多层螺旋CT双期增强扫描与CT平扫在肝小细胞癌中的诊断价值研究

目的探讨多层螺旋CT双期增强扫描与CT平扫在肝小细胞癌中的诊断价值。方法将118例肝小细胞癌患者作为研究对象,并将其按照检查方法的不同随机分成观察组59例与对照组59例,观察组患者行多层螺旋CT双期增强扫描检查,对照组患者行CT平扫检查,分别对两组患者的肝小细胞癌确诊率、CT扫描时病灶的密度及图像表现、不同扫描时相肿瘤与肝脏密度差值的变化情况进行对比。结果观察组肝小细胞癌患者的确诊率要明显高于对照组患者。观察组肝小细胞癌患者中瘤内密度均匀患者34例、占57. 6%,有瘤内密度不均匀患者25例、占42. 4%;病灶边界显示清楚患者40例、占67. 8%,病灶边界显示模糊患者19例、占32. 2%。对照组肝小细胞癌患者中低密度影患者47例、占79. 7%,高密度影患者12例、占20. 3%,瘤内密度均匀患者45例、占76. 3%,瘤内密度不均匀患者14例、占23. 7%,病灶边界显示清楚患者22例、占37. 3%,病灶边界显示模糊患者37例、占62. 7%。观察组动脉期、门脉期及对照组患者的肿瘤与肝脏密度差值均存在明显差异,其中观察组门脉期肿瘤与肝脏密度差值最大,对照组肿瘤与肝脏密度差值最小。结论多层螺旋CT双期增强扫描在肝小细胞癌诊断中的确诊率较高,具有较高的临床应用价值。

MSCT三期增强扫描对肝小细胞癌确诊率的影响

目的:探讨多层螺旋CT(MSCT)三期增强扫描对肝小细胞癌确诊率的影响。方法:选取2020年8月~2021年9月本院收治的80例肝小细胞癌患者,以病理诊断为金标准,根据检查方法不同分为MSCT三期增强扫描组、CT平扫组,对比两组扫描效果。结果:MSCT三期增强扫描组动脉期检出38个病灶(95.00%);门静脉期检出27个病灶(67.50%);延迟期共检出36个病灶(90.00%)。MSCT三期增强扫描组动脉期、延迟期病灶检出率高于门静脉期、平扫组(P<0.05);两组动脉期、门静脉期、延迟期MSCT扫描的高密度、低密度强化对比,差异有统计学意义(P<0.05);MSCT三期增强扫描组动脉期、门静脉期、延迟期的肝脏、肿瘤及肿瘤与肝脏密度差值均高于平扫组(P<0.05)。结论:MSCT三期增强扫描可准确反映肝小细胞癌病灶强化特征,确诊率较高,可为临床诊断提供可靠的影像学依据,对肝小细胞癌早期诊断具有重要意义。

CT平扫与MSCT双期增强鉴别早期肝细胞癌效果研究

目的探讨CT平扫与多层螺旋CT(MSCT)双期增强鉴别早期肝细胞癌效果。方法选取2019年1月-2020年6月河南科技大学第一附属医院就诊的114例早期肝细胞癌患者,依照检查方式的不同将患者分为对照组(n=58)与研究组(n=56),分别采用CT平扫检查与MSCT双期增强扫描检查,对比两组患者临床检查结果。结果以病理活检为金标准,研究组早期肝细胞癌动脉期准确率为92.86%,门脉期准确率83.93%;对照组早期肝细胞癌准确率65.52%。研究组早期肝细胞癌诊断准确率高于对照组(P<0.05);研究组患者进行中MSCT双期增强后低密度影与等密度影占比各为3.58%,高密度影占比92.86%;肿瘤内密度均匀占比64.29%,肿瘤内密度不均占比35.71%;肿瘤边界清晰占比73.21%,肿瘤边界不清晰占比26.76%。对照组Ct平扫后低密度影占比81.03%,等密度影占比15.52%,高密度影占比3.45%;肿瘤内密度均匀占比82.76%,肿瘤内密度不均占比17.24%;肿瘤边界清晰占比36.21%,肿瘤边界不清晰占比63.79%。对照组患者与研究组患者动脉期、门脉期肿瘤与肝脏密度差存在差异(P<0.05),其中门脉期密度差最大,对照组最小。结论MSCT双期增强扫描在诊断早期肝细胞癌中诊断准确率显著高于CT平扫,可进行临床推广使用,诊断价值较高。

