),HNF4A and forkhead box protein A3 (FOXA3)synergistically reprograms hepatocellular carcinoma (HCC)cells to hepatocyte-like cells (reprogrammed hepatocytes, rHeps).Our results show that rHeps lose the malignant phenotypes of cancer cells and retrieve hepatocyte-specific characteristics including hepatocyte-like morphology;global expression pattern of genes and specific biomarkers of hepatocytes;and the unique hepatic functions of albumin (ALB)secretion,glycogen synthesis,low-density lipoprotein (LDL)uptake,urea production, cytochrome P450 enzymes induction and drug metabolism.Intratumoral injection of these three factors efficiently shrank patientderived tumor xenografts and reprogrammed HCC cells in vivo.Most importantly,transplantation of rHeps in the liver of fumarylacetoacetate hydrolase-deficient (Fah^-/-)mice led to the reconstruction of hepatic lobules and the restoration of hepatic function.Mechanistically,exogenous expression of HNF1A,HNF4A and FOXA3 in HCC cells initiated the endogenous expression of numerous hepatocyte nuclear factors,which promoted the conversion of HCC cells to hepatocyte-like cells.Collectively,our results indicate the successful conversion of hepatoma cells to hepatocyte-like cells,not only extending our current knowledge of cell reprogramming but also providing a route towards a novel therapeutic strategy for cancer. | Zhuo Cheng Zhiying He Yongchao Cai Cheng Zhang Gongbo Fu Hengyu Li Wen Sun Changcheng Liu Xiuliang Cui Beifang Ning Daimin Xiang Tengfei Zhou Xiaofeng Li Weifen Xie Hongyang Wang Jin Ding | 2019 | Cell Research2019，29，2： | 3 |
| 16 | Expression of alpha-fetoprotein messenger RNA in BEL-7404 human hepatoma cells and effect of L-4-oxalysine on the expression显示文摘ExpressionofalphafetoproteinmessengerRNAinBEL7404humanhepatomacelsandefectofL4oxalysineontheexpressionWANGXingWangandXU... | WANG XingWang and XU BinKeywords oxalysine liver neoplasms fetoprotein tumor cell, cultured RNA, messenger gene expression in situ hybridization immunohistochemistry | 1998 | World Journal of Gastroenterology1998，4，4： | 3 |
| 17 | Anticancer effect of the extracts from Polyalthia evecta against human hepatoma cell line(HepG2)显示文摘Objective:To investigate the anticancer activity of Polyalthia evecta(P.evecta)(Pierre) Finet & Gagnep against human hepatoma cell line(HepG2).Methods:The anticancer activity was based on(a) the cytotoxicity against human hepatoma cells(HepG2) assessed using a neutral red assay and(b) apoptosis induction determined by evaluation of nuclei morphological changes after DAP1 staining.Preliminary phytochemical analysis of the crude extract was assessed by HPLC analysis.Results:The 50% ethanol-water crude leaf extract of P.evecta(EW-L) showed greater potential anticancer activity with high cytotoxicity[IC_(50)=(62.8±7.3)μg/mL]and higher selectivity in HepG2 cells than normal Vero cells[selective index(SI)=7.9].The SI of EW-L was higher than the positive control,melphalan(SI=1.6) and the apoptotic cells(46.4±2.6)%induced by EW-L was higher than the melphalan(41.6±2.1)%(P<0.05).The HPLC chromatogram of the EW-L revealed the presence of various kinds of polyphenolics and flavonoids in it.Conclusions: P.evecta is a potential plant with anticancer activity.The isolation of pure compounds and determination of the bioactivity of individual compounds will be further performed. | Sasipawan Machana Natthida Weerapreeyakul Sahapat Barusrux | 2012 | Asian Pacific Journal of Tropical Biomedicine2012，2，5： | 3 |
| 18 | Role of liver resection in the management of multinodular hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC) is the third leadingcause of cancer related deaths worldwide. Various treatment modalities have been applied to HCC depend-ing on the tumor load, functional capacity of the liver and the general condition of the patient. According to Barcelona Clinic Liver Cancer staging strategy and The American Association for the Study of Liver Disease guidelines, surgical resection is not advocated in the tretment of multinodular HCC. Despite this, many recent clinical studies show that, resection can achieve good results in patients with multinodular HCC and 5-year survival rate around 40% can be reached. If resection or transplantation is not performed, these patients are usually managed with palliative procedures such as transarterial chemoembolization, radioembolization and cytotoxic chemotherapy and 5-year survival of this group of patients will be extremely low. Although survival rates are lower and complications may be increased in this group of patients, liver resection can safely be performed in selected patients in experienced centers for the management of multinodular HCC. | Osman Abbasoglu | 2015 | World Journal of Hepatology2015，7，20： | 3 |
| 19 | Differentiation of human hepatoma cells induced by the expression of antisense PKCα | 王向阳 柳惠图 | 1998 | Progress in Natural Science:Materials International1998，8，3： | 3 |
| 20 | Antitumoral activity of low density lipoprotein-aclacinomycin complex in mice bearing H_(22) tumor显示文摘INTRODUCTIONCancer cells,which proliferate rapidly need largeamounts of cholesterol for new membrane synthesis,and high LDL receptor (LDLR) activity.LDL hasbeen proposed as a useful discriminatory vehicle forthe delivery of cytotoxic drugs to tumor cells.LDL presents many advantages as drug | Bi WX Xu SD Zhang PH Kong F | 2000 | World Journal of Gastroenterology2000，6，1： | 3 |
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