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Volume 24,Issue 11,2017 Table of Contents
2017, 24(11):1247-1253.
DOI: 10.3872/j.issn.1007-385X.2017.11.001
Abstract:
T cell dysfunction in tumor microenvironment is the key mechanism of tumor escaping from immune surveillance. T cell dysfunction induced by up-regulating expression of immune checkpoint molecules is a hot point of the current research. The clinical trials of blocking immune checkpoint, PD-1 and CTLA-1, have shown encouraging efficacy in the many patients with advanced cancer. It was confirmed that there was T cell dysfunction in tumor microenvironment and reversing T cell dysfunction could play a potentiality in tumor therapy. However, the novel immunotherapy methods exhibited a long-lasting clinical efficacy in a small number of the patients with cancer only,which suggest heterogeneity and complexity of the tumor microenvironment. Recently, the research in unicellular level further clarified phenotypic characteristics and clinical significance of T cell dysfunction in tumor microenvironment, which reveals that epigenetics and metabolic changes are the important mechanisms resulting in T cell dysfunction in the tumor microenvironment and suggests the novel methods for reversing T cell dysfunction in the tumor microenvironment. This paper focus on the latest research progresses of the T cell dysfunction in the tumor microenvironment and strategy of reversing the T cell dysfunction.
T cell dysfunction in tumor microenvironment is the key mechanism of tumor escaping from immune surveillance. T cell dysfunction induced by up-regulating expression of immune checkpoint molecules is a hot point of the current research. The clinical trials of blocking immune checkpoint, PD-1 and CTLA-1, have shown encouraging efficacy in the many patients with advanced cancer. It was confirmed that there was T cell dysfunction in tumor microenvironment and reversing T cell dysfunction could play a potentiality in tumor therapy. However, the novel immunotherapy methods exhibited a long-lasting clinical efficacy in a small number of the patients with cancer only,which suggest heterogeneity and complexity of the tumor microenvironment. Recently, the research in unicellular level further clarified phenotypic characteristics and clinical significance of T cell dysfunction in tumor microenvironment, which reveals that epigenetics and metabolic changes are the important mechanisms resulting in T cell dysfunction in the tumor microenvironment and suggests the novel methods for reversing T cell dysfunction in the tumor microenvironment. This paper focus on the latest research progresses of the T cell dysfunction in the tumor microenvironment and strategy of reversing the T cell dysfunction.
2017, 24(11):1254-1259.
DOI: 10.3872/j.issn.1007-385X.2017.11.002
Abstract:
Objective: To analyze effect of demethylation of bridging integrator- 1 (Bin1) on expression of Bin1 gene and proliferation ability of the esophageal squamous cell carcinoma (ESCC) EC109 cell, and preliminarily to explore its possible action mechanism. Methods: Methylation specific Polymerase Chain Reaction (MSP) assay was used to detect methylation status of Bin1 promoter region in the EC109 cell after treatment with demethylation drug, 5-Aza-2’-deoxycytidine (5-Aza-dc). qPCR, Western blotting and MTT assays were used to detect effect of treatment with 5-Aza-dc only and treatment with 5-Aza-dc plus transfection with Bin1 gene interference fragments (Bin1 siRNA) on expressions of Bin1 mRNA and its protein in the EC109 cell as well as proliferation ability of the EC109 cell respectively. Cell cycles of the EC109 cell and expressions of cell cycle-related proteins (Cyclin D1 and CDK4) in the EC109 cell were tested by flow cytometry assay and Western blotting respectively. Results: Demethylation of Bin1 gene promoter region occurred in the EC109 cell after treatment with 5-Aza-dc. In the EC109 cell treated with 5-Aza-dc, expressions of Bin1 mRNA and its protein obviously up-regulated, proliferation ability of the EC109 cell remarkably decreased, the EC109 cell was blocked at G0/G1 stage, proportion of the EC109 cell at S stage evidently reduced, as well as expressions of Cyclin D1 and CDK4 proteins were markedly down-regulated (all P<0.05). After the EC109 cell in demethylation status was transfected with Bin1 siRNA, expressions of Bin1 mRNA and its protein significantly decreased and proliferation ability of the EC109 cell evidently enhanced (all P<0.05).Conclusion: Bin1 gene promoter region in the EC109 cell appeared in complete demethylation status. Demethylation of 5-Aza-dc could enhance expression of Bin1 in the EC109 cell of ESCC, which could induce cell cycle arrest and inhibit proliferation of the EC109 cell through decrease of cell cycle- related protein expression. It was confirmed that epigenetic changes could be related to malignant proliferation of the ESCC cell, which could provide novel idea for therapy of the esophageal carcinoma.
Objective: To analyze effect of demethylation of bridging integrator- 1 (Bin1) on expression of Bin1 gene and proliferation ability of the esophageal squamous cell carcinoma (ESCC) EC109 cell, and preliminarily to explore its possible action mechanism. Methods: Methylation specific Polymerase Chain Reaction (MSP) assay was used to detect methylation status of Bin1 promoter region in the EC109 cell after treatment with demethylation drug, 5-Aza-2’-deoxycytidine (5-Aza-dc). qPCR, Western blotting and MTT assays were used to detect effect of treatment with 5-Aza-dc only and treatment with 5-Aza-dc plus transfection with Bin1 gene interference fragments (Bin1 siRNA) on expressions of Bin1 mRNA and its protein in the EC109 cell as well as proliferation ability of the EC109 cell respectively. Cell cycles of the EC109 cell and expressions of cell cycle-related proteins (Cyclin D1 and CDK4) in the EC109 cell were tested by flow cytometry assay and Western blotting respectively. Results: Demethylation of Bin1 gene promoter region occurred in the EC109 cell after treatment with 5-Aza-dc. In the EC109 cell treated with 5-Aza-dc, expressions of Bin1 mRNA and its protein obviously up-regulated, proliferation ability of the EC109 cell remarkably decreased, the EC109 cell was blocked at G0/G1 stage, proportion of the EC109 cell at S stage evidently reduced, as well as expressions of Cyclin D1 and CDK4 proteins were markedly down-regulated (all P<0.05). After the EC109 cell in demethylation status was transfected with Bin1 siRNA, expressions of Bin1 mRNA and its protein significantly decreased and proliferation ability of the EC109 cell evidently enhanced (all P<0.05).Conclusion: Bin1 gene promoter region in the EC109 cell appeared in complete demethylation status. Demethylation of 5-Aza-dc could enhance expression of Bin1 in the EC109 cell of ESCC, which could induce cell cycle arrest and inhibit proliferation of the EC109 cell through decrease of cell cycle- related protein expression. It was confirmed that epigenetic changes could be related to malignant proliferation of the ESCC cell, which could provide novel idea for therapy of the esophageal carcinoma.
2017, 24(11):1260-1265.
