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AIM:To study the effcts of caspase recruitment domain membrane-associated guanylate kinase protein 3 (CARMA3) knockdown on the growth, migration and invasion of human colonic carcinoma HCT116 cells and to analyze the mechanism.METHODS:A colonic carcinoma cell line with CARMA3 over-expression was selected.The CARMA3 gene in the HCT116 cells was knocked down by lentivirus technique.After screening by puromycin, the stably-transfected HCT116-shCARMA3 cell line was constructed.CARMA3 expression at mRNA and protein levels was detected by real-time PCR and Western blot,respectively.The cell proliferation was analyzed by WST-1 assay and RTCA S16 system.The colony formation ability was measured by colony-forming assay.The cell cycle was analyzed by flow cytometry.The cell morphological changes were observed under microscope.The abilities of migration and invasion in vitro were observed by wound healing assay and Transwell assay.The changes of related molecules were determined by Western blot to explore the mechanism.RESULTS:The expression of CARMA3 at mRNA and protein levels in the HCT116 cells was the highest in the 4 colonic carcinoma cell lines.HCT116-shCARMA3 cells with stably-silenced CARMA3 gene were successfully established.Among them, HCT116-shCARMA3-93 cells showed the greatest inhibition of CARMA3 at mRNA and protein levels.Therefore,HCT116-shCARMA3-93 cells were chosen as the cell model.Compared with control group, the morphological changes of the HCT116-shCARMA3-93 cells had epithelial-mesenchymal transition (EMT) reversion.The abilities of proliferation, colony formation, migration and invasion in the HCT116-shCARMA3-93 cells were obviously suppressed (P<0.01).G0 /G1 phase proportion was increased and S phase proportion was correspondingly decreased (P<0.05).Bcl10 and NF-κB were down-regulated, and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT-1)showed no change.Cyclin D1 was decreased obviously and cyclin A declined slightly.Metastasis-related mar-kers matrix metalloproteinase (MMP)-2 and MMP-9 were reduced,MMP-7 remained unchanged, while tissue inhibitor of metalloproteinase(TIMP)-1 and TIMP-2 were up-regulated.Furthermore, EMT-associated molecule E-cadherin was increased, while N-cadherin, Snail, Slug and Twist were decreased to some extent.CONCLUSION:CARMA3 has an impact on the growth,migration and invasion of colonic carcinoma cell line, which is possibly related to NF-κB signaling pathway to change cell cycle and metastasis-related markers and to regulate EMT.
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Objective:To explore the association of microsatellite polymorphism of MICA gene with susceptibility to esophageal cancer.Methods: PCR-STR microsatellite genotyped technique was used to detect the polymorphism of MICA in Exon 5 in 103 cases of esophageal cancer and 84 cases of normal controls.Constructed of eukaryotic expression vector in esophageal carcinoma with high frequency of occurrence of the MICA allele.NK cells killing effect to 293T cells after alleles MICA transfected were assayed by LDH and the effect on target was 20∶1.ELISA was used to test supernatants sMICA of 293T cell after transfected.Results: Identified five allelic genes in MICA Exon 5 with esophageal cancer.Each allele and its frequency respectively were:MICA-A4(9.71%),MICA-A5(22.3%),MICA-A5.1(40.8%),MICA-A6(15.5%),MICA-A9(11.7%).MICA-A5.1 showed significant difference comparison with the control group.After 293T cell line was transfected MICA allele,MICA-A5.1 group was less sensitive to NK cytotoxicity compared to other groups[(30.4±6.3)%,P<0.05].The secretion of soluble MICA increased(135.7±6.2)pg/ml.Conclusion: Esophageal cancer was relevent with the MICA-A5.1 polymorphism of MICA Exon 5 alleles.Its risk is higher than other alleles.
