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Volume 13,Issue 5,2006 Table of Contents
2006, 13(5):321-324.
DOI: 10.3872/j.issn.1007-385X.2006.5.001
Abstract:
2006, 13(5):325-328.
DOI: 10.3872/j.issn.1007-385X.2006.5.002
Abstract:
2006, 13(5):329-331.
DOI: 10.3872/j.issn.1007-385X.2006.5.003
Abstract:
2006, 13(5):332-337.
DOI: 10.3872/j.issn.1007-385X.2006.5.004
Abstract:
Objective: To prepare monoclonal antibody for inhibition of adhesion between esophageal carcinoma and pulmonary vascular endothelia, so as to pave a way for the targeted treatment of esophageal carcinoma metastasis.Methods: Tumor cells were separated from esophageal carcinoma tissues and were used to immunize Balb/c mouse. The spleen cells of the immunized mouse were fused with SP2/0 cells. The anti-adhesion antibodies were then screened and identified by ELISA, immunohistochemistry, immunofluorescence, tumor-endothelial cell adhesion assay, and Western blotting. Results: Totally 1 134 clones of monoclonal antibodies were obtained after fusion. Among the 486 clones which could interact with the membrane of the esophageal carcinoma, 294 clones had no or weak reactions with normal esophageal epithelia. The 15 selected clones significantly suppressed the adherence between esophageal cancer cells and lung endothelia. Western blotting displayed that 2 of the clones reacted with the antigens having a molecular weight of 30 000 and 60 000, respectively.Conclusion: We have successfully obtained several clones of functional monoclonal antibodies which can suppress the adherence of esophageal carcinoma cells with lung micro-vascular endothelia, and 2 of the clones show promise in anti metastasis therapy of esophageal carcinoma.
Objective: To prepare monoclonal antibody for inhibition of adhesion between esophageal carcinoma and pulmonary vascular endothelia, so as to pave a way for the targeted treatment of esophageal carcinoma metastasis.Methods: Tumor cells were separated from esophageal carcinoma tissues and were used to immunize Balb/c mouse. The spleen cells of the immunized mouse were fused with SP2/0 cells. The anti-adhesion antibodies were then screened and identified by ELISA, immunohistochemistry, immunofluorescence, tumor-endothelial cell adhesion assay, and Western blotting. Results: Totally 1 134 clones of monoclonal antibodies were obtained after fusion. Among the 486 clones which could interact with the membrane of the esophageal carcinoma, 294 clones had no or weak reactions with normal esophageal epithelia. The 15 selected clones significantly suppressed the adherence between esophageal cancer cells and lung endothelia. Western blotting displayed that 2 of the clones reacted with the antigens having a molecular weight of 30 000 and 60 000, respectively.Conclusion: We have successfully obtained several clones of functional monoclonal antibodies which can suppress the adherence of esophageal carcinoma cells with lung micro-vascular endothelia, and 2 of the clones show promise in anti metastasis therapy of esophageal carcinoma.
2006, 13(5):338-342.
DOI: 10.3872/j.issn.1007-385X.2006.5.005
Abstract:
Objective: To investigate the effects of three-dimensional microstructures of silicon and glass substrates on the growth of breast cancer cell line MCF-7. Methods: Three-dimensional microstructures (grooves, pentagons, and gear wheels) of silicon and glass substrates were fabricated by micro-fabrication technology, and were then co-cultured with MCF-7 cells for 1- 4 days. Phase contrast microscope and scanning electron microscopy were used to observe the distribution, size, shape, and growth of MCF-7 cells, MTT was used to analyze the effects of the microstructures on the proliferation of MCF-7 cells, and flow cytometry was used to analyze the amounts of apoptosis cells. Results: These microstructures, including grooves, pentagram and gear wheels, were successfuly fabricated by micro-fabrication technology. MCF-7 cells were prone to grow on the bottom of grooves, pentagram and gear wheels; few cells were observed on the top and sidewalls of microstructures. Round suspension cells gradually increased as the cell culture time increased. Few cells existed on the surface of control silicon substrate, and the adhesive cells were easily detached from the substrate; however, abundant spindle-shaped MCF-7 cells grew evenly on the surface of glass substrate. MTT analysis showed that as the culture time increased, the inhibition of cell proliferation on the microstructures on the glass and silicon substrates decreased gradually (P<0.01，P<0.05); flow cytometry analysis showed that as the culture time increased, apoptosis cell number also increased gradually (P<0.01，P<0.05). Conclusion: Micron level microstructures, such as grooves, pentagram and gear wheels on the substrates of silicon and glass, can inhibit the growth of MCF-7 cells and induce cell apoptosis, which hold much potential for application in tumor therapy.