DOI: 10.3872/j.issn.1007-385X.2017.11.003
Abstract:
Objective: To explore effect of silencing glioma associated oncogene homolog 2 (Gli2) on proliferation and apoptosis of the liver cancer SMMC-7721 cell and its possible action mechanism. Methods: Infection of the SMMC-7721 cell with recombinant shRNA-Gli2 lentivirus was used to screen the best jamming sequence for silence effect. The SMMC-7721 cell of interference group was infected with the best jamming sequence lentivirus,the SMMC-7721 cell of control group was infected with shRNA-NC shRNA-Gli2 lentivirus and the SMMC-7721 cell of blank group didn’t with any treatment. CCK-8 and Western blotting assays were used to detect proliferation activity of the SMMC-7721 cell in various groups. Flow cytometry assay was used to test apoptosis of the SMMC-7721 cell in various groups. Expressions of Cli2, cyclinD1, Bax and Bcl-2 mRNA and their proteins were detected by qPCR and Western blotting. Results: Infection rate of the recombinant lentivirus was about 90%. Silence effect of the recombinant shRNA-Gli2-1 lentivirus was the best. Expressions of Gli2 mRNA and its protein in the SMMC-7721 cell of interference group were remarkably lower than those in the SMMC-7721 cells of control and blank groups (all P<0.05), and differences of Gli2 mRNA and its protein expressions between the SMMC-7721 cells of control group and blank group were not significant (P>0.05). Proliferation and cell colony forming number of the SSMC-7721 cell in interference group were obviously less than those of the SSMC-7721 cell in control and blank groups (all P<0.05). Apoptosis rate of the SMMC-7721 cell in interference group evidently higher than those of the SMMC-7721 cell in control and blank groups (P<0.01). Expressions of cyclinD1 and Bax mRNA and their proteins in the SMMC-7721 cell of interference group were observably lower than those in the SMMC-7721 cells of control and blank groups (all P<0.05), but expressions of Bcl-2 mRNA and protein in the SMMC-7721 cell of interference group were observably higher than those in the SMMC-7721 cells of control and blank groups (all P<0.05). Conclusion:Silencing expression of Gli2 gene could inhibit growth of the liver cancer SMMC-7721 cell, and promote apoptosis of the liver cancer cell, its mechanism might relate to down-regulation of cyclin D1 and Bax as well as upregulation of Bcl-2.
Objective: To explore effect of silencing glioma associated oncogene homolog 2 (Gli2) on proliferation and apoptosis of the liver cancer SMMC-7721 cell and its possible action mechanism. Methods: Infection of the SMMC-7721 cell with recombinant shRNA-Gli2 lentivirus was used to screen the best jamming sequence for silence effect. The SMMC-7721 cell of interference group was infected with the best jamming sequence lentivirus,the SMMC-7721 cell of control group was infected with shRNA-NC shRNA-Gli2 lentivirus and the SMMC-7721 cell of blank group didn’t with any treatment. CCK-8 and Western blotting assays were used to detect proliferation activity of the SMMC-7721 cell in various groups. Flow cytometry assay was used to test apoptosis of the SMMC-7721 cell in various groups. Expressions of Cli2, cyclinD1, Bax and Bcl-2 mRNA and their proteins were detected by qPCR and Western blotting. Results: Infection rate of the recombinant lentivirus was about 90%. Silence effect of the recombinant shRNA-Gli2-1 lentivirus was the best. Expressions of Gli2 mRNA and its protein in the SMMC-7721 cell of interference group were remarkably lower than those in the SMMC-7721 cells of control and blank groups (all P<0.05), and differences of Gli2 mRNA and its protein expressions between the SMMC-7721 cells of control group and blank group were not significant (P>0.05). Proliferation and cell colony forming number of the SSMC-7721 cell in interference group were obviously less than those of the SSMC-7721 cell in control and blank groups (all P<0.05). Apoptosis rate of the SMMC-7721 cell in interference group evidently higher than those of the SMMC-7721 cell in control and blank groups (P<0.01). Expressions of cyclinD1 and Bax mRNA and their proteins in the SMMC-7721 cell of interference group were observably lower than those in the SMMC-7721 cells of control and blank groups (all P<0.05), but expressions of Bcl-2 mRNA and protein in the SMMC-7721 cell of interference group were observably higher than those in the SMMC-7721 cells of control and blank groups (all P<0.05). Conclusion:Silencing expression of Gli2 gene could inhibit growth of the liver cancer SMMC-7721 cell, and promote apoptosis of the liver cancer cell, its mechanism might relate to down-regulation of cyclin D1 and Bax as well as upregulation of Bcl-2.
2017, 24(11):1266-1270.
DOI: 10.3872/j.issn.1007-385X.2017.11.004
Abstract:
Objective: To explore effect of cytokine interleukin 21 (IL-21) on the activity of cytokine-induced killer (CIK) cell killing in vitro the esophageal cancer EC9706 cell, and preliminarily to analyze its possible molicular mechanism. Methods: Human peripheral blood mononuclear cells were isolated with sterile operation in vitro,which were respectively cultured into CIK cells in routine medium or in routine medium plus IL-21. Flow cytometry assay was used to detect immunophenotypes of CIK cells cultured with the two medium. Lactate dehydrogenase (LDH) release method was used to exam the activities of the two cultured CIK cells killing the esophageal cancer EC9706 cell. Concentrations of IFN-γ in liquid supernatant cultured the two types of CIK cell were checked by ELISA. Results: There not were any significant difference of proliferation number of the CIK cells between routine culture and routine culture plus IL-21. Proportion of CD3+CD56+ cell, expression rates of granzyme B and perforin in CD3+ cell of the CIK cell cultured by routine medium plus IL-21 were evidently higher than those of the CIK cell cultured by routine medium (CD3+CD56+ cell: [26.95±3.53]% vs [16.18±1.04]%；granzyme B: [33.29±2.30]% vs [23.58±2.28]%；perforin: [59.70±1.91]% vs [45.96±2.67]%, all P<0.05). At effector/target ratio of 20∶1 and 30∶1,killing activities against the EC9706 cell of the CIK cell cultured with routine medium plus IL-21 were all remarkably higher than those of the CIK cell cultured with routine medium（at E/T 20:1 [43.66±1.99]% vs [34.59±1.75]%;at E/T 30∶1 [142.7±13.4]% vs [42.6±3.3]%，all P<0.05). Concentration of IFN-γ in liquid supernatant cultured the CIK cell in routine medium plus IL- 21 was obviously higher than that cultured the CIK cell in routine medium [(157.2±10.3) ng/L vs (46.2±4.3) ng/L，P<0.05]. Conclusion: IL-21 could enhance killing activity of the CIK cell against the esophageal cancer EC9706 cell through increasing proportion of CD3+CD56+ cell, expression rates of granzyme B and perforin in CD3+ cell as well as raising the secretion of IFN-γ by the CIK cell.