Detection of small hepatocellular carcinoma:Comparison of dynamic enhancement magnetic resonance imaging and multiphase multirow-detector helical CT scanning

AIM: To compare the gadolinium-enhanced multiphase dynamic magnetic resonance imaging (MRI) and multiphase multirow-detector helical CT (MDCT) scanning for detection of small hepatocellular carcinoma (HCC). METHODS: MDCT scanning and baseline MRI with SE T1-WI and T2-WI sequence combined with FMPSPGR sequence were performed in 37 patients with 43 small HCCs. Receiver operating characteristic (ROC) curves were plotted to analyze the results for modality. RESULTS: The areas below ROC curve (Az) were calculated. There was no statistical difference in dynamic enhancement MDCT and MRI. The detection rate of small HCC was 97.5%-97.6% on multiphase MDCT scanning and 90.7%-94.7% on MRI, respectively. The sensitivity of detection for small HCC on MDCT scanning was higher than that on dynamic enhancement MRI. The sensitivity of detection for minute HCC (tumor diameter ≤ 1 cm) was 90.0%-95.0% on MDCT scanning and 70.0%-85.0% on MRI, respectively. CONCLUSION: MDCT scanning should be performed for early detection and effective treatment of small HCC in patients with chronic hepatitis and cirrhosis during follow-up.

Factors for early tumor recurrence of single small hepatocellular carcinoma after percutaneous radiofrequency ablation therapy

AIM: To evaluate the factors affecting the early tumor recurrence within one year in cirrhotic patients having a single small hepatocellular carcinoma (HCC) after complete tumor necrosis by radiofrequency ablation (RFA)therapy.METHODS: Thirty patients with a single small HCC received RFA therapy by a RFA 2000 generator with LeVeen needle. Tri-phase computerized tomogram was followed every 2 to3 mo after RFA. The clinical effects and tumor recurrence were recorded.RESULTS: The initial complete tumor necrosis rate was 86.7%. Twenty-two patients were followed for more than one year. The local and overall recurrence rates were 13.6% and 36.4%, 33.3% and 56.2%, 46.6% and 56.2%at 12, 24 and 30 mo, respectively. No major complication or procedure-related mortality was found. The risk factors for early local tumor recurrence within one year were larger tumor size, poor pathologic differentiation of tumor cells and advanced tumor staging. The age of patients with new tumor formation within one year was relatively younger (55.1±8.3 vs 66.7±10.8, P = 0.029).CONCLUSION: Large tumor size, poor pathologic differentiation of tumor cells and advanced tumor staging are the risk factors for early local tumor recurrence within one year, and young age is the positive predictor for new tumor formation within one year.

Establishment of an orthotopic transplantation tumor model of hepatocellular carcinoma in mice

AIM:To improve the outcome of orthotopic transplantation in a mouse model,we used an absorbable gelatin sponge(AGS) in nude mice to establish an orthotopic implantation tumor model.METHODS:MHCC-97L hepatocellular carcinoma(HCC)cells stably expressing the luciferase gene were injected into the subcutaneous region of nude mice.One week later,the ectopic tumors were harvested and transplanted into the left liver lobe of nude mice.The AGS was used to establish the nude mouse orthotopic implantation tumor model.The tumor suppressor gene,paired box gene 5(PAX5),which is a tumor suppressor in HCC,was transfected into HCC cells to validate the model.Tumor growth was measured by bioluminescence imaging technology.Semi-quantitative reverse transcription polymerase chain reaction(RT-PCR) and histopathology were used to confirm the tumorigenicity of the implanted tumor from the MHCC-97L cell line.RESULTS:We successfully developed an orthotopic transplantation tumor model in nude mice with the use of an AGS.The success rate of tumor transplantation was improved from 60% in the control group to 100% in the experimental group using AGS.The detection of fluorescent signals showed that tumors grew in all live nude mice.The mice were divided into 3 groups:AGS-,AGS+/PAX5-and AGS+/PAX5 +.Tumor size was significantly smaller in PAX5 transfected nude mice compared to control mice(P < 0.0001).These fluorescent signal results were consistent with observations made during surgery.Pathologic examination further confirmed that the tissues from the ectopic tumor were HCC.Results from RT-PCR proved that the HCC originated from MHCC-97L cells.CONCLUSION:Using an AGS is a convenient and efficient way of establishing an indirect orthotopic liver transplantation tumor model with a high success rate.