Objective: To investigate the effects of three-dimensional microstructures of silicon and glass substrates on the growth of breast cancer cell line MCF-7. Methods: Three-dimensional microstructures (grooves, pentagons, and gear wheels) of silicon and glass substrates were fabricated by micro-fabrication technology, and were then co-cultured with MCF-7 cells for 1- 4 days. Phase contrast microscope and scanning electron microscopy were used to observe the distribution, size, shape, and growth of MCF-7 cells, MTT was used to analyze the effects of the microstructures on the proliferation of MCF-7 cells, and flow cytometry was used to analyze the amounts of apoptosis cells. Results: These microstructures, including grooves, pentagram and gear wheels, were successfuly fabricated by micro-fabrication technology. MCF-7 cells were prone to grow on the bottom of grooves, pentagram and gear wheels; few cells were observed on the top and sidewalls of microstructures. Round suspension cells gradually increased as the cell culture time increased. Few cells existed on the surface of control silicon substrate, and the adhesive cells were easily detached from the substrate; however, abundant spindle-shaped MCF-7 cells grew evenly on the surface of glass substrate. MTT analysis showed that as the culture time increased, the inhibition of cell proliferation on the microstructures on the glass and silicon substrates decreased gradually (P<0.01，P<0.05); flow cytometry analysis showed that as the culture time increased, apoptosis cell number also increased gradually (P<0.01，P<0.05). Conclusion: Micron level microstructures, such as grooves, pentagram and gear wheels on the substrates of silicon and glass, can inhibit the growth of MCF-7 cells and induce cell apoptosis, which hold much potential for application in tumor therapy.
GAN Hui-zhu
,
ZHANG Gui-zhen
,
ZHANG Feng-chun
,
BU Li-sa
,
YANG Shao juan
,
GAO Shen
,
ZHENG De-ming
2006, 13(5):343-348.
DOI: 10.3872/j.issn.1007-385X.2006.5.006
Abstract:
Objective: To reverse multidrug resistance (MDR) of human breast cancer cell line (MCF-7/AdrR) to adriamycin (ADM) with short hairpin RNA (shRNA) expression vectors. Methods: Two shRNA expression vectors harboring MDR1 gene were constructed and introduced into MCF-7/AdrR cells. Expression of MDR1 mRNA was assessed by RT-PCR and P-gp expression was determined by Western blotting. The apoptosis and sensibility of the breast cancer cells to ADM were evaluated by flow cytometry and MTT assays, respectively. Cellular daunorubicin accumulation was assayed by laser scanning confocal microscope (LSCM).Results: RT-PCR showed that MDR1 mRNA expression was significantly reduced to 37.6 % (P<0.05) and 28.0% (P<0.01) in MCF-7/AdrA cells stably transfected with pSilencerTM 3.1-H1 neo MDR1-A and MDR1-B shRNA, respectively. Western blotting showed that P-gp expression was inhibited significantly and specifically. Resistance against ADM was decreased from 162-fold to 108-fold (P<0.05 ) and 50-fold (P<0.01 ). Furthermore, shRNA vectors significantly enhanced the cellular daunorubicin accumulation. MDR1 shRNA vectors combined with ADM significantly induced the apoptosis of MCF-7/AdrR cells. Conclusion: shRNA vectors can effectively reverse MDR and can restore the sensitivity of drug-resistance cancer cells to conventional chemotherapeutic agents.
Objective: To reverse multidrug resistance (MDR) of human breast cancer cell line (MCF-7/AdrR) to adriamycin (ADM) with short hairpin RNA (shRNA) expression vectors. Methods: Two shRNA expression vectors harboring MDR1 gene were constructed and introduced into MCF-7/AdrR cells. Expression of MDR1 mRNA was assessed by RT-PCR and P-gp expression was determined by Western blotting. The apoptosis and sensibility of the breast cancer cells to ADM were evaluated by flow cytometry and MTT assays, respectively. Cellular daunorubicin accumulation was assayed by laser scanning confocal microscope (LSCM).Results: RT-PCR showed that MDR1 mRNA expression was significantly reduced to 37.6 % (P<0.05) and 28.0% (P<0.01) in MCF-7/AdrA cells stably transfected with pSilencerTM 3.1-H1 neo MDR1-A and MDR1-B shRNA, respectively. Western blotting showed that P-gp expression was inhibited significantly and specifically. Resistance against ADM was decreased from 162-fold to 108-fold (P<0.05 ) and 50-fold (P<0.01 ). Furthermore, shRNA vectors significantly enhanced the cellular daunorubicin accumulation. MDR1 shRNA vectors combined with ADM significantly induced the apoptosis of MCF-7/AdrR cells. Conclusion: shRNA vectors can effectively reverse MDR and can restore the sensitivity of drug-resistance cancer cells to conventional chemotherapeutic agents.
2006, 13(5):349-352.