Objective: To explore effect of cytokine interleukin 21 (IL-21) on the activity of cytokine-induced killer (CIK) cell killing in vitro the esophageal cancer EC9706 cell, and preliminarily to analyze its possible molicular mechanism. Methods: Human peripheral blood mononuclear cells were isolated with sterile operation in vitro,which were respectively cultured into CIK cells in routine medium or in routine medium plus IL-21. Flow cytometry assay was used to detect immunophenotypes of CIK cells cultured with the two medium. Lactate dehydrogenase (LDH) release method was used to exam the activities of the two cultured CIK cells killing the esophageal cancer EC9706 cell. Concentrations of IFN-γ in liquid supernatant cultured the two types of CIK cell were checked by ELISA. Results: There not were any significant difference of proliferation number of the CIK cells between routine culture and routine culture plus IL-21. Proportion of CD3+CD56+ cell, expression rates of granzyme B and perforin in CD3+ cell of the CIK cell cultured by routine medium plus IL-21 were evidently higher than those of the CIK cell cultured by routine medium (CD3+CD56+ cell: [26.95±3.53]% vs [16.18±1.04]%；granzyme B: [33.29±2.30]% vs [23.58±2.28]%；perforin: [59.70±1.91]% vs [45.96±2.67]%, all P<0.05). At effector/target ratio of 20∶1 and 30∶1,killing activities against the EC9706 cell of the CIK cell cultured with routine medium plus IL-21 were all remarkably higher than those of the CIK cell cultured with routine medium（at E/T 20:1 [43.66±1.99]% vs [34.59±1.75]%;at E/T 30∶1 [142.7±13.4]% vs [42.6±3.3]%，all P<0.05). Concentration of IFN-γ in liquid supernatant cultured the CIK cell in routine medium plus IL- 21 was obviously higher than that cultured the CIK cell in routine medium [(157.2±10.3) ng/L vs (46.2±4.3) ng/L，P<0.05]. Conclusion: IL-21 could enhance killing activity of the CIK cell against the esophageal cancer EC9706 cell through increasing proportion of CD3+CD56+ cell, expression rates of granzyme B and perforin in CD3+ cell as well as raising the secretion of IFN-γ by the CIK cell.
5 Effects of HuR siRNA on proliferation, migration and invasion of the lung adenocarcinoma A549 cells
2017, 24(11):1271-1275.
DOI: 10.3872/j.issn.1007-385X.2017.11.005
Abstract:
Objective: To explore effect of HuR siRNA on proliferation, migration and invasion of the human lung adenocarcinoma cell line A549 and its possible mechanism. Methods: After the A549 cells were transfected by HuR siRNA and cultured for 24 hours, CCK-8 assay and clone formation assay were used to detect proliferation ability of the A549 cells. Migration and invasion abilities of the A549 cells were respectively detected by scratch and Transwell assays. mRNA and protein expressions of HuR and matrix metalloproteinose-9 (MMP-9) were detected by RTqPCR and Western blotting assays. Results: HuR siRNA inhibited proliferation, migration and invasion of the human lung cancer cell line A549. HuR siRNA significantly reduced mRNA and protein expressions of HuR and MMP-9 in the A549 cells (P<0.01). Conclusion: Down-regulation of HuR could inhibit proliferation, migration and invasion of the lung adenocarcinoma A549 cells, and the inhibitions of migration and invasion of the A549 cells might be related to down-regulation of MMP-9.
Objective: To explore effect of HuR siRNA on proliferation, migration and invasion of the human lung adenocarcinoma cell line A549 and its possible mechanism. Methods: After the A549 cells were transfected by HuR siRNA and cultured for 24 hours, CCK-8 assay and clone formation assay were used to detect proliferation ability of the A549 cells. Migration and invasion abilities of the A549 cells were respectively detected by scratch and Transwell assays. mRNA and protein expressions of HuR and matrix metalloproteinose-9 (MMP-9) were detected by RTqPCR and Western blotting assays. Results: HuR siRNA inhibited proliferation, migration and invasion of the human lung cancer cell line A549. HuR siRNA significantly reduced mRNA and protein expressions of HuR and MMP-9 in the A549 cells (P<0.01). Conclusion: Down-regulation of HuR could inhibit proliferation, migration and invasion of the lung adenocarcinoma A549 cells, and the inhibitions of migration and invasion of the A549 cells might be related to down-regulation of MMP-9.
2017, 24(11):1276-1280.
DOI: 10.3872/j.issn.1007-385X.2017.11.006
Abstract:
Objective: To explore effect of sodium tanshinone IIA sulfonate (STS) on migration of the cervix carcinoma Hela cell and its possible mechanism. Methods：Effects of STS in different concentrations, specific antibody to integrin β3 (LM609), and transfection with integrin β3 over-expression plasmid on migration of the cervix carcinoma HeLa cell were detected by Transwell assay. Immunoblotting test was used to detect effects of STS in different concentrations and different times of STS stimulation on expression of integrin β3 in the HeLa cell. Effect of STS on viability of the HeLa cell was tested by CCK-8 assay. Results：STS in concentration-dependent manner reduced significantly migration of the HeLa cell (P<0.01). LM609 remarkably decreased migration rate of the HeLa cell (P<0.01). Migration rate of the HeLa cell transfected with over-expression integrin β3 plasmid and stimulated by STS was markedly more increase than those of the HeLa cell stimulated by STS only as well as the HeLa cell transfected with empty plasmid and stimulated by STS (P<0.01). STS in concentration- and timing-dependent manners reduced expression of integrin β3 in the HeLa cell (P<0.05). There was no significant difference in number of the viable cells between the HeLa cell stimulated with different concentrations of STS groups and the HeLa cells in blank control group (P>0.05). Conclusion：STS could reduce expression of integrin β3 in the cervix carcinoma HeLa cell, and significantly decrease migration of the HeLa cell，LM609 which is a specific antibody against integrin β3 could also reduced migration of the HeLa cells, and transfection with integrin β3 over- expression plasmid could reduce the inhibition of STS on migration of the HeLa cell. The results of this paper shown that STS might inhibits migration of the HeLa cell via decrease of integrin β3 expression, which might provide theoretical basis and experimental evidence for further explain molecular mechanism of STS anti-carcinoma and clinical application of STS.
Objective: To explore effect of sodium tanshinone IIA sulfonate (STS) on migration of the cervix carcinoma Hela cell and its possible mechanism. Methods：Effects of STS in different concentrations, specific antibody to integrin β3 (LM609), and transfection with integrin β3 over-expression plasmid on migration of the cervix carcinoma HeLa cell were detected by Transwell assay. Immunoblotting test was used to detect effects of STS in different concentrations and different times of STS stimulation on expression of integrin β3 in the HeLa cell. Effect of STS on viability of the HeLa cell was tested by CCK-8 assay. Results：STS in concentration-dependent manner reduced significantly migration of the HeLa cell (P<0.01). LM609 remarkably decreased migration rate of the HeLa cell (P<0.01). Migration rate of the HeLa cell transfected with over-expression integrin β3 plasmid and stimulated by STS was markedly more increase than those of the HeLa cell stimulated by STS only as well as the HeLa cell transfected with empty plasmid and stimulated by STS (P<0.01). STS in concentration- and timing-dependent manners reduced expression of integrin β3 in the HeLa cell (P<0.05). There was no significant difference in number of the viable cells between the HeLa cell stimulated with different concentrations of STS groups and the HeLa cells in blank control group (P>0.05). Conclusion：STS could reduce expression of integrin β3 in the cervix carcinoma HeLa cell, and significantly decrease migration of the HeLa cell，LM609 which is a specific antibody against integrin β3 could also reduced migration of the HeLa cells, and transfection with integrin β3 over- expression plasmid could reduce the inhibition of STS on migration of the HeLa cell. The results of this paper shown that STS might inhibits migration of the HeLa cell via decrease of integrin β3 expression, which might provide theoretical basis and experimental evidence for further explain molecular mechanism of STS anti-carcinoma and clinical application of STS.