A potential oncogenic role of the commonly observed E2F5 overexpression in hepatocellular carcinoma

AIM: To explore the expression pattern of E2F5 in primary hepatocellular carcinomas (HCCs) and elucidate the roles of E2F5 in hepatocarcinogenesis. METHODS: E2F5 expression was analyzed in 120 primary HCCs and 29 normal liver tissues by immunohistochemistry analysis. E2F5-small interfering RNA was transfected into HepG2, an E2F5-overexpressed HCC cell line. After E2F5 knockdown, cell growth capacity and migrating potential were examined. RESULTS: E2F5 was significantly overexpressed in primary HCCs compared with normal liver tissues (P = 0.008). The E2F5-silenced cells showed significantly reduced proliferation (P = 0.004). On the colony formation and soft agar assays, the number of colonies was significantly reduced in E2F5-silenced cells (P = 0.004 and P = 0.009, respectively). E2F5 knockdown resulted in the accumulation of G0/G1 phase cells and a reduction of S phase cells. The number of migrating/invading cells was also reduced after E2F5 knockdown (P = 0.021). CONCLUSION: To our knowledge, this is the first evidence that E2F5 is commonly overexpressed in primary HCC and that E2F5 knockdown significantly repressed the growth of HCC cells.

Fibrosing cholestatic hepatitis following cytotoxic chemotherapy for small-cell lung cancer

Fibrosing cholestatic hepatitis(FCH) is a variant of viral hepatitis reported in hepatitis B virus or hepatitis C virus infected liver,renal or bone transplantation recipients and in leukemia and lymphoma patients after conventional cytotoxic chemotherapy.FCH constitutes a well-described form of fulminant hepatitis having extensive fibrosis and severe cholestasis as its most characteristic pathological findings.Here,we report a case of a 49-year-old patient diagnosed with small-cell lung cancer who developed this condition following conventional chemotherapy-induced immunosuppression.This is the first reported case in the literature of FCH after conventional chemotherapy for a solid tumor.In addition to a detailed report of the case,a physiopathological examination of this potentially life-threatening condition and its treatment options are discussed.

Growth factor receptors and related signalling pathways as targets for novel treatment strategies of hepatocellular cancer

Growth factors and their corresponding receptors are commonly overexpressed and/or dysregulated in many cancers including hepatocellular cancer （HCC）. Clinical trials indicate that growth factor receptors and their related signalling pathways play important roles in HCC cancer etiology and progression, thus providing rational targets for innovative cancer therapies. A number of strategies including monoclonal antibodies, tyrosine kinase inhibitors （＂small molecule inhibitors＂） and antisense oligonucleotides have already been evaluated for their potency to inhibit the activity and downstream signalling cascades of these receptors in HCC. First clinical trials have also shown that multi-kinase inhibition is an effective novel treatment strategy in HCC. In this respect sorafenib, an inhibitor of Raf-, VEGF- and PDGF-signalling, is the first multi-kinase inhibitor that has been approved by the FDA for the treatment of advanced HCC. Moreover, the serine-threonine kinase of mammalian target of rapamycin （mTOR） upon which the signalling of several growth factor receptors converge plays a central role in cancer cell proliferation, roTOR inhibition of HCC is currently also being studied in preclinical trials. As HCCs represent hypervascularized neoplasms, inhibition of tumour vessel formation via interfering with the VEGF/VEGFR system is another promising approach in HCC treatment. This review will summarize the current status of the various growth factor receptor-based treatment strategies and in view of the multitude of novel targeted approaches, the rationale for combination therapies for advanced HCC treatment will also be taken into account.