DOI: 10.3872/j.issn.1007-385X.2006.5.007
Abstract:
Objective: To analyze the expression of HLA class Ⅰ molecules and MHC classⅠ related chain A and B (MICA/MICB) in human nasopharyngeal carcinoma cell line (CNE2) and multi-drug resistant nasopharyngeal carcinoma cell line (CNE2/ DDP), and to assess their influence on NK cell-mediated lysis.Methods: Expression of HLA classⅠ molecules and MICA/MICB on the surface of CNE2 and CNE2/DDP cell lines was analyzed by flow cytometry. Cytotoxicity of NK cells (isolated from 3 healthy persons) against CNE2 and CNE2/DDP cells were detected by LDH releasing assay at different effect-to-target cell ratios (E∶T). In blocking experiments, anti-MHC class Ⅰ monoclonal antibody (mAb) (W6/32, a pan anti-HLA class Ⅰ antibody) and anti-MHC class I chain related molecules mAb (BAMO-1, specificly against MICA and MICB) were added to the target cells at a E∶T ratio of 10∶1. Results:It was found that the expression of HLA class Ⅰ molecules and MICA/MICB on CNE2 was higher than that on CNE2/DDP(Ｐ<0.01). Cytotoxicity of NK cells against CNE2 and CNE2/DDP cells was (9.37±2.14) %, (4.37±0.63 )% at E∶T ratio of 5∶1, (27.14±1.82)%, (15.79±2.87)% at E∶T ratio of 10∶1, (36.40±4.28)%, (26.20±4.18)% at E∶T ratio of 20∶1, and (54.67±2.80)%, (40.29±2.73)% at E∶T ratio of 30∶1, respectively. NK cells displayed higher cytotoxicity against parental CNE2 cells than multi-drug resistant CNE2/DDP cells(P<0.01). Expression of HLA classⅠ molecules and MICA/MICB on CNE2, CNE2/DDP cells was correlated with NK cell-mediated lysis. Blocking experiments confirmed that the killing of CNE2, CNE2/DDP cells was efficiently inhibited by BAMO-1, whereas efficiently increased by W6/32. Conclusion: Low expression of MICA/MICB in multi-drug resistant tumor cell lines leads to reduction of their susceptibility to NK lysis.
Objective: To analyze the expression of HLA class Ⅰ molecules and MHC classⅠ related chain A and B (MICA/MICB) in human nasopharyngeal carcinoma cell line (CNE2) and multi-drug resistant nasopharyngeal carcinoma cell line (CNE2/ DDP), and to assess their influence on NK cell-mediated lysis.Methods: Expression of HLA classⅠ molecules and MICA/MICB on the surface of CNE2 and CNE2/DDP cell lines was analyzed by flow cytometry. Cytotoxicity of NK cells (isolated from 3 healthy persons) against CNE2 and CNE2/DDP cells were detected by LDH releasing assay at different effect-to-target cell ratios (E∶T). In blocking experiments, anti-MHC class Ⅰ monoclonal antibody (mAb) (W6/32, a pan anti-HLA class Ⅰ antibody) and anti-MHC class I chain related molecules mAb (BAMO-1, specificly against MICA and MICB) were added to the target cells at a E∶T ratio of 10∶1. Results:It was found that the expression of HLA class Ⅰ molecules and MICA/MICB on CNE2 was higher than that on CNE2/DDP(Ｐ<0.01). Cytotoxicity of NK cells against CNE2 and CNE2/DDP cells was (9.37±2.14) %, (4.37±0.63 )% at E∶T ratio of 5∶1, (27.14±1.82)%, (15.79±2.87)% at E∶T ratio of 10∶1, (36.40±4.28)%, (26.20±4.18)% at E∶T ratio of 20∶1, and (54.67±2.80)%, (40.29±2.73)% at E∶T ratio of 30∶1, respectively. NK cells displayed higher cytotoxicity against parental CNE2 cells than multi-drug resistant CNE2/DDP cells(P<0.01). Expression of HLA classⅠ molecules and MICA/MICB on CNE2, CNE2/DDP cells was correlated with NK cell-mediated lysis. Blocking experiments confirmed that the killing of CNE2, CNE2/DDP cells was efficiently inhibited by BAMO-1, whereas efficiently increased by W6/32. Conclusion: Low expression of MICA/MICB in multi-drug resistant tumor cell lines leads to reduction of their susceptibility to NK lysis.
2006, 13(5):353-357.
DOI: 10.3872/j.issn.1007-385X.2006.5.008
Abstract:
Objective: To screen for proteins which can interact with phosphotyrosine-interacting domain (PID) of differentially expressed gene in human ovarian cancer cell line DOC-2 by yeast-two hybrid technique, so as to provide evidence for the signal pathway of DOC-2. Methods: The cDNA sequence of human DOC-2 gene was amplified and its PID domain (nDOC-2) was subcloned into the bait vector pGBKT7 of yeast two-hybrid system; the product was then used to screen an embryo brain cDNA library and the proteins interacting with nDOC-2 were identified. Quadrople dropout(QDO) medium and X-α-gal were used for selecting the positive clones. PCA was used to analyze the amplified sequence. After elimination of the false positive clones, the positive clones were sequenced and analyzed by bioinformatic methods. Results:Twenty-one candidate positive clones were obtained and 3 of them were plasmids encoding Homo sapiens partial mRNA for betaglycan (TBR III gene), Homo sapiens protocadherin gamma subfamily C 3 (PCDHGC3), and APLP1（amyloid beta precursor-like protein 1）.Conclusion: The proteins obtained in this study may play important roles in the signal pathway of DOC-2, which provides a new orientation for DOC-2 gene therapy of ovarian cancers
Objective: To screen for proteins which can interact with phosphotyrosine-interacting domain (PID) of differentially expressed gene in human ovarian cancer cell line DOC-2 by yeast-two hybrid technique, so as to provide evidence for the signal pathway of DOC-2. Methods: The cDNA sequence of human DOC-2 gene was amplified and its PID domain (nDOC-2) was subcloned into the bait vector pGBKT7 of yeast two-hybrid system; the product was then used to screen an embryo brain cDNA library and the proteins interacting with nDOC-2 were identified. Quadrople dropout(QDO) medium and X-α-gal were used for selecting the positive clones. PCA was used to analyze the amplified sequence. After elimination of the false positive clones, the positive clones were sequenced and analyzed by bioinformatic methods. Results:Twenty-one candidate positive clones were obtained and 3 of them were plasmids encoding Homo sapiens partial mRNA for betaglycan (TBR III gene), Homo sapiens protocadherin gamma subfamily C 3 (PCDHGC3), and APLP1（amyloid beta precursor-like protein 1）.Conclusion: The proteins obtained in this study may play important roles in the signal pathway of DOC-2, which provides a new orientation for DOC-2 gene therapy of ovarian cancers
2006, 13(5):358-361.