2017, 24(11):1281-1286.
DOI: 10.3872/j.issn.1007-385X.2017.11.007
Abstract:
Objective: To comparatively analyze clinical efficacy of single- unit and double- unit nonrelative cord blood transplantation for treatment of hematologic diseases. Methods: Clinical data of the 185 patients received single-unit umbilical cord blood transplantation (SU-UCBT) and the 66 patients received double-unit umbilical cord blood transplantation (DU-UCBT) in 8 domestic transplant centers during 2006 to 2016 were retrospectively analyzed.It was compared that implantation rates, implantation time of neutrophil granulocyte and platelet between SUUCBT and DU-UCBT, as well as occurrence of acute graft vs host disease (aGVHD) and survival rates of the patients with malignant hematonosis and with non malignant hematonosis after SU-UCBT and DU-UCBT. Results:Implantation rates of the patients received SU-UCBT and DU-UCBT were 78.9% and 70.7% respectively, among them implantation rates of the patients with malignant hematonosis were 89.1% for SU-UCBT and 82.5% for DUUCBT as well as implantation rates of the patients with non malignant hematonosis were 64.0% for SU-UCBT and 53.8% for DU-UCBT, implantation rates of SU-UCBT and DU-UCBT were similar (P>0.05). In the patients received SU-UCBT and DU-UCBT, median implantation times of neutrophil granulocyte were all 18 d, median implantation times of platelet were 40 d and 27 d respectively, the difference was not remarkable (P>0.05). Incidence rates of aGVHD at I, II, III, IV grades in the patients received SU-UCBT and DU-UCBT were 22.6%, 22.6%, 8.2%,12.3% and 21.3%, 14.9%, 10.6%, 10.6% respectively, all of the differences were not evident (all P>0.05). Median survival time in the recipients of SU-UCBT and DU-UCBT were 1 460 d (17~2 200 d) and 988 d (21~2 200 d), and their cumulative survival rate of 6 years were respectively 42.5% and 40.4%, all differences were not obvious (P>0.05). Conclusion: Between the patients successfully received SU-UCBT and DU-UCBT, implantation times of neutrophil granulocyte and platelet, incidence rate of aGVHD, survival time and cumulative survival rate of 6 years were not significant, which suggests that DU-UCBT could be a safe and effective selection of UCBT. However, the evaluation system of SU-UCBT and DU-UCBT still needs to be perfected and implantation mechanism of DUUCBT needs to make a thorough inquiry, so as to scientifically guide selection of UCBT.
Objective: To comparatively analyze clinical efficacy of single- unit and double- unit nonrelative cord blood transplantation for treatment of hematologic diseases. Methods: Clinical data of the 185 patients received single-unit umbilical cord blood transplantation (SU-UCBT) and the 66 patients received double-unit umbilical cord blood transplantation (DU-UCBT) in 8 domestic transplant centers during 2006 to 2016 were retrospectively analyzed.It was compared that implantation rates, implantation time of neutrophil granulocyte and platelet between SUUCBT and DU-UCBT, as well as occurrence of acute graft vs host disease (aGVHD) and survival rates of the patients with malignant hematonosis and with non malignant hematonosis after SU-UCBT and DU-UCBT. Results:Implantation rates of the patients received SU-UCBT and DU-UCBT were 78.9% and 70.7% respectively, among them implantation rates of the patients with malignant hematonosis were 89.1% for SU-UCBT and 82.5% for DUUCBT as well as implantation rates of the patients with non malignant hematonosis were 64.0% for SU-UCBT and 53.8% for DU-UCBT, implantation rates of SU-UCBT and DU-UCBT were similar (P>0.05). In the patients received SU-UCBT and DU-UCBT, median implantation times of neutrophil granulocyte were all 18 d, median implantation times of platelet were 40 d and 27 d respectively, the difference was not remarkable (P>0.05). Incidence rates of aGVHD at I, II, III, IV grades in the patients received SU-UCBT and DU-UCBT were 22.6%, 22.6%, 8.2%,12.3% and 21.3%, 14.9%, 10.6%, 10.6% respectively, all of the differences were not evident (all P>0.05). Median survival time in the recipients of SU-UCBT and DU-UCBT were 1 460 d (17~2 200 d) and 988 d (21~2 200 d), and their cumulative survival rate of 6 years were respectively 42.5% and 40.4%, all differences were not obvious (P>0.05). Conclusion: Between the patients successfully received SU-UCBT and DU-UCBT, implantation times of neutrophil granulocyte and platelet, incidence rate of aGVHD, survival time and cumulative survival rate of 6 years were not significant, which suggests that DU-UCBT could be a safe and effective selection of UCBT. However, the evaluation system of SU-UCBT and DU-UCBT still needs to be perfected and implantation mechanism of DUUCBT needs to make a thorough inquiry, so as to scientifically guide selection of UCBT.
2017, 24(11):1287-1292.
DOI: 10.3872/j.issn.1007-385X.2017.11.008
Abstract:
Objective: To detect expression of human interleukin 11 (IL-11) gene in tissue and blood specimens of the patients with diffuse large B-cell lymphoma (DLBCL), and to explore the relationship between expression of IL-11 gene and prognosis of the patients with DLBCL as well as its effect on thrombocytopenia of the patients with DLBCL after chemotherapy. Methods: Tissue and blood specimens of 88 patients with DLBCL and 42 patients with reactive lymphoid hyperplasia (RLH) who were made a definite diagnosis in Department of Hematology, the First Hospital of Handan City of Hebei Province during January 2012 to December 2016 were collected. qPCR was used to detect expression of IL-11 in the tumor tissues and blood specimens. Univariate and multivariate Cox regression analyses were used to analyze relationship of IL-11 expression in the tissues with clinical pathological features and prognosis of the patients with DLBCL as well as independent factors effecting prognosis of the patients. Correlationship between expression of IL-11 and thrombocytopenia after chemotherapy in the patients with DLBCL was analyzed,as wall as relationships of the IL-11 expression with overall survival (OS) and progression free survival (PFS)were analyzed by Kaplan-Meier assay. Results: Comparing with the patients with RLH in control group, expressions of IL-11 in tissue and blood of the patients with DLBCL were significant higher (in tissue: 7.002±0.357 vs 1.507±0.139; in blood: 6.700±0.337 vs 1.446±0.126, all P<0.01). In the patients with DLBCL, expression of IL-11 was correlated to tumor size, clinical staging, B cell symptom, sensitivity of chemotherapy and IPI index (all P<0.01). OS and PFS of the patients with high expression of IL-11 were shorter than those of the patients with low expression of IL-11 (all P<0.01). Expression of IL-11, sensitivity of chemotherapy and IPI index were independent factors affecting prognosis of the patients with DLBCL. In the patients with thrombocytopenia after chemotherapy, expression of IL-11 in serum and platelet count were negative correlated(r=-0.732, P<0.01). Conclusion: IL-11 was highly expressed in tissue and blood of the patients with DLBCL. OS and PFS of the DLBCL patients with high expression of IL-11 were significantly shortened, in whom, platelet severely reduced after chemotherapy. IL-11 might be expected to become an independent biological marker which could judge prognosis of the patients with DLBCL.