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Objective:To investigate the cytotoxic effects of CTL cell induced by DCs loaded with exosomes derived from hepatoma Huh-7 cells(T-exo).Methods: Exosomes derived from hepatoma Huh-7 cells were isolated and purified by combination of ultrafiltration centrifugation and sucrose density gradient centrifugation.Morphology of exosomes was observed under transmission electron microscopy and the expression of CD 9,CD63,HSP70 and AFP was detected by Western blot.DCs were induced with peripheral blood monocytes isolated from healthy donors.Flow cytometry was used to analysis surface markers of the DCs loaded with T-exo.WST-1 light absorption measurement was adopted to evaluate the T cell proliferation ability.Annexin-V/PI Flow cytometry were respectively used to examined cytotoxicity against the tumor cells.Results:Exosomes isolated and extracted from culture supernatant of Huh-7 cells presented as circular or elliptical vesicle with bilayer membrane , unequal in size , and with diameter of 50 to 100 nm.Western blot showed that the T-exo expressed CD9,CD63,HSP70 and AFP molecules.DCs loaded with T-exo caused significantly higher T cell pro-liferation and cytotoxic effect against AFP positive Huh-7 cells as compare to gainst AFP negative SMMC 7721 cells and un-loaded control group ( P<0.05 ).Conclusion: T-exosome loaded-DC can promote proliferation and induce significant cytotoxic effect of CTL against Huh-7 cells.
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Objective To develop a simple method of determination of sorafenib in serum by reversed-phase high performance liquid chromatography (RP-HPLC) and to explore its application in sorafenib therapeutic drug monitoring (TDM).Methods Sorafenib extracted by ethyl ether-petroleum (9∶1) with internal standard of erlotinib from serum was wiped off in 60 ℃ water bath.Sorafenib was redissolved by mobile buffer and analyzed by 40 μl.Chromatographic column was Symmetry Rp18 (5 μm,4.6 mm×250 mm,waters) column in normal temperature.The mobile buffer was 28 mmol/L acetate buffer (pH 5.8)-acetonitrile (37∶63).Sorafenib and erlotinib were detected in 249 nm and 335 nm,respectively.Results The concentration range of sorafenib was 0.50-20.00 μg/ml (r =0.9999).The within-day and between-day accuracies of sorafenib were less than 4.77 % and 8.79 %,respectively.The average recovery rate was 98.48 %.Sorafenib was stable in serum or after extraction.The concentrations of sorafenib in two patients were detected.Conclusion Detection of sorafenib in serum by RP-HPLC is simple and accurate,which is available to determine sorafenib in serum.The TDM of sorafenib has clinical significance.
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Objective: To explore the significance of Th17 in hepatocellular carcinoma, expecially with HBV infection.Methods:Cytometric bead array(CBA) was employed to detect 5 cytokines(IL-2,IL-4,IL-6,IFN-γ,IL-17A)from 39 tumor and non-tumor tissues of HCC and combined clinical data for comparative statistic analysis.Results:The expression of IL-2,IL-4,IFN-γin liver cancer tissue[(4.61±0.28),(3.37±0.58),(3.08±1.08)pg/ml,respectively] was significant lower than non-cancer tissue [(5.57±0.59),(3.77±0.70),(3.69±1.20)pg/ml,respectively].Otherwise,the expression of IL-6,IL-17A in cancer tissue [(280.09±254.68), (2.66±1.66) pg/ml, respectively] was higher than non-cancer [(6.58 ±1.92), (1.49 ±0.98) pg/ml, respectively].And,whatever cancer or non-cancer tissue,the expression of IL-17A in tissue[(3.45±1.86)pg/ml] with high HBV load (>1 000 U/ml) was significant higher than tissue with low HBV load[(1.97±1.16)pg/ml].Conclusion: IL-17A was highly expressed in HCC,and IL-2,IL-4,IFN-γmay inhibit its expression,and IL-6 may promote it.Hepatitis B virus infection may promote Th17 expression,thereby reducing patient′s prognosis.
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Objective To induce the immune tolerance of heart grafts with infusion of isogeneic bone marrow mesenchymal stem cells (BMSCs) in heart transplant rats.Method Donor Wistar rats and recipient F344 rats were randomly divided into 4 groups:acute rejection group (group A),Wistar rats as the donors and F344 rats as the recipients for heart transplantation; low dose cyclosporin A(CsA) group (group B),recipient F344 rats given low dose CsA; BMSCs group (group C),recipient F344 rats given isogeneic BMSCs; BMSC and low dose CsA group (group D),the recipient F344 rats given isogeneic BMSCs and low dose CsA.The serum cytokine levels were determined,and the donor heart pathological changes and survival were observed postoperatively.The relative level of Foxp3 mRNA expression in the spleen of the recipient F344 rats was also observed.Result The blood levels of interleukin-2 (IL-2) and interferon-γ(INF-γ) were significantly reduced,but IL-4 and IL-10 levels were increased (P<0.05),and the survival time of donor heart was significantly prolonged in group D as compared with groups A,B and C (P<0.05 for all).Heart pathological examination revealed a mild acute rejection in group D,moderate acute rejection in groups B and C group,and severe acute rejection in group A respectively.The expression of Foxp3 mRNA was significantly lower in group A than in groups B,C and D (P<0.05 for all),and that in group D was significantly higher than in groups B and C (P<0.05 for both),but there was no significant difference between between groups B and C (P>0.05).Conclusion Intravenous administration of BMSCs can alleviate immunorejection in heterotopic rat heart transplantation.Low-dose CsA acts synergistically with BMSCs to significantly inhibit acute rejection after heart transplantation.The partial mechanisms involve the suppressive effect of BMSCs on the expression of Foxp3 mRNA and modulation on cytokine.