Platelet-activating factor in cirrhotic liver and hepatocellular carcinoma

AIM： Platelet-activating factor （PAF） is a pro-inflammatory and angiogenic lipid mediator. Here we aimed to investigate levels of PAF, lyso-PAF （the PAF precursor）, phospholipase A2 （PLA2, the enzymatic activity generating lyso-PAF）, acetylhydrolase activity （AHA, the PAF degrading enzyme） and PAF receptor （PAF-R） transcripts in cirrhotic liver and hepatocellular carcinoma （HCC）. METHODS： Twenty-nine patients with HCC were enrolled in this study. Cirrhosis was present in fourteen patients and seven had no liver disease. Tissue PAF levels were investigated by a platelet-aggregation assay. Lyso- PAF was assessed after its chemical acetylation into PAR AHA was determined by degradation of [^3H]-PAE PLA2 levels were assessed by EIA. PAF-R transcripts were investigated using RT-PCR. RESULTS： Elevated amounts of PAF and PAF-R transcripts 1 （leukocyte-type） were found in cirrhotic tissues as compared with non-cirrhotic ones. Higher amounts of PAF and PAF-R transcripts 1 and 2 （tissue-type） were found in HCC tissues as compared with non-tumor tissues. PLA2, lyso-PAF and AHA levels were not changed in cirrhotic tissues and HCC. CONCLUSION： While the role of PAF is currently unknown in liver physiology, this study suggests its potential involvement in the inflammatory network found in the cirrhotic liver and in the angiogenic response during HCC.

Inhibition effect of natural killer T cells on transplantation hepatocellular carcinoma in mice

Objective:The aim of this study was to investigate the inhibition effect of natural killer T(NKT) cells on transplantation hepatocellular carcinoma in mice.Methods:α-galactosylceramide(α-GalCer)-pulsed DC and Hep S were prepared as stimulus.Hepatoma xenograft model was established and mice were randomly divided into 4 groups(n=13 each group):(1) control group,intravenous injection of the same volume of saline.(2) mature DC group,intravenous injection of mature DC cells(4×106 cells).(3) α-GalCer-pulsed HepS group,intravenous injection of α-GalCer-pulsed HepS(4×106 cells).(4) α-GalCer-pulsed mature DC group,intravenous injection of α-GalCer-pulsed DC(4×106 cells).The changes of tumor volume in mice and survival period were measured every 2 days.Percentage of NKT cells in spleens and cytotoxicity of spleen cells were detected by flow cytometry.Tumor tissues were analyzed by histopathological examination.Results:In α-GalCer-pulsed Heps and DC groups,the average survival period was prolonged and tumor volume was markedly decreased,spleen cells and NKT cells were significantly increased,and tumor necrosis was evident,compared to the control group.Conclusion:α-GalCer-pulsed DC and HepS could activate NKT cells in vivo,also increase NKT cells cytotoxicity,inhibit the growth of hepatomas and prolong survival period.

Systematic Investigation of Berberine for Treating Hepatocellular Carcinoma Based on Network Pharmacology

Objective Liver cancer is the 4th leading cause of cancer death worldwide,and hepatocellular carcinoma(HCC)accounts for the largest proportion of these deaths.Berberine is a quaternary amine compound extracted from plants such as Coptidis Rhizoma(Huang Lian,黄连)and Phellodendri Chinensis Cortex(Huang Bo,黄柏)and is considered as a potential candidate for treating HCC.This study used network pharmacology methods,reveal the core mechanism of action of berberine in the treatment of HCC,clarify its medicinal value,and locate the anti-tumor mechanism of berberine.Methods Structural information of Berberine(PubChem CID:2353)was obtained from the NCBI PubChem;ADME parameter were obtained from the Traditional Chinese Medicine Systems Pharmacology(TCMSP)database;Berberine prediction targets were collected from symmap,stitch and targetnet databases;HCC significant targets were retrieved from OncoDB.HCC and Liverome;A PPI network was established at STRING,Prediction target of berberine therapy for HCC are collected by gene mapping;The core target,pathway,biological process(BP),cellular component(CC),and molecular function(MF)of berberine in the treatment of HCC were predicted by topological analysis and enrichment analysis;the visualized"target pathway"network diagram of berberine in the treatment of HCC was established by the software of Cytoscape.Results Through PubChem and tcmsp databases,the good drugforming properties of berberine were identified;32 prediction targets of berberine were collected in symmap,stitch and targetnet databases;566 related targets of HCC were collected in oncodb.hcc and liverome databases;10 targets of berberine treatment for HCC were predicted by gene mapping,and a PPI with 10 nodes and 34 edges was established Through topological analysis and enrichment analysis,6 topologically important targets,6 related pathways and 16 BP,6 cc and 7 MF involved in Berberine treatment of HCC were obtained.Conclusions The anticancer effect of berberine is mainly involved in the regulation of cells of hepatoma cells through complex interactions between the TB52,MAPK1,CCND1,PTGS2,ESR1 that act on Hub nodes and their associated 6 pathways.The cycle is related to the immune inflammatory response,including biological processes such as proliferation and apoptosis of liver cancer cells.