Objective: To detect expression of human interleukin 11 (IL-11) gene in tissue and blood specimens of the patients with diffuse large B-cell lymphoma (DLBCL), and to explore the relationship between expression of IL-11 gene and prognosis of the patients with DLBCL as well as its effect on thrombocytopenia of the patients with DLBCL after chemotherapy. Methods: Tissue and blood specimens of 88 patients with DLBCL and 42 patients with reactive lymphoid hyperplasia (RLH) who were made a definite diagnosis in Department of Hematology, the First Hospital of Handan City of Hebei Province during January 2012 to December 2016 were collected. qPCR was used to detect expression of IL-11 in the tumor tissues and blood specimens. Univariate and multivariate Cox regression analyses were used to analyze relationship of IL-11 expression in the tissues with clinical pathological features and prognosis of the patients with DLBCL as well as independent factors effecting prognosis of the patients. Correlationship between expression of IL-11 and thrombocytopenia after chemotherapy in the patients with DLBCL was analyzed,as wall as relationships of the IL-11 expression with overall survival (OS) and progression free survival (PFS)were analyzed by Kaplan-Meier assay. Results: Comparing with the patients with RLH in control group, expressions of IL-11 in tissue and blood of the patients with DLBCL were significant higher (in tissue: 7.002±0.357 vs 1.507±0.139; in blood: 6.700±0.337 vs 1.446±0.126, all P<0.01). In the patients with DLBCL, expression of IL-11 was correlated to tumor size, clinical staging, B cell symptom, sensitivity of chemotherapy and IPI index (all P<0.01). OS and PFS of the patients with high expression of IL-11 were shorter than those of the patients with low expression of IL-11 (all P<0.01). Expression of IL-11, sensitivity of chemotherapy and IPI index were independent factors affecting prognosis of the patients with DLBCL. In the patients with thrombocytopenia after chemotherapy, expression of IL-11 in serum and platelet count were negative correlated(r=-0.732, P<0.01). Conclusion: IL-11 was highly expressed in tissue and blood of the patients with DLBCL. OS and PFS of the DLBCL patients with high expression of IL-11 were significantly shortened, in whom, platelet severely reduced after chemotherapy. IL-11 might be expected to become an independent biological marker which could judge prognosis of the patients with DLBCL.
2017, 24(11):1293-1298.
DOI: 10.3872/j.issn.1007-385X.2017.11.009
Abstract:
Objective: To explore expression status of periostin (POSTN) in the mammary cancer, para-cancer and normal mammary tissues and its clinical significance. Methods: The mammary cancer, para- cancer and normal mammary tissues of 45 patients with mammary cancer，which were taken out by exairesis in Department of Galactophore,Third Affiliated Hospital of Kunming Medical University during May 2012 to December 2016. In addition,from the tissues fifteen amicrobic mammary cancer and normal mammary tissues were selected for primary cell culture.The primary cultured cells were identified by HE staining and immunohistochemistry assays. Expression status of POSTN mRNA in the mammary cancer, para-cancer and normal mammary tissues as well as in the cancer associated fibroblast (CAF) and normal fibroblast (NF) were detected by real-time quality PCR (qPCR). Correlation analysis was used to analyze the relationship between expression level of POSTN in the mammary tissue and clinical pathological features of the patients with mammary cancer. Location of POSTN protein in the mammary cancer tissue was identified by HE staining and immunohistochemistry of the mammary cancer tissue chips. Results: Expression level of POSTN mRNA in the mammary cancer tissue was significantly higher than those in the para-cancer and normal mammary tissues (P<0.05), expression level of POSTN mRNA was similar between CAF and NF (P>0.05).POSTN protein mainly expressed in substances of the mammary cancer tissues and less expressed in the mesenchyma of the mammary cancer tissue. Expression level of POSTN mRNA in the mammary cancer tissue was negatively correlated to estrogen receptor (ER) of the patients with mammary cancer (P<0.05). Conclusion: POSTN was mainly expressed in substances of the mammary cancer tissues, high expression of which in the mammary tissues could be related to occurrence and development of the mammary cancer.
Objective: To explore expression status of periostin (POSTN) in the mammary cancer, para-cancer and normal mammary tissues and its clinical significance. Methods: The mammary cancer, para- cancer and normal mammary tissues of 45 patients with mammary cancer，which were taken out by exairesis in Department of Galactophore,Third Affiliated Hospital of Kunming Medical University during May 2012 to December 2016. In addition,from the tissues fifteen amicrobic mammary cancer and normal mammary tissues were selected for primary cell culture.The primary cultured cells were identified by HE staining and immunohistochemistry assays. Expression status of POSTN mRNA in the mammary cancer, para-cancer and normal mammary tissues as well as in the cancer associated fibroblast (CAF) and normal fibroblast (NF) were detected by real-time quality PCR (qPCR). Correlation analysis was used to analyze the relationship between expression level of POSTN in the mammary tissue and clinical pathological features of the patients with mammary cancer. Location of POSTN protein in the mammary cancer tissue was identified by HE staining and immunohistochemistry of the mammary cancer tissue chips. Results: Expression level of POSTN mRNA in the mammary cancer tissue was significantly higher than those in the para-cancer and normal mammary tissues (P<0.05), expression level of POSTN mRNA was similar between CAF and NF (P>0.05).POSTN protein mainly expressed in substances of the mammary cancer tissues and less expressed in the mesenchyma of the mammary cancer tissue. Expression level of POSTN mRNA in the mammary cancer tissue was negatively correlated to estrogen receptor (ER) of the patients with mammary cancer (P<0.05). Conclusion: POSTN was mainly expressed in substances of the mammary cancer tissues, high expression of which in the mammary tissues could be related to occurrence and development of the mammary cancer.
2017, 24(11):1299-1303.
DOI: 10.3872/j.issn.1007-385X.2017.11.010
Abstract:
Objective: To explore expression of taurine upregulated gene 1 (TUG1) in tissue specimens of the patients with diffuse large B-cell lymphoma (DLBCL) and to analyze correlation between expression of TUG1 and clinical features as well as prognosis of the patients with DLBCL. Methods: Tissue specimens of 108 patients who were diagnosed as DLBCL in Department of Hematology, the 1st Hospital affiliated to Southwestern Medical University during January 2011 to December 2016 and 47 patients with reactive lymphoid hyperplasia (RLH) during the same period were collected. qPCR assay was used to detect expressions of TUG1 mRNA in the tissue specimens of the patients with DLBCL or RLH. The relationship between expression level of TUG1 mRNA and clinical pathological features of the patients with DLBCL as well as factors affecting survival time and prognosis of the patients with DLBCL were analyzed by Chi-Square test, Kaplan-Meier assay, univariate and multivariate assays respectively. Results:Expression of TUG1 mRNA in the patients with DLBCL was obviously higher than that in the patients with RLH (6.108±0.332 vs 1.231±0.095, P<0.01). Expression of TUG1 mRNA was evidently related to disease staging,tumor size, B cell symptom, IPI index, GCB subtype and chemotherapy sensitivity in the patients with DLBCL (all P<0.01). Expression of TUG1 mRNA, disease staging and tumor size were the factors affecting over survival time (OS) of the patients with DLBCL (all P<0.05). Expression of TUG1 mRNA, disease staging, IPI index and chemotherapy sensitivity were the factors effecting on prognosis of the patients with DLBCL. Conclusion: TUG1 mRNA was highly expressed in the DLBCL tissues and was the independent factor effecting on prognosis of the patients with DLBCL. TUG1 might be as a novel marker which evaluates prognosis of the patients with DLBCL and as a po-tential target point for gene therapy of DLBCL.