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Objective To explore the relevance of expression of MHC class Ⅰ-related molecules A (MICA) molecule and NK cells immunotherapy in esophageal cancer patients after operation.To analyze the significance of MICA expression in NK cell immunotherapy.Methods 100 patients of esophageal cancer were divided into 3 group,surgical alone group,MICA negative with NK therapy group (MICA-group) and MICA positive with NK therapy group (MICA+ group).The immunity indicators and tumor markers including the levels of CD3+,CD4+ T cells,ratio of CD4+/CD8+, NK cells,Treg cells,the levels of Th1/Th2/Th17 cytokine,the antibody IgA,IgM,IgG and the tumor markers of CEA,SCC,CA199,CYFRA21-1 were detected before treatment and after treatment 60 days.Results The positives rates of CD3+,CD4+ T cells,NK cells and the ratio of CD4+/CD8+ in peripheral blood from MICA+ patients group were higher than those of before treatment [(68.3±7.6) % vs (56.2±4.1) %,(39.8±8.2) % vs (30.8±4.7) %,(22.2±4.7) % vs (18.7±5.5) %,(1.49±0.30) vs (1.15±0.61),P < 0.05],meanwhile the levels of Treg cells was lower than those of before treatment [(8.1± 4.0) % vs (13.4±4.5) %,P < 0.05].There was no statistical significant difference of positive rate of CD8+ T cells [(26.9±6.2) % vs (27.8±7.1) %,P > 0.05].The levels of Th1 cytokin (IL-2,IFN-γand TNF-α) increased and Th2 cytokin (IL-4,IL-6 and IL-10) decreased after treatment.The level of Th17 cytokine was not different significantly (P > 0.05).The content of IgA,IgM,IgG in MICA+ group were effectively improved after treatment.The tumor markers CEA,SCC,CA199,CYFRA21-1 had no statistically change before and after treatment.Conclusion The results indicate that NK cells immunotherapy can enhance the cellular immunity and humoral immunity of MICA positive esophageal cancer patients after operation.
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Objective:To explore the role of NKG2D ligand MHC-I related molecule A (MICA) in chemotherapy combined with NK cell immunotherapy in patients with advanced esophageal cancer after surgery. Methods:A total of 90 patients with esophageal cancer from Fujian Provincial Tumor Hospital were divided into three groups after surgery:40 patients of chemotherapy alone, 25 patients of chemotherapy combined with NK cell therapy with negative expression of MICA (MICA-group), and 25 patients of chemotherapy combined with NK cells therapy with positive expression of MICA (MICA+group). The efficacy was then compared. Results:Compared with the chemotherapy alone and MICA-groups, the positive rates of CD3+, CD4+T cells, NK cells, and the CD4+/CD8+ratio in peripheral blood from MICA+group were higher than those before treatment (64.2%± 6.4%vs. 51.3%± 5.6%, 39.8%± 8.2%vs. 29.5%± 3.2%, 25.3%± 2.1%vs. 16.4%±4.3%, 1.4%± 0.5%vs. 1.1%± 0.7%;P0.05). Conclusion:Treatment with chemotherapy and autologous NK cells on patients with advanced esophageal carcinoma and MICA positive expression can be safely transfused with only minor side effects and can effectively improve a patient's immune system, quality of life, and survival.