DOI: 10.3872/j.issn.1007-385X.2006.5.009
Abstract:
Objective: To construct a liver targeting gene transfer vector using hepatitis B virus envelope particles. Methods: Hepatitis B viruses were obtained from the supernatant of HepG 2.2.15 cells by a PEG8000 system and were inactivated by β-propiolactone to prepare hepatitis B virus envelope. The hepatitis B virus envelope was used to pack 5.3 kb pIRES2-EGFP to assess their packing ability. Subsequently, the products were studied with ELISA, PCR, SDS-PAGE, and electron microscopy. Finally, the product was used to transfect HepG2 cells and the green fluorescent protein (GFP) expression was observed under a fluorescent microscope. The rate of GFP positive cells was determined by flow cytometer.Results: The acquired hepatitis B virus envelope retained the surface protein HBsAg+pre S1+pre S2, but with no virus DNA. The prepared envelope had high packing ability for GFP and the packed GFP had a high transfection rate in HepG2 cell. Conclusion: Hepatitis B virus envelope has been successfully obtained from the supernatant of HepG 2215 cells with a PEG8000 system and β-propiolactone.
Objective: To construct a liver targeting gene transfer vector using hepatitis B virus envelope particles. Methods: Hepatitis B viruses were obtained from the supernatant of HepG 2.2.15 cells by a PEG8000 system and were inactivated by β-propiolactone to prepare hepatitis B virus envelope. The hepatitis B virus envelope was used to pack 5.3 kb pIRES2-EGFP to assess their packing ability. Subsequently, the products were studied with ELISA, PCR, SDS-PAGE, and electron microscopy. Finally, the product was used to transfect HepG2 cells and the green fluorescent protein (GFP) expression was observed under a fluorescent microscope. The rate of GFP positive cells was determined by flow cytometer.Results: The acquired hepatitis B virus envelope retained the surface protein HBsAg+pre S1+pre S2, but with no virus DNA. The prepared envelope had high packing ability for GFP and the packed GFP had a high transfection rate in HepG2 cell. Conclusion: Hepatitis B virus envelope has been successfully obtained from the supernatant of HepG 2215 cells with a PEG8000 system and β-propiolactone.
2006, 13(5):362-366.
DOI: 10.3872/j.issn.1007-385X.2006.5.010
Abstract:
Objective: To observe the targeting therapy of the hdsFv-RC-RNase recombinant single chain immunotoxin on the xenograft of the human hepatocellular carcinoma in nude mice and to explore its clinical potentiality. Methods: The prokaryotic expression vector TIG-hdsFv-RC-RNase was transformed into E.coli BL21（DE3）plys to largely express recombinant single chain immunotoxin hdsFv-RC-RNase against hepatocellular carcinoma induced by IPTG. The expressed product was purified via Ni-NTA affinity chromatography under native conditions and mildly refolded. The ELISA was used to analyze its immunological activity of antigen-binding capability. The xenogrft model of the human hepatocellular carcinoma in nude mice was established and the targeting therapy of hdsFv-RC-RNase was evaluated. Results:After induced by IPTG, a new protein band with Mr 41 000 was found in the supernatant of the bacteria and expressed in a soluble form. The expressed product was purified to homogeneity via Ni-NTA affinity chromatography under native conditions. The results of ELISA showed the refolded hdsFv-RC-RNase had the specific antigen-binding capability to the human hepatocellular carcinoma cell, but not to the normal hepatocyte (P＜0.01). The targeting therapy on the xenograft in nude mice indicated that the efficiency of the hdsFv-RC-RNase was 100%(P＜0.01). The tumor inhibition rate reached 79.38%. Conclusion: The recombinant immunotoxin hdsFv-RC-RNase has been obtained sussefully, which has high activity and targeting therapy on hepatocellular carcinoma xinograft in nude mice. It may be used as targeting drug in therapy of hepatocellular carcinoma.