Objective: To explore expression of taurine upregulated gene 1 (TUG1) in tissue specimens of the patients with diffuse large B-cell lymphoma (DLBCL) and to analyze correlation between expression of TUG1 and clinical features as well as prognosis of the patients with DLBCL. Methods: Tissue specimens of 108 patients who were diagnosed as DLBCL in Department of Hematology, the 1st Hospital affiliated to Southwestern Medical University during January 2011 to December 2016 and 47 patients with reactive lymphoid hyperplasia (RLH) during the same period were collected. qPCR assay was used to detect expressions of TUG1 mRNA in the tissue specimens of the patients with DLBCL or RLH. The relationship between expression level of TUG1 mRNA and clinical pathological features of the patients with DLBCL as well as factors affecting survival time and prognosis of the patients with DLBCL were analyzed by Chi-Square test, Kaplan-Meier assay, univariate and multivariate assays respectively. Results:Expression of TUG1 mRNA in the patients with DLBCL was obviously higher than that in the patients with RLH (6.108±0.332 vs 1.231±0.095, P<0.01). Expression of TUG1 mRNA was evidently related to disease staging,tumor size, B cell symptom, IPI index, GCB subtype and chemotherapy sensitivity in the patients with DLBCL (all P<0.01). Expression of TUG1 mRNA, disease staging and tumor size were the factors affecting over survival time (OS) of the patients with DLBCL (all P<0.05). Expression of TUG1 mRNA, disease staging, IPI index and chemotherapy sensitivity were the factors effecting on prognosis of the patients with DLBCL. Conclusion: TUG1 mRNA was highly expressed in the DLBCL tissues and was the independent factor effecting on prognosis of the patients with DLBCL. TUG1 might be as a novel marker which evaluates prognosis of the patients with DLBCL and as a po-tential target point for gene therapy of DLBCL.
2017, 24(11):1304-1308.
DOI: 10.3872/j.issn.1007-385X.2017.11.011
Abstract:
Objective: To explore expression of extracellular matrix protein spondin2 (SPON2) in human gastric carcinoma tissue and its relationship with occurrence of the gastric carcinoma. Methods: Gastric adenocarcinoma and para-carcinoma tissues of 75 patients who hospitalized in Zhangjiagang Hospital affiliated to Suzhou University for eradication of the gastric carcinoma during June 2014 to July 2016 were collected. Immunoflorescence staining was used to survey localization of SPON2 protein in cells of the gastric carcinoma and the para-carcinoma tissues.Expressions of SPON2 in the gastric carcinoma and the para-carcinoma tissues were detected by immunohistochemical staining. Relationship between expression of SPON2 protein and clinicopathological features of the patients with gastric carcinoma was analyzed. Results: SPON2 protein was localized in cytomembrane, cytoplasm and extracellular matrix of the gastric carcinoma cells. Expression of SPON2 protein in the gastric carcinoma tissue was significantly higher than that in the para-carcinoma tissue (72.0% vs 16.0%, P<0.01). There was no relationship between expression of SPON2 protein and tumor cell differentiation, gender, age of the patients with gastric carcinoma, as well as there were significant relationships between expression of SPON2 protein and tumor size, TNM staging, invasion degree, lymph node metastasis (all P<0.05). Conclusion: High expression of SPON2 protein in the gastric carcinoma tissue was related to occurrence and development of the gastric carcinoma, which suggests that SPON2 protein might become a novel marker of early clinical diagnosis and a potential therapeutic target of the gas-tric carcinoma as well as could forecast prognosis of the patients with gastric carcinoma.
Objective: To explore expression of extracellular matrix protein spondin2 (SPON2) in human gastric carcinoma tissue and its relationship with occurrence of the gastric carcinoma. Methods: Gastric adenocarcinoma and para-carcinoma tissues of 75 patients who hospitalized in Zhangjiagang Hospital affiliated to Suzhou University for eradication of the gastric carcinoma during June 2014 to July 2016 were collected. Immunoflorescence staining was used to survey localization of SPON2 protein in cells of the gastric carcinoma and the para-carcinoma tissues.Expressions of SPON2 in the gastric carcinoma and the para-carcinoma tissues were detected by immunohistochemical staining. Relationship between expression of SPON2 protein and clinicopathological features of the patients with gastric carcinoma was analyzed. Results: SPON2 protein was localized in cytomembrane, cytoplasm and extracellular matrix of the gastric carcinoma cells. Expression of SPON2 protein in the gastric carcinoma tissue was significantly higher than that in the para-carcinoma tissue (72.0% vs 16.0%, P<0.01). There was no relationship between expression of SPON2 protein and tumor cell differentiation, gender, age of the patients with gastric carcinoma, as well as there were significant relationships between expression of SPON2 protein and tumor size, TNM staging, invasion degree, lymph node metastasis (all P<0.05). Conclusion: High expression of SPON2 protein in the gastric carcinoma tissue was related to occurrence and development of the gastric carcinoma, which suggests that SPON2 protein might become a novel marker of early clinical diagnosis and a potential therapeutic target of the gas-tric carcinoma as well as could forecast prognosis of the patients with gastric carcinoma.
HAN Tao
,
LUAN Yuting
,
GE Yanan
,
WANG Shiyu
,
YANG Xiaodan
,
LIU Lu
,
LIU Zhaozhe
,
LIU Yongye
,
ZHENG Zhendong
2017, 24(11):1309-1314.
DOI: 10.3872/j.issn.1007-385X.2017.11.012
Abstract:
Objective: To explore independent risk factors affecting prognosis of the patients with liver cancer and their correlative features to action target points of targeting drug for liver cancer (sorafenib) via survey and analysis of bio-information. Methods: Data of gene expression, survival time and survival status of the 79 patients with liver cancer who finally died were selected from the 248 patients with liver cancer in the TCGA data base, the died patients were divided into 2 groups according to medium survival time of 360 days as a dividing line. Differential genes were screened out among data of the gene expression in patients of the 2 groups by DEseq algorithm. Without considering other mingled factors and only considering a single factor of differential gene expression and its correlation with survival time of the patients, uni-variate analysis of the differential genes was made by Kaplan-Meier assay.Survival analysis of a matrix integrated with the differential gene expression obtained by the analysis，survival time and survival status of the patients was made by COX regression model, in order to look for independent risk factors affecting prognosis of the patients with liver cancer. Based on STRING data base, a protein interconnected network was constructed with the obtained differential genes and action target points of sorafenib, targeting drug for liver cancer, to seek relationship of the action target points of sorafenib with the differential genes. Results: Fifty two differential genes that could affect prognosis of the patients with liver cancer were obtained by preliminary screening of DEseq algorithm. Twenty six differential genes relating to survival time of the patients were obtained by Kaplan-Meier assay. Three differential genes (SQSTM1, ANXA10 and STMN1) were finally confirmed as independent risk factors affecting prognosis of the patients with liver cancer by COX analysis. The protein-protein interaction network revealed that the action target points of sorafenib, targetin drug for liver cancer, were closely related to multiple differential genes. ANXA10 involved in combine of calcium ion and combination of calcium dependent phospholipids. STMN1 and SQSTM1 played a important role in multiple signaling pathways. Conclusion: ANXA10,STMN1 and SQSTM1 could be independent risk factors affecting prognosis of the patients with liver cancer, which might be used as action target points of targeting drug developed or prediction index of prognosis of the patients in future.