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Objective To investigate the corresponds between NF-κB p65 activation and k-ras mutations.Methods NF-κB p65 activation was analyzed by immunochemistry in 167 colorectal cancer specimens in which the k-ras mutation status was confirmed.Resluts Among 167 colorectal cancer specimens screened,59 (35.3 %) had k-ras mutations and 63 (37.7 %) had NF-κB p65 activation.k-ras mutations and NF-κB p65 nuclear expression were no significant difference in different sex,age,ECOG score,pathological types,degrees of pathological differentiation,TNM stage,and metastases on lymph nodes (P> 0.05).The positive nuclear expression rate of NF-κB p65 was 50.8 % (30/59) in specimens with k-ras mutations and 30.6 % (33/108) in specimens with wild type k-ras.There was obviously statistical difference between them (P =0.010).Conclusion NF-κB p65 activation in coloretal cancer was associated with k-ras mutations.
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Objective To explore the expressions and significances of the tumor stem cell markers CD133-2,CD24 and CD44s in head and neck squamous cell carcinoma (HNSCC) tissues and their association with the clinical pathologic characteristics.Methods Expressions of CD133-2,CD24 and CD44s were analyzed by immunohistochemistry (SP) in 83 cases of primary HNSCC tissues and 46 cases of normal epithelia.Clinicopathological indexes were assessed.Results In primary HNSCC tissues and normal epithelia,the expression rates of CD133-2 and CD24 were 9.64 % (8/83),21.74 % (10/46) and 90.36 % (75/83),46.67 % (21/46)respectively,which had statistically significances (x2 =15.040,5.818,P < 0.05).CD44s expression was detected in primary HNSCC tissues and normal epithelia,but their staining scores had statistical significance (Z =-4.262,P < 0.05).In primary HNSCC tissues,the expression of CD133-2 had negative correlation with differentiation degree (x2 =7.246,P < 0.05),but CD24 and CD44s had positive correlation with differentiation degree (x2 =9.005,44.765,P < 0.05).In addition,the expression of CD44s in primary HNSCC tissues had negative correlation with T classification (x2 =4.650,P < 0.05).Conclusion The expressions of CD24 and CD44s in primary HNSCC tissues are highly up-regulated with tumor cells differentiation,and further research needs to be performed to discover whether or not CD24 and CD44s could be the markers of tumor stem cells of HNSCC.The expression of CD133-2 in primary HNSCC tissues is highly down-regulated with tumor cell differentiation.As one of the tumor stem cell markers of HNSCC,CD133-2 may play an important role in the development and clinical outcomes of tumor.
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Objective To evaluate the clinical effects of cytokine-induced killer (CIK) cells combined with chemotherapy on the treatment of patients with advanced colorectal cancer.Methods CIK cells were prepared from 50 ml peripheral blood mononuclear cells by stimulated with IL-2,IFN-γ,anti-CD3 monoclone antibody,IL-1 for 8 d.The clinical effects and survival rate were compared between CIK cells combined with chemotherapy group and the chemotherapy group (50 patients with advanced colorectal cancer for each).T cells and NK cells of patients were tested by FCM before and after CIK cells treatment.The improvement of quality of life and toxicity of this therapy were observed.Results The percentages of CD3+,CD4+,CD8+ T cells and NK cells were (54.779±14.228) %,(30.821±11.554) %,(16.676±6.256) %,(18.705±9.347) % before CIK cells transfusion.After transfusion,the percentages were (65.236±14.901) %,(37.292±8.880) %,(25.229±6.711) %,(22.950±8.933) %,respectively.The percentages were expanded greatly (P < 0.05).The patients quality of life were improved clearly with lower toxicity.The DCR of CIK cells combined with chemotherapy group (64 %,32/50) was higher than the chemotherapy group (40 %,20/50) (P < 0.05).The survival rate between two groups had no statistical significance (P > 0.05).Conclusion Administration of CIK cells combined with chemotherapy can enhance immune function in patients with advanced colorectal cancer and improve their quality of life,and get good clinical efficacy.