Objective: To observe the targeting therapy of the hdsFv-RC-RNase recombinant single chain immunotoxin on the xenograft of the human hepatocellular carcinoma in nude mice and to explore its clinical potentiality. Methods: The prokaryotic expression vector TIG-hdsFv-RC-RNase was transformed into E.coli BL21（DE3）plys to largely express recombinant single chain immunotoxin hdsFv-RC-RNase against hepatocellular carcinoma induced by IPTG. The expressed product was purified via Ni-NTA affinity chromatography under native conditions and mildly refolded. The ELISA was used to analyze its immunological activity of antigen-binding capability. The xenogrft model of the human hepatocellular carcinoma in nude mice was established and the targeting therapy of hdsFv-RC-RNase was evaluated. Results:After induced by IPTG, a new protein band with Mr 41 000 was found in the supernatant of the bacteria and expressed in a soluble form. The expressed product was purified to homogeneity via Ni-NTA affinity chromatography under native conditions. The results of ELISA showed the refolded hdsFv-RC-RNase had the specific antigen-binding capability to the human hepatocellular carcinoma cell, but not to the normal hepatocyte (P＜0.01). The targeting therapy on the xenograft in nude mice indicated that the efficiency of the hdsFv-RC-RNase was 100%(P＜0.01). The tumor inhibition rate reached 79.38%. Conclusion: The recombinant immunotoxin hdsFv-RC-RNase has been obtained sussefully, which has high activity and targeting therapy on hepatocellular carcinoma xinograft in nude mice. It may be used as targeting drug in therapy of hepatocellular carcinoma.
2006, 13(5):367-370.
DOI: 10.3872/j.issn.1007-385X.2006.5.011
Abstract:
Objective: To inhibit c-myc gene expression in human rectal cancer cell line Colo320 by small interfering RNA technique, so as to assess the role of c-myc in Colo320 cells. Methods: The c-myc gene specific siRNA was designed and prepared by in vitro transcription. The prepared c-myc siRNA was transfected into Colo320 cells. After cultured for 48-96 hours, the cells were harvested. c-myc mRNA and protein level was monitored by fluorescence real time reverse transcription-poly merase chain reaction, c-myc protein expression was detected by Western blotting, and the cell proliferation activities were assayed by tetrazolium bromide (MTT) colorimetry and clone test. Results: Compared with control group, the mRNA of pGensil-c-myc-1, 2, 3, and 4 in Colo320 cells was obviously decreased in c-myc siRNA transfected cells. C-myc protein expression was also decreased obviously. MTT assay and clone test showed that c-myc siRNA apparently slowed down the proliferation of Colo320 cells. Conclusion: Our results suggest that RNA interference exists in Colo320 cell line; c-myc siRNA can specifically inhibit the expression of c-myc gene in Colo320 cells, subsequently inhibits the proliferation of Colo320 cells.
Objective: To inhibit c-myc gene expression in human rectal cancer cell line Colo320 by small interfering RNA technique, so as to assess the role of c-myc in Colo320 cells. Methods: The c-myc gene specific siRNA was designed and prepared by in vitro transcription. The prepared c-myc siRNA was transfected into Colo320 cells. After cultured for 48-96 hours, the cells were harvested. c-myc mRNA and protein level was monitored by fluorescence real time reverse transcription-poly merase chain reaction, c-myc protein expression was detected by Western blotting, and the cell proliferation activities were assayed by tetrazolium bromide (MTT) colorimetry and clone test. Results: Compared with control group, the mRNA of pGensil-c-myc-1, 2, 3, and 4 in Colo320 cells was obviously decreased in c-myc siRNA transfected cells. C-myc protein expression was also decreased obviously. MTT assay and clone test showed that c-myc siRNA apparently slowed down the proliferation of Colo320 cells. Conclusion: Our results suggest that RNA interference exists in Colo320 cell line; c-myc siRNA can specifically inhibit the expression of c-myc gene in Colo320 cells, subsequently inhibits the proliferation of Colo320 cells.
ZHANG Wen-ying
,
LOU Guo-liang
,
SHI Ping
,
ZHOU Jun-ping
,
WANG Liang-hua
,
JIAO Bing-hua
,
XIE Jun
2006, 13(5):371-375.
DOI: 10.3872/j.issn.1007-385X.2006.5.012
Abstract:
Objective: To study the inhibitory effect of indoleamine 2,3-dioxygenase(IDC)-modified dendritic cells on proliferation responses of allogeneic T-cell in transplantation of the hematopoietic stem cells in vitro. Methods： BALB/c mice bone marrow-derived dendritic cells were transfected with recombinant adenovirus harboring AdIDO gene. IDO mRNA was detected by RT-PCR in DCs transfected with AdmIDO and the changes of DCs phenotype were analyzed by FACS. Naive T lymphocytes from the spleen of C57BL/6 mice were co-cultured with BALB/c mouse-derived IDO-DC and Mixed lymphocyte reaction were performed to evaluate the alloantigen-specific hyporesponsivness and T cell apoptosis.
Objective: To study the inhibitory effect of indoleamine 2,3-dioxygenase(IDC)-modified dendritic cells on proliferation responses of allogeneic T-cell in transplantation of the hematopoietic stem cells in vitro. Methods： BALB/c mice bone marrow-derived dendritic cells were transfected with recombinant adenovirus harboring AdIDO gene. IDO mRNA was detected by RT-PCR in DCs transfected with AdmIDO and the changes of DCs phenotype were analyzed by FACS. Naive T lymphocytes from the spleen of C57BL/6 mice were co-cultured with BALB/c mouse-derived IDO-DC and Mixed lymphocyte reaction were performed to evaluate the alloantigen-specific hyporesponsivness and T cell apoptosis.