Galactosylated chitosan/5-fluorouracil nanoparticles inhibit mouse hepatic cancer growth and its side effects

AIM： To observe the curative effect of galactosylated chitosan （GC）/5-fluorouracil （5-FU） nanoparticles in liver caner mice and its side effects. METHODS： The GC/5-FU nanoparticle is a nanomate- rial made by coupling GC and 5-FU. The release experiment was performed in vitro. The orthotropic liver cancer mouse models were established and divided into control, GC, 5-FU and GC/5-FU groups. Mice in the control and GC group received an intravenous injection of 200 μL saline and GC, respectively. Mice in the 5-FU and GC/5-FU groups received 200 μL （containing 0.371 mg 5-FU） 5-FU and GC/5-FU, respectively. The tumor weight and survival time were observed. The cell cycle and apoptosis in tumor tissues were monitored by flow cytometry. The expression of p53, Bax, Bcl-2, caspase-3 and poly adenosine 50-diphosphate-ribose polymerase 1 （PARP-1） was detected by immunohistochemistry, reverse transcription-polymerase chain reaction and Western blot. The serum blood biochemical parameters and cytotoxic activity of natural killer （NK） cell and cy- totoxicity T lymphocyte （CTL） were measured. RESULTS： The GC/5-FU nanoparticle is a sustained release system. The drug loading was 6.12% ± 1.36%, the encapsulation efficiency was 81.82% ± 5.32%, and the Zeta potential was 10.34 ± 1.43 mV. The tu- mor weight in the GC/5-FU group （0.4361±0.1153 g vs 1.5801 ± 0.2821 g, P 〈 0.001） and the 5-FU （0.7932±0.1283 g vs 1.5801 ±0.2821 g, P 〈 0.001） was sig- nificantly lower than that in the control group; GC/5- FU treatment can significantly lower the tumor weight （0.4361± 0.1153 g vs 0.7932±0.1283 g, P 〈 0.001）, and the longest median survival time was seen in the GC/5-FU group, compared with the control （12 d vs 30 d, P 〈 0.001）, GC （13 d vs 30 d, P 〈 0.001） and 5-FU groups （17 d vs 30 d, P 〈 0.001）. Flow cytom- etry revealed that compared with the control, GC/5- FU caused a higher rate of G0-G1 arrest （52.79% ± 13.42% vs 23.92%±9.09%, P = 0.014 ） and apopto- sis （2.55% ±1.10% vs 11.13% ±11.73%, P 〈 0.001） in hepatic cancer cells. Analysis of the apoptosis path- ways showed that GC/5-FU upregulated the expression of p53 at both the protein and the mRNA levels, which in turn lowered the ratio of Bcl-2lBax expression; this led to the release of cytochrome C into the cytosol from the mitochondria and the subsequent activation of caspase-3. Upregulation of caspase-3 expression de- creased the PARP-1 at both the mRNA and the protein levels, which contributed to apoptosis. 5-FU increased the levels of aspartate aminotransferase and alanine aminotransferase, and decreased the numbers of platelet, white blood cell and lymphocyte and cytotoxic activities of CTL and NK cells, however, there were no such side effects in the GC/5-FU group. CONCLUSION： GC/5-FU nanoparticles can significant- ly inhibit the growth of liver cancer in mice via the p53 apoptosis pathway, and relieve the side effects and im- munosuppression of 5-FU.

Phase Ⅲ Clinical Trials of the Cell Differentiation Agent-2 （CDA-2）： Therapeutic Efficacy on Breast Cancer, Non-Small Cell Lung Cancer and Primary Hepatoma