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Objective To investigate the expression of arginase Ⅰ(ARG1)in hepatocellular carcinoma(HCC)and to analyze its correlation with clinicopathological features.Methods The expression of ARG1 at protein level in 167 samples of HCC and corresponding adjacent liver tissue was detected with high-throughput tissue microarray technique and immunohistochemistry.The correlation between ARG1 expression and clinicopathological features was analyzed with x2 test and Spearman rank correlation analysis.The expression of ARG1 at mRNA level in 68 samples of HCC and corresponding adjacent liver tissue was determined by real-time polymerase chain reaction(real-time PCR).Results The expression of ARG1 at protein level in HCC(3.540±3.702)was significantly lower than that of the corresponding adjacent liver tissues(10.290 ± 2.303)(t=-22.421,P=0.000).The ARG1 expression was correlated with differentiation degree of HCC,histological grade,vascular invasion,preoperative level of α-fetoprotein(AFP)and recurrence after operation(all P<0.05).The ARG1 expression at mRNA level in 68 HCC tissue[0.0997(0.213)]was lower than that of the corresponding adjacent liver tissues[0.563(0.459)],and the difference was statistical significant(u=-6.544,P=0.000).Conclusion Low expression of ARG1 in HCC may take part inHCC genesis and development.Detecting the expression of ARG1 may be helpful in HCC diagnosis,differentiation degree and prognosis assessment.
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Objective To analyze the influence of peptidimer-c on the gene expression profiling of K562 cells and investigate the mechanism of peptidimer-c inducing the apoptosis and inhibiting proliferation of K562cells.Methods Trypan blue staining technique was performed for counting the number of living K562 cells treated with peptidimer-c.The ultrastructure changes of K562 cells treated with peptidimer-c was observed under transmission electron microscope.The Human U133 Plus 3.0 gene chips were used to detect the differentially expressed genes of K562 cells treated with peptidimer-c.Reverse transcription PCR was conducted to confirm some genes identified by gene chips.Results Peptidimer-c could induce the apoptosis and inhibit the proliferation of K562 cells.Peptidimer-c caused widely changes of the gene expression profiles of K562 cells.The chip data suggested that there were 529 differentially expressed genes,of which 455 genes were up-regulated and 74 genes were down-regulated.The relevant apoptotic genes were down-regulated markedly,including JUN,AXUD1,TNFRSF10B,etc.Fifteen of the differentially expressed genes were detected by RT-PCR,which was consistent with the chip data.Conclusion Peptidimer-c may induce aooptosis of K562 cells by activating the TNF/TNFR family and the JUN family.
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In recent years, the study on the molecular mechanism of tumorigenesis and cancer cell signals promotes the application of cancer-targeted therapy, which aims at cell receptors, key genes, and regulatory molecules in cancer cells. However, the polymorphism of targeting genes/molecules determines the clinical efficiency of these therapies. The application of gene polymorphism diagnosis in cancer-targeted therapy was reviewed.
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The current strategies of anti-cancer therapy are mainly based on the evidence-based medicine, which is much better than be based on the doctor's experience. But we still need to make attempts to find the right drugs and doses for each patient. The patients with the same disease may receive different response to the same treatment because of their inherited and somatic genetic variability. This results in greatly different therapeutic outcome. The determination of anti-cancer drugs and the doses based on the individual genotype will open up a new era of personalized therapy.
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Objective:To study the alteration of K-ras mutations in different stages of colorectal cancer(CRC) and its influence on the progression of CRC. Methods:The 20 paraffin-embedded tissues, including primary foci, metastatic lymph nodes, remoter metastatic foci, colorectal adenoma, and normal colorectal tissues, were collected from 20 patients with colorectal cancer. The sequence of PCR-amplified products were analyzed. Results:The wild K-ras gene was expressed in normal colorectal tissues. The mutation frequency of K-ras gene was 20.0% (4/20) in colorectal adenoma, 30.0% (6/20) in primary foci, 25.0% (5/20) in metastatic lymph nodes, and 30% (6/20) in remote metastatic lesions. In the samples with K-ras mutations, the consistency of the types of K-ras mutations between primary foci and colorectal carcinoma, lymph node metastatic lesions, remote metastatic lesions was 0.0%(0/4), 40.0%(2/5), and 50.0%(3/6), respectively.Conclusion:The colorectal adenoma, metastatic lymph nodes and remote metastatic lesions were not suited for K-ras analysis as routine samples in clinical practice. If the samples of primary lesions were not available, the detection results of metastatic lymph nodes and remote metastatic remote lesions will provide some reference values. K-ras gene had several different mutations in the progression of CRC.