2006, 13(5):376-380.
DOI: 10.3872/j.issn.1007-385X.2006.5.013
Abstract:
Objective: To investigate the expression of Cyclin G mRNA in leukemia patients and its clinical significance. Methods: RT-PCR was used to analyze the expression of Cyclin G mRNA in the mononuclear cells of 129 leukemia patients and 10 healthy controls. Results: (1) The expression of Cyclin G in acute leukemia (AL) and chronic leukemia (CL) patients was significantly higher than that in healthy controls (both P<0.05), but there was no significant difference between AL and CL patients. (2) The Cyclin G positive rates of newly diagnosed/recurrent cases in AL, acute myeloid leukaemia (AML), acute lymphoblastic leukemia (ALL) groups were respectively 71.3%, 66.7%, and 85.7%, all significantly higher than those of their corresponding remission cases（P<0.05 or P<0.01）and that of healthy controls (P<0.01). (3) The Cyclin G positive rates in newly diagnosed cases of different ages, sexes, and percent of immature cells were similar; the positive rates of newly diagnosed cases with WBC > 50×109/L in AL and AML groups were significantly higher than those with WBC ≤ 50×109/L. (4) Fifty-three of the newly diagnosed cases were Cyclin G positive. The remission rate of patients with high Cyclin G expression（51.7%）was significantly lower than that with low Cyclin G expression（79.1%）(P<0.05). Conclusion: The high expression of Cyclin G may be correlated with the pathogenesis of leukemia and may be one of the factors for the poor prognosis of leukemia.
Objective: To investigate the expression of Cyclin G mRNA in leukemia patients and its clinical significance. Methods: RT-PCR was used to analyze the expression of Cyclin G mRNA in the mononuclear cells of 129 leukemia patients and 10 healthy controls. Results: (1) The expression of Cyclin G in acute leukemia (AL) and chronic leukemia (CL) patients was significantly higher than that in healthy controls (both P<0.05), but there was no significant difference between AL and CL patients. (2) The Cyclin G positive rates of newly diagnosed/recurrent cases in AL, acute myeloid leukaemia (AML), acute lymphoblastic leukemia (ALL) groups were respectively 71.3%, 66.7%, and 85.7%, all significantly higher than those of their corresponding remission cases（P<0.05 or P<0.01）and that of healthy controls (P<0.01). (3) The Cyclin G positive rates in newly diagnosed cases of different ages, sexes, and percent of immature cells were similar; the positive rates of newly diagnosed cases with WBC > 50×109/L in AL and AML groups were significantly higher than those with WBC ≤ 50×109/L. (4) Fifty-three of the newly diagnosed cases were Cyclin G positive. The remission rate of patients with high Cyclin G expression（51.7%）was significantly lower than that with low Cyclin G expression（79.1%）(P<0.05). Conclusion: The high expression of Cyclin G may be correlated with the pathogenesis of leukemia and may be one of the factors for the poor prognosis of leukemia.
2006, 13(5):381-383.
DOI: 10.3872/j.issn.1007-385X.2006.5.014
Abstract:
目的： 探讨Ki-67抗原和P53蛋白在非霍奇金淋巴瘤（NHL）的表达及其临床意义。方法： 采用免疫组化SP方法检测52例NHL及12例淋巴结反应性增生（RH）Ki-67和P53的表达情况,结合临床及病理资料进行分析。结果： Ki-67和P53在RH中的阳性表达率非常明显低于NHL(P<0.01),侵袭性NHL表达水平明显高于惰性NHL(P<0.05);两者在NHL中的表达呈正相关。Ki 67和P53在NHL的表达与患者性别、年龄、临床分期、有无全身症状、淋巴瘤细胞来源、首发部位无关。LDH＜250 μg/L的NHL Ki-67和P53阳性表达率明显低于LDH≥250 μg/L NHL中的阳性表达率(P<0.01)。Ki-67、P53阳性表达率≥25%的NHL患者与阳性表达率<25%的NHL患者相比较，平均生存期明显缩短(P<0.05)。结论： Ki-67和P53与NHL的发生发展有关,并可为预后判断提供参考依据。
目的： 探讨Ki-67抗原和P53蛋白在非霍奇金淋巴瘤（NHL）的表达及其临床意义。方法： 采用免疫组化SP方法检测52例NHL及12例淋巴结反应性增生（RH）Ki-67和P53的表达情况,结合临床及病理资料进行分析。结果： Ki-67和P53在RH中的阳性表达率非常明显低于NHL(P<0.01),侵袭性NHL表达水平明显高于惰性NHL(P<0.05);两者在NHL中的表达呈正相关。Ki 67和P53在NHL的表达与患者性别、年龄、临床分期、有无全身症状、淋巴瘤细胞来源、首发部位无关。LDH＜250 μg/L的NHL Ki-67和P53阳性表达率明显低于LDH≥250 μg/L NHL中的阳性表达率(P<0.01)。Ki-67、P53阳性表达率≥25%的NHL患者与阳性表达率<25%的NHL患者相比较，平均生存期明显缩短(P<0.05)。结论： Ki-67和P53与NHL的发生发展有关,并可为预后判断提供参考依据。
2006, 13(5):384-386.