OBJECTIVE The objective of this study was to explore the effect of CDA-2, a selective inhibitor of abnormal methylation enzymes in cancer cells, on the therapeutic efficacy of cytotoxic chemotherapy. METHODS Advanced cancer patients, all of whom had previously undergone chemotherapy, were randomly divided into 2 groups, one receiving chemotherapy only as the control group, and the other receiving CDA-2 in addition to chemotherapy as the combination group. The therapeutic efficacies and the toxic maniestations of the 2 groups were compared based on the WHO criteria. RESULTS Of 454 cancer patients enrolled in phase Ⅲ clinical trials of CDA-2, 80, 188, and 186 were breast cancer, NSCLC, and primary hepatoma patients, respectively. Among them 378 patients completed treatments according to the protocols. The results showed that the overall effective rate of the combination group was 2.6 fold that of the control group, 4.8 fold in the case of breast cancer, 2.3 fold in the case of primary hepatoma, and 2.2 fold in the case of NSCLC. Surprisingly, the combination therapy appeared to work better for stage Ⅳ than stage Ⅲ patients. CDA-2 did not contribute additional toxicity. On the contrary, it reduced toxic manifestations of chemotherapy, particularly regarding white blood cells, nausea and vomiting. CONCLUSION Modulation of abnormal methylation enzymes by CDA-2 is definitely helpful to supplement chemotherapy. It significantly increased the therapeutic efficacy and reduced the toxic manifestation of cytotoxic chemotherapy on breast cancer and NSCLC.

Enhancement of leukocyte adhesion after percutaneous irradiation in rats with hepatocellular carcinoma

AIM: To evaluate the effects of percutaneous radiation on leukocyte-endothelium interaction (LEI) in experimental hepatocellular carcinoma (HCC). METHODS: Twelve ACI rats underwent HCC-inoculation, six of which on day 12 received low-dose external radiation and six did not. After 12 h intravital microscopy was performed. RESULTS: LEI was significantly reduced in tumor tissue. However,irradiation of liver sinusoids and tumor tissue with 6 Gy led to a significant activation of leukocyte adhesion in the tumor with a marked increase of the proinflammatory cytokine TNF-α. CONCLUSION: The findings indicate that the immune-logical tumor-endothelial barrier can be overcome by external irradiation.

Axl glycosylation mediates tumor cell proliferation, invasion and lymphatic metastasis in murine hepatocellular carcinoma

AIM: To investigate the effects of Axl deglycosylation on tumor lymphatic metastases in mouse hepatocellular carcinoma cell lines. METHODS: Western blotting was used to analyze the expression profile of Axl glycoprotein in mouse hepa-tocellular carcinoma cell line Hca-F treated with tunicamycin and PNGase F 3-(4,5)-dimethylthiazol(-zyl)-3,5- diphenyltetrazolium bromide (MTT) assay, extracellular matrix (ECM) invasion assay (in vitro ) and tumor metastasis assay (in vivo ) were utilized to evaluate the effect of Axl deglycosylation on the Hca-F cell proliferation, invasion and lymphatic metastasis. RESULTS: Tunicamycin and PNGase F treatment markedly inhibited Axl glycoprotein synthesis and expression, proliferation, invasion, and lymphatic metastasis both in vitro and in vivo . In the MTT assay, proliferation was apparent in untreated Hca-F cells compared with treated Hca-F cells. In the ECM invasion assay (in vitro ), treated cells passed through the ECMatrix gel in significantly smaller numbers than untreated cells (tunicamycin 5 μg/mL: 68 ± 8 vs 80 ± 9, P=0.0222; 10 μg/mL: 50 ± 6vs 80 ± 9,P=0.0003; 20 μg/mL: 41 ± 4 vs 80 ± 9, P=0.0001); (PNGase F 8 h: 66 ± 7 vs 82 ± 8, P=0.0098; 16 h: 49 ± 4 vs 82 ± 8, P=0.0001; 24 h: 34 ± 3 vs 82 ± 8, P=0.0001). In the tumor metastasis assay (in vivo ), average lymph node weights of the untreated Hca-F group compared with treated Hca-F groups (tunicamycin 5 μg/mL: 0.84 ± 0.21 g vs 0.72 ± 0.19 g, P=0.3237; 10 μg/mL: 0.84 ± 0.21 g vs 0.54 ± 0.11 g, P=0.0113; 20 μg/mL: 0.84 ± 0.21 g vs 0.42 ± 0.06 g, P=0.0008); (PNGase F 8 h: 0.79 ± 0.15 g vs 0.63 ± 0.13 g, P=0.0766; 16 h: 0.79 ± 0.15 g vs 0.49 ± 0.10 g, P=0.0022; 24 h: 0.79 ± 0.15 g vs 0.39 ± 0.05 g, P=0.0001). Also, average lymph node volumes of the untreated Hca-F group compared with treated Hca-F groups (tunicamycin 5 μg/mL: 815 ± 61 mm 3 vs 680 ± 59 mm 3 , P=0.0613; 10 μg/mL: 815 ± 61 mm 3 vs 580 ± 29 mm 3 , P=0.0001; 20 μg/mL: 815 ± 61 mm 3 vs 395 ± 12 mm 3 , P=0.0001); (PNGase F 8 h: 670 ± 56 mm 3 vs 581 ± 48 mm 3 , P=0.0532; 16 h: 670 ± 56 mm 3 vs 412 ± 22 mm 3 , P=0.0001; 24 h: 670 ± 56 mm 3 vs 323 ± 11 mm 3 , P=0.0001). CONCLUSION: Alteration of Axl glycosylation can at-tenuate neoplastic lymphatic metastasis. Axl N-glycans may be a universal target for chemotherapy.