Objective: To explore independent risk factors affecting prognosis of the patients with liver cancer and their correlative features to action target points of targeting drug for liver cancer (sorafenib) via survey and analysis of bio-information. Methods: Data of gene expression, survival time and survival status of the 79 patients with liver cancer who finally died were selected from the 248 patients with liver cancer in the TCGA data base, the died patients were divided into 2 groups according to medium survival time of 360 days as a dividing line. Differential genes were screened out among data of the gene expression in patients of the 2 groups by DEseq algorithm. Without considering other mingled factors and only considering a single factor of differential gene expression and its correlation with survival time of the patients, uni-variate analysis of the differential genes was made by Kaplan-Meier assay.Survival analysis of a matrix integrated with the differential gene expression obtained by the analysis，survival time and survival status of the patients was made by COX regression model, in order to look for independent risk factors affecting prognosis of the patients with liver cancer. Based on STRING data base, a protein interconnected network was constructed with the obtained differential genes and action target points of sorafenib, targeting drug for liver cancer, to seek relationship of the action target points of sorafenib with the differential genes. Results: Fifty two differential genes that could affect prognosis of the patients with liver cancer were obtained by preliminary screening of DEseq algorithm. Twenty six differential genes relating to survival time of the patients were obtained by Kaplan-Meier assay. Three differential genes (SQSTM1, ANXA10 and STMN1) were finally confirmed as independent risk factors affecting prognosis of the patients with liver cancer by COX analysis. The protein-protein interaction network revealed that the action target points of sorafenib, targetin drug for liver cancer, were closely related to multiple differential genes. ANXA10 involved in combine of calcium ion and combination of calcium dependent phospholipids. STMN1 and SQSTM1 played a important role in multiple signaling pathways. Conclusion: ANXA10,STMN1 and SQSTM1 could be independent risk factors affecting prognosis of the patients with liver cancer, which might be used as action target points of targeting drug developed or prediction index of prognosis of the patients in future.
TIE Xiaojing
,
SHEN Fengqian
,
QU Fulian
,
ZHANG Yan
,
YI Zhenying
,
LIU Peijie
,
GAO Ling
,
LI Ning
,
XU Zhiqiao
2017, 24(11):1315-1319.
DOI: 10.3872/j.issn.1007-385X.2017.11.013
Abstract:
Objective: To explore efficacy of apatinib plus S-1 to treat the patients with recurrent and metastatic esophageal cancer as 2nd line therapy and its toxic and side effects. Methods: Twenty-four patients with recurrent and metastatic esophageal cancer who diagnosed and remedied in Department of Oncology, the Central Hospital of Kaifeng during June 2015 to December 2016 were collected. Them were divided into Observation and Control groups. Ten patients in the Observation group took orally apatinib plus S-1 as chemotherapy, apatinib was orally taken in 500 mg/d and S-1 taken according to body surface area for 1 to 14 days. Twenty eight days were as one cycle.Fourteen patients in the Control group were treated with routine S-1. Results: After two cycles, efficacy of the chemotherapy was evaluated as CR 0 case; PR 5 cases; SD 3 cases and PD 2 cases. ORR was 50% (5/10) and DCR was 80% (8/10). Before the chemotherapy, baseline diameter sum of 20 target lesions was 71.5 cm, diameter sum of the 20 target lesions became 40.5 cm after 2 cycles of the chemotherapy, and the diameter sum decreased by 43.36%compared with the baseline diameter sum. After six patients completed 4 cycles of the combination chemotherapy,the patients whose efficacy evaluation were effective or stable continued to take orally apatinib alone for maintenance therapy, the longest PFS of the patients was 9 months and their shortest PFS 6 months. Sever drug-related toxic and side effects didn’t be observed. Conclusion: Efficacy of apatinib plus S-1 to treat the patients with recurrent and metastatic esophageal cancer as 2nd line therapy might be better, and its safety and tolerability could be acceptable.
Objective: To explore efficacy of apatinib plus S-1 to treat the patients with recurrent and metastatic esophageal cancer as 2nd line therapy and its toxic and side effects. Methods: Twenty-four patients with recurrent and metastatic esophageal cancer who diagnosed and remedied in Department of Oncology, the Central Hospital of Kaifeng during June 2015 to December 2016 were collected. Them were divided into Observation and Control groups. Ten patients in the Observation group took orally apatinib plus S-1 as chemotherapy, apatinib was orally taken in 500 mg/d and S-1 taken according to body surface area for 1 to 14 days. Twenty eight days were as one cycle.Fourteen patients in the Control group were treated with routine S-1. Results: After two cycles, efficacy of the chemotherapy was evaluated as CR 0 case; PR 5 cases; SD 3 cases and PD 2 cases. ORR was 50% (5/10) and DCR was 80% (8/10). Before the chemotherapy, baseline diameter sum of 20 target lesions was 71.5 cm, diameter sum of the 20 target lesions became 40.5 cm after 2 cycles of the chemotherapy, and the diameter sum decreased by 43.36%compared with the baseline diameter sum. After six patients completed 4 cycles of the combination chemotherapy,the patients whose efficacy evaluation were effective or stable continued to take orally apatinib alone for maintenance therapy, the longest PFS of the patients was 9 months and their shortest PFS 6 months. Sever drug-related toxic and side effects didn’t be observed. Conclusion: Efficacy of apatinib plus S-1 to treat the patients with recurrent and metastatic esophageal cancer as 2nd line therapy might be better, and its safety and tolerability could be acceptable.
2017, 24(11):1320-1325.