DOI: 10.3872/j.issn.1007-385X.2006.5.015
Abstract:
目的： 观察反应停联合VAD方案治疗难治性多发性骨髓瘤的临床疗效。方法： 将16例多发性骨髓瘤患者随机分为两组，治疗组9例采用反应停联合VAD方案，反应停起始剂量为100 mg/d，每周增加50 mg/d,最大剂量为200~400 mg/d，持续12周以上；对照组7例采用单纯VAD方案，28 d为1疗程，治疗3个疗程。结果： 治疗组总有效率为66.7%，对照组总有效率为42.9%，两组间疗效有显著性差异（P＜0.05）。治疗组出现较对照组相对明显的不良反应有便秘、失眠，对症治疗后缓解。结论： 反应停联合VAD方案治疗多发性骨髓瘤疗效明显优于单用化疗组。
目的： 观察反应停联合VAD方案治疗难治性多发性骨髓瘤的临床疗效。方法： 将16例多发性骨髓瘤患者随机分为两组，治疗组9例采用反应停联合VAD方案，反应停起始剂量为100 mg/d，每周增加50 mg/d,最大剂量为200~400 mg/d，持续12周以上；对照组7例采用单纯VAD方案，28 d为1疗程，治疗3个疗程。结果： 治疗组总有效率为66.7%，对照组总有效率为42.9%，两组间疗效有显著性差异（P＜0.05）。治疗组出现较对照组相对明显的不良反应有便秘、失眠，对症治疗后缓解。结论： 反应停联合VAD方案治疗多发性骨髓瘤疗效明显优于单用化疗组。
2006, 13(5):387-389.
DOI: 10.3872/j.issn.1007-385X.2006.5.016
Abstract:
淋巴结转移是肿瘤分期的重要内容和预后指标。淋巴管生成不仅参与了正常胚胎淋巴管发育、组织修复，而且在肿瘤淋巴结转移等病理状况下也具有十分重要的作用。近年来多种淋巴管内皮标记物如LYVE-1、Prox-1、Podoplanin的发现和淋巴管生成模型的建立，使得人们逐渐认识到淋巴管生成因子VEGF-C、VEGF-D的表达和分子调控，以及其受体VEGFR-3在促进肿瘤淋巴结转移过程中的地位。抗肿瘤淋巴管生成已经成为肿瘤生物治疗的新靶点，并证实阻断VEGF-C/VEGF-D/VEGFR-3信号通路可以抑制肿瘤淋巴结转移。
淋巴结转移是肿瘤分期的重要内容和预后指标。淋巴管生成不仅参与了正常胚胎淋巴管发育、组织修复，而且在肿瘤淋巴结转移等病理状况下也具有十分重要的作用。近年来多种淋巴管内皮标记物如LYVE-1、Prox-1、Podoplanin的发现和淋巴管生成模型的建立，使得人们逐渐认识到淋巴管生成因子VEGF-C、VEGF-D的表达和分子调控，以及其受体VEGFR-3在促进肿瘤淋巴结转移过程中的地位。抗肿瘤淋巴管生成已经成为肿瘤生物治疗的新靶点，并证实阻断VEGF-C/VEGF-D/VEGFR-3信号通路可以抑制肿瘤淋巴结转移。
2006, 13(5):390-392.
DOI: 10.3872/j.issn.1007-385X.2006.5.017
Abstract:
肿瘤细胞在乏氧环境中会发生一系列生物学行为的改变，包括肿瘤侵袭性和转移能力的增加，其中乏氧诱导因子 -1α（hypoxia induciactor 1α, HIF-1α）起关键作用。HIF 1α可作用于多个环节促进肿瘤转移。在细胞运动方面：肝细胞生长因子(HGF)的受体c-Met在乏氧时增加，能促进细胞活动性并通过与肝细胞生长因子结合而增加细胞的侵袭性；基质降解方面：肿瘤细胞侵袭转移能力与其产生或诱导MMPs的能力密切相关，HIF 1可引起MMPs的表达增加，进而促进恶性肿瘤的转移；细胞黏附方面：HIF-1α可通过对肿瘤细胞黏附分子表达的影响而促进肿瘤转移；血管生成方面：乏氧能引起VEGF表达的上调，在肿瘤发生早期向血管生成型转变过程中，HIF-1α介导了VEGF的上调；细胞凋亡方面：HIF 1上调凋亡抑制因子Bcl-2，抑制凋亡，从而增强肿瘤转移力。HIF-1α亦可上调凋亡抑制因子p21，从而抑制凋亡使肿瘤恶性程度增加易于转移。对HIF-1α的研究可能是治疗肿瘤、减少恶性肿瘤转移的一种新途径。
肿瘤细胞在乏氧环境中会发生一系列生物学行为的改变，包括肿瘤侵袭性和转移能力的增加，其中乏氧诱导因子 -1α（hypoxia induciactor 1α, HIF-1α）起关键作用。HIF 1α可作用于多个环节促进肿瘤转移。在细胞运动方面：肝细胞生长因子(HGF)的受体c-Met在乏氧时增加，能促进细胞活动性并通过与肝细胞生长因子结合而增加细胞的侵袭性；基质降解方面：肿瘤细胞侵袭转移能力与其产生或诱导MMPs的能力密切相关，HIF 1可引起MMPs的表达增加，进而促进恶性肿瘤的转移；细胞黏附方面：HIF-1α可通过对肿瘤细胞黏附分子表达的影响而促进肿瘤转移；血管生成方面：乏氧能引起VEGF表达的上调，在肿瘤发生早期向血管生成型转变过程中，HIF-1α介导了VEGF的上调；细胞凋亡方面：HIF 1上调凋亡抑制因子Bcl-2，抑制凋亡，从而增强肿瘤转移力。HIF-1α亦可上调凋亡抑制因子p21，从而抑制凋亡使肿瘤恶性程度增加易于转移。对HIF-1α的研究可能是治疗肿瘤、减少恶性肿瘤转移的一种新途径。
2006, 13(5):393-396.