Relationship between hepatitis B virus infection and hepatic metastasis in non-small cell lung cancer

Objective: The purpose of the study was to explore the relationship between hepatitis B virus(HBV) infection and hepatic metastasis in non-small cell lung cancer(NSCLC). Methods: Four hundred and eighty cases of NSCLC were retrospectively analyzed from January 2003 to January 2010, and the prevalence of hepatic metastasis of NSCLC in patients with and without hepatitis B virus infection were compared. Results: In the HBV carriers' group, the prevalence of synchronous hepatic metastasis and metachronous hepatic metastasis were 13.2% and 5.9%, respectively. Meanwhile in the non-HBV group, those were 21.6% and 9.5% respectively. A significant difference between the two groups was found(P < 0.05). Conclusion: The prevalence of synchronous hepatic metastasis and metachronous hepatic metastasis in non-small cell lung cancer with HBV infection are lower than those in non-HBV infection group. Hepatic metastasis is infrequent in HBV infected cases of NSCLC.

STUDY ON SMALL HEPATOCELLULAR CARCINOMAAND ITS EXTENSION

This paper summarizes the 'study On small hepatocellular carcinoma and its extensionII in Liver CancerInstitute, Zhongshan Hospital Of Shanghai MedicaI University during the past 25 years. The results 1ndl-cated that it was an impOrtant approach to obtain long-term HCC survivOrs, of the 239 patients with 5-yearsurvival, small HCC resection accounted for 51. 4 %. It was an effective apprOach to lmprove the prognosisof HCC in the entire series, the 5-year survlval of lnpatients treated ln authorsI institution was 4. 8% in1958~1970, l2. 2 % in 197l ~ 1983, and 46. 7 % in l984~ 1995; which were correlated to the increaseProportion of small HCC resection in the series; it was more effective as compared to large HCC resection,the 5 year survival was 6l. 3 % (n= 645 ) versus 33. 6 % (n= 950). ExtensiOns of small HCC study includ-ed early detection and treatment of small recurrent HCC, Of the l47 patients wlth re-resection, the 5-yearsurvival was 48. 9% caIculated frOm the time Of first resectiOn. Another extenslon was conversiOn Of largeHCC intO small HCC, using multimodality combination treatment, 72 out of the 663 patients wlth surgical-ly verified unresectable HCCs have been converted to resectable, 5-year survival being 62' l %, wh1ch wascomparable tO that of small HCC resection. Studies on related basic aspect of small HCC such as cell originof recurrence, and mOlecular aspect of small HCC, indicated that biOlOgical characterlstics, particularly thetumor invasiveness, remalned the key link for further prolong survival after small HCC resection. Recent-ly, a'patient-like' human HCC metastatic medel in nude mice has been established. Experimental inter-ventions have also been tried. Clinical trials fOr preventiOn of recurrence after small HCC resection haveshown preliminary encouraging results. However, the IIcOst-effectivenessn Of screening, the invasiveness ofHCC, the multicentric origin, the coexisted Child C cirrhosis, etc., remained great chal1enge.

Label-free quantification of differentially expressed proteins in mouse liver cancer cells with high and low metastasis rates by a SWATH acquisition method

Label-free quantification is a valuable tool for the analysis of differentially expressed proteins identified by mass spectrometry methods.Herein,we used a new strategy:data-dependent acquisition mode identification combined with label-free quantification by SWATH acquisition mode,to study the differentially expressed proteins in mouse liver cancer metastasis cells.A total of 1528 protein groups were identified,among which 1159 protein groups were quantified and 249 protein groups were observed as differentially expressed proteins(86 proteins up-regulated and 163 down-regulated).This method provides a commendable solution for the identification and quantification of differentially expressed proteins in biological samples.