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Objective To investigate the advantages of detection for EGFR gene mutations by denaturing high performance liquid chromatography (DHPLC) technology. Methods DHPLC was used to detect EGFR gene mutations at exon 19 and 21 in 49 cases of non-small cell lung cancer (NSCLC) patients,and the direct DNA sequencing was used to verify the accuracy of DHPLC detection. Results EGFR gene mutation was identified from 13 of 49 cases by DHPLC,including deletion mutation at exon 19 in 10 cases (76.92 %) and alternative mutations at exon 21 in 3 cases (23.08 %). Mutation results of DHPLC was consistent with DNA direct sequencing. The results of the direct DNA sequencing were the same as those of DHPLC. The sensitivity of mutation test by DHPLC was 100 %. Conclusion DHPLC technology can be used for large scale screening of EGFR gene mutation with rapid and accuracy.
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Objective To observe the expression of cytotoxicity and receptors on NK cells in breast cancer,and investigate the impact of soluble MICA(sohble MHC class Ⅰ-related molecules A,sMICA) on NK cells receptors expression and cytotoxicity.Methods ELISA was used to examine the sMICA in peripheral blood.The expressions of activated receptor(NKG2D),killer inhibitory receptor (KIR)(CD158b) and NK cells were identified by flow cytometry(FCM).Cytotoxicity of NK cells to breast cancer were tested by MTT.Results sMICA was (205.36±71.27)ng/L in breast cancer patients and 81.6 % samples were detected.There were positive correlations between sMICA levels with breast cancer stages.There were no difference of NK cells percentage between breast cancer and healthy person.The cytotoxicity of NK cells and expressions of NKG2D were obviously lower in breast cancer with sMICA(+) than in healthy person,but CD158b was higher in healthy person.After cultured with sMICA,NK cells cytotoxicity decreased from(76.2±6.7)% to(48.4±4.1)% and the expression of NKG2D reduced from(92.5±7.1)% to (62.5±6.4)%,but the the expression of CD158b increased from(10.6±3.2)% to (43.6±3.4)%.IL-15 up regulated the expression of NKG2D and NK cells cytotoxicity,but decreased the expression of CD158b by co-culturation with IL-15 and sMICA in sMICA+ patients with breast cancer.Conclusion sMICA reduced the expression of NKG2D and increased the expression of Kill,which lead to the down regulation of NK cells cytotoxicity.IL-15 can reverse this effect.
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Objective To screen serum biomarkers in patients with hepatocelhlar carcinoma by using surface-enhanced laser desorption and ionization time-of-flight mass spectrometry(SELDI-TOF-MS)technique and to evaluate its clinical implication in the patients whose alpha-fetoprotein were negative in the sera. Methods Proteomic spectra were generated by mass spectroscopy in 112 cases, including 57 cases AFP-negative hepatocellular carcinoma,and 55 cases of healthy control. The consequence was analyzed and the characteristic preteomic peaks was selected by using Biomarker Wizard. Results Seven low expressed potential biomarker were indentified with the mass-to-charge ratio of 4.2×103, 4.1×103, 6.7×103, 5.7×103, 6.5×103, 6.9×103, 5.8×103. The sensitivity for diagnosing hepatic cancer were 88.23 % and specificity was 92.31%. These peaks were not correlated with age, sex, tumor mass size, pathology grading and cirrhosis in hepatocellular carcinoma. Conclusion SELDI-TOF-MS offers a unique platform for the proteomic detection of hepatocellular carcinoma.It also offers an auxiliary diagnosis method to the patients whose alpha-fetoprotein are negative in the serum.
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Background and purpose: Renal-cell carcinoma (RCC) is susceptible to immune therapy including the use of the nonmyeloablative allogeneic transplantation(NAT). However, NST can produce severe toxicity, so it might not be appropriate for many patients with metastatic RCC. Other novel allogeneic immunotherapies have been designed to induce an autologous immune response directed against the malignancy. This study evaluated the efficacy and safety of infusions of partially HLA-matched irradiated allogeneic blood mononuclear cells for advanced renal-cell carcinoma. Methods: Patients with histologically proven diagnosis of advanced RCC received infusions of partially HLA-matched allogeneic blood mononuclear cells. Repeat infusions were given every 8 weeks. Treatment was continued until disease progressed, unacceptable toxicity, or patient (or donor) choice. Results: Eight patients were enrolled. After every infusion, 6 patients received an oral administration of thalidomide daily with 100-300 mg/d for 2 months. One patient had durable complete response. Five stable diseases and two progress diseases were observed. In eight patients, time to progression and survival were 320 and 879+days, respectively. Severe toxicity was not observed. Conclusion: Infusions of partially HLA-matcbed irradiated allogeneic blood mononuclear cells for advanced RCC may induce some antitumor effects and deserves further study.