DOI: 10.3872/j.issn.1007-385X.2006.5.018
Abstract:
目前发现血管内皮生长因子（vascular endothelial growth factors, VEGFs）家族包括7个成员：VEGF-A，胎盘生长因子（placenta growth factor,PlGF)，VEGF-B，VEGF-C，VEGF-D，VEGF-E 和蛇毒VEGF(snake venom VEGF,svVEGF )；其同源受体有酪氨酸激酶受体VEGFR -1(Flt-1)、VEGFR-2(KDR)、VEGFR-3(Flt-4)等多种类型。其中，VEGF-A与VEGFR-1 和VEGFR-2结合在血管生成中起关键作用，而VEGF-C、VEGF-D与VEGFR-2、VEGFR-3结合在淋巴管生成中起关键作用。胃癌血管生成、淋巴管生成对胃癌的发生发展及转移至关重要。近年研究表明，VEGF-A在胃癌组织中高表达,并在胃癌血管生成中起关键作用；VEGF-C、 VEGF-D在胃癌组织中高表达，而在胃癌淋巴管生成中起关键作用；VEGF-A、 VEGF-C及-VEGF-D与胃癌血管转移、淋巴管转移呈正相关。因此，研究VEGFs家族成员在胃癌生长及侵袭转移中的作用及其机制，可为胃癌的抗血管、抗淋巴管治疗提供新的靶点。
目前发现血管内皮生长因子（vascular endothelial growth factors, VEGFs）家族包括7个成员：VEGF-A，胎盘生长因子（placenta growth factor,PlGF)，VEGF-B，VEGF-C，VEGF-D，VEGF-E 和蛇毒VEGF(snake venom VEGF,svVEGF )；其同源受体有酪氨酸激酶受体VEGFR -1(Flt-1)、VEGFR-2(KDR)、VEGFR-3(Flt-4)等多种类型。其中，VEGF-A与VEGFR-1 和VEGFR-2结合在血管生成中起关键作用，而VEGF-C、VEGF-D与VEGFR-2、VEGFR-3结合在淋巴管生成中起关键作用。胃癌血管生成、淋巴管生成对胃癌的发生发展及转移至关重要。近年研究表明，VEGF-A在胃癌组织中高表达,并在胃癌血管生成中起关键作用；VEGF-C、 VEGF-D在胃癌组织中高表达，而在胃癌淋巴管生成中起关键作用；VEGF-A、 VEGF-C及-VEGF-D与胃癌血管转移、淋巴管转移呈正相关。因此，研究VEGFs家族成员在胃癌生长及侵袭转移中的作用及其机制，可为胃癌的抗血管、抗淋巴管治疗提供新的靶点。
2006, 13(5):397-399.
DOI: 10.3872/j.issn.1007-385X.2006.5.019
Abstract:
P27蛋白属于细胞周期调控蛋白Cip／kip家族，是细胞周期负性调节因子，在人体多种恶性肿瘤细胞增殖、分化以及细胞凋亡调控中起着非常重要的作用。MAPK和PI3K/PKB信号途径均能够介导P27的降解或失活，其表达的下调与乳腺癌的发生及进展密切相关，故可能是一种新的肿瘤标志物及肿瘤预后指标。P27在乳腺癌的化学疗法、放射治疗以及激素治疗中具有一定的应用价值。通过人工调节p27表达水平及外部干涉p27作用通路可能在乳腺癌的基因疗法中具有广阔的应用前景。
P27蛋白属于细胞周期调控蛋白Cip／kip家族，是细胞周期负性调节因子，在人体多种恶性肿瘤细胞增殖、分化以及细胞凋亡调控中起着非常重要的作用。MAPK和PI3K/PKB信号途径均能够介导P27的降解或失活，其表达的下调与乳腺癌的发生及进展密切相关，故可能是一种新的肿瘤标志物及肿瘤预后指标。P27在乳腺癌的化学疗法、放射治疗以及激素治疗中具有一定的应用价值。通过人工调节p27表达水平及外部干涉p27作用通路可能在乳腺癌的基因疗法中具有广阔的应用前景。
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Supported by:Beijing E-Tiller Technology Development Co., Ltd.