DOI: 10.3872/j.issn.1007-385X.2017.11.014
Abstract:
患者来源的肿瘤异种移植（patient-derived tumor xenografts，PDTX）模型，因其较好地保留了原代肿瘤的遗传、分子、形态结构等方面的特征，维持了肿瘤干细胞的特性，能反映患者肿瘤的遗传多样性，并且在对治疗的反应性上也与患者保持较高的一致性，现已越来越多地被应用于临床前期研究。近年来，NSG(NOD/LtSz-Prkdcscid Il2rgtm1Wjl/J)、NOG(NOD.Cg-PrkdcscidIL2rgtm1Sug/JicCrl)和NCG(NOD-Prkdcem26Cd52Il2rgem26Cd22/Nju）等免疫缺陷小鼠的研发成功，推动了新一代PDTX模型研究的快速发展。由于新一代PDTX模型建立所需样本量小，经过冷冻的组织与新鲜组织成瘤率无明显差异，为一些难以获取大量样本的肿瘤组织提供了研究材料。笔者对近年来PDTX模型用于个性化治疗方案的筛选制定、药物的临床前研究、肿瘤耐药机制的研究、肿瘤标志物及敏感指标的筛选、肿瘤微环境的研究以及患者预后的评估等的发展现状作一综述。
患者来源的肿瘤异种移植（patient-derived tumor xenografts，PDTX）模型，因其较好地保留了原代肿瘤的遗传、分子、形态结构等方面的特征，维持了肿瘤干细胞的特性，能反映患者肿瘤的遗传多样性，并且在对治疗的反应性上也与患者保持较高的一致性，现已越来越多地被应用于临床前期研究。近年来，NSG(NOD/LtSz-Prkdcscid Il2rgtm1Wjl/J)、NOG(NOD.Cg-PrkdcscidIL2rgtm1Sug/JicCrl)和NCG(NOD-Prkdcem26Cd52Il2rgem26Cd22/Nju）等免疫缺陷小鼠的研发成功，推动了新一代PDTX模型研究的快速发展。由于新一代PDTX模型建立所需样本量小，经过冷冻的组织与新鲜组织成瘤率无明显差异，为一些难以获取大量样本的肿瘤组织提供了研究材料。笔者对近年来PDTX模型用于个性化治疗方案的筛选制定、药物的临床前研究、肿瘤耐药机制的研究、肿瘤标志物及敏感指标的筛选、肿瘤微环境的研究以及患者预后的评估等的发展现状作一综述。
2017, 24(11):1326-1330.
DOI: 10.3872/j.issn.1007-385X.2017.11.015
Abstract:
细胞外囊泡(extracellular vesicles, EVs)是细胞旁分泌产生的一种亚细胞成分，主要分为外泌体(exosome)、微囊泡(microvesicle)两种类型，正常细胞和肿瘤细胞均可分泌EVs。肺癌细胞分泌的EVs参与肺癌生物学功能和肿瘤微环境调节，对肺癌的发生发展发挥重要作用。由于EVs包含的物质及特殊的分子结构决定其在肺癌的早期诊断、作为免疫调节剂、化疗药物载体等方面具有独特的临床应用价值，因此本篇综述主要介绍肺癌中EVs 研究的进展，为肺癌的早期诊断、治疗及预后提供重要的依据。
细胞外囊泡(extracellular vesicles, EVs)是细胞旁分泌产生的一种亚细胞成分，主要分为外泌体(exosome)、微囊泡(microvesicle)两种类型，正常细胞和肿瘤细胞均可分泌EVs。肺癌细胞分泌的EVs参与肺癌生物学功能和肿瘤微环境调节，对肺癌的发生发展发挥重要作用。由于EVs包含的物质及特殊的分子结构决定其在肺癌的早期诊断、作为免疫调节剂、化疗药物载体等方面具有独特的临床应用价值，因此本篇综述主要介绍肺癌中EVs 研究的进展，为肺癌的早期诊断、治疗及预后提供重要的依据。
2017, 24(11):1331-1335.
DOI: 10.3872/j.issn.1007-385X.2017.11.016
Abstract:
胃癌是由多基因改变、多因素参与和多阶段发生的一个复杂病变过程, 研究表明微小RNA（microRNA，miRNA）与胃癌的发生发展密切相关，可参与多种信号通路调节，与多种信号通路相互作用, 通过激活或抑制相关信号通路影响胃癌细胞的增殖、侵袭、转移及药物敏感性等生物学功能。目前，胃癌中研究比较广泛的与miRNA 功能相关的信号通路主要集中于PI3K/AKT、Wnt/β-Catenin/Tcf、Ras/Raf/MEK/ERK、p53 及TGF-β 等信号通路，本文对胃癌中这些miRNA功能相关信号通路的研究进展作一综述。
胃癌是由多基因改变、多因素参与和多阶段发生的一个复杂病变过程, 研究表明微小RNA（microRNA，miRNA）与胃癌的发生发展密切相关，可参与多种信号通路调节，与多种信号通路相互作用, 通过激活或抑制相关信号通路影响胃癌细胞的增殖、侵袭、转移及药物敏感性等生物学功能。目前，胃癌中研究比较广泛的与miRNA 功能相关的信号通路主要集中于PI3K/AKT、Wnt/β-Catenin/Tcf、Ras/Raf/MEK/ERK、p53 及TGF-β 等信号通路，本文对胃癌中这些miRNA功能相关信号通路的研究进展作一综述。
2017, 24(11):1336-1338.
DOI: 10.3872/j.issn.1007-385X.2017.11.017
Abstract:
目的：探讨靶向生长分化因子15（growth differentiation factor 15，GDF15）基因siRNA 对人肺腺癌SPCA1 细胞增殖和迁移的影响。方法：根据基因数据库（GenBank）设计并合成3 条人GDF15 基因siRNA（GDF15-siRNA161、GDF15-siRNA290 和GDF15-siRNA860）和阴性对照NC-siRNA 序列，采用qPCR法测定转染不同GDF15-siRNA 的SPCA1 细胞中GDF15 mRNA表达水平，筛选有效抑制GDF15 基因表达的siRNA。CCK-8 法和划痕实验分别检测转染有效GDF15-siRNA 和NC-siRNA 的SPCA1 细胞增殖和迁移能力。结果：3 条GDF15-siRNA 对SPCA1 细胞GDF15 mRNA表达均有明显抑制（P<0.01），其中GDF15-siRNA161抑制最为明显。和转染NC-siRNA 的SPCA1 细胞相比，转染GDF15-siRNA161的SPCA1 细胞增殖明显减慢[ （0.46±0.03）vs（0.52±0.01），P<0.01]，转染GDF15-siRNA161的SPCA1 细胞迁移速度明显低于转染NC-siRNA的SPCA1 细胞（P<0.01）。结论：有效沉默人肺腺癌SPCA1 细胞GDF15基因表达能抑制肺腺癌细胞的增殖和迁移，GDF15 可能成为人肺腺癌基因治疗的候选靶点。
目的：探讨靶向生长分化因子15（growth differentiation factor 15，GDF15）基因siRNA 对人肺腺癌SPCA1 细胞增殖和迁移的影响。方法：根据基因数据库（GenBank）设计并合成3 条人GDF15 基因siRNA（GDF15-siRNA161、GDF15-siRNA290 和GDF15-siRNA860）和阴性对照NC-siRNA 序列，采用qPCR法测定转染不同GDF15-siRNA 的SPCA1 细胞中GDF15 mRNA表达水平，筛选有效抑制GDF15 基因表达的siRNA。CCK-8 法和划痕实验分别检测转染有效GDF15-siRNA 和NC-siRNA 的SPCA1 细胞增殖和迁移能力。结果：3 条GDF15-siRNA 对SPCA1 细胞GDF15 mRNA表达均有明显抑制（P<0.01），其中GDF15-siRNA161抑制最为明显。和转染NC-siRNA 的SPCA1 细胞相比，转染GDF15-siRNA161的SPCA1 细胞增殖明显减慢[ （0.46±0.03）vs（0.52±0.01），P<0.01]，转染GDF15-siRNA161的SPCA1 细胞迁移速度明显低于转染NC-siRNA的SPCA1 细胞（P<0.01）。结论：有效沉默人肺腺癌SPCA1 细胞GDF15基因表达能抑制肺腺癌细胞的增殖和迁移，GDF15 可能成为人肺腺癌基因治疗的候选靶点。
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.