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Volume 24,Issue 9,2017 Table of Contents
2017, 24(9):929-937.
DOI: 10.3872/j.issn.1007-385X.2017.09.001
Abstract:
Many advances in the treatment of cancer have been driven by the development of targeted therapies that inhibit oncogenic signaling pathways and tumor-associated angiogenesis, as well as by the therapies that acti-vate immune system to unleash antitumor immunity. Many clinically approved therapies, including monoclonal anti-bodies，antibody-drug conjugates，bispecific antibodies and immune checkpoints, have become important strategies for cancer treatment. Recently, tumor immunotherapy is becoming more and more popular, and antibody medicines acquiring above mentioned immune-modulating effects, such as increasing tumor antigenicity or promoting intratu-moral T cell infiltration, had achieved great clinical benefits; monoclonal antibody medicine in combination with tu-mor immunotherapy, molecular targeted antibody medicine, chemotherapy or small molecular inhibitors and even surgery, will further enlarge the application value of antibody medicines in tumor therapies.
Many advances in the treatment of cancer have been driven by the development of targeted therapies that inhibit oncogenic signaling pathways and tumor-associated angiogenesis, as well as by the therapies that acti-vate immune system to unleash antitumor immunity. Many clinically approved therapies, including monoclonal anti-bodies，antibody-drug conjugates，bispecific antibodies and immune checkpoints, have become important strategies for cancer treatment. Recently, tumor immunotherapy is becoming more and more popular, and antibody medicines acquiring above mentioned immune-modulating effects, such as increasing tumor antigenicity or promoting intratu-moral T cell infiltration, had achieved great clinical benefits; monoclonal antibody medicine in combination with tu-mor immunotherapy, molecular targeted antibody medicine, chemotherapy or small molecular inhibitors and even surgery, will further enlarge the application value of antibody medicines in tumor therapies.
2017, 24(9):938-943.
DOI: 10.3872/j.issn.1007-385X.2017.09.002
Abstract:
Objective: To study the cytotoxicity of specific cytotoxic T lymphocyte (CTL) induced by EBV-LPM2A peptide on human EBV associated gastric cancer cells in vitro. Methods: The peripheral blood mononucle-ar cells (PBMC) of HLA-A2 positive gastric cancer patients from Cancer Center of Drum Tower Hospital Affiliated to Medical School of Nanjing University, human gastric adenocarcinoma cell line (AGS) and human EBV positive adenocarcinoma cell line (AGS-EBV) were selected. By modified in vitro cell culture technique, specific CTL was amplified from human PBMCs with the induction of HLA-A2 restricted EBV-LMP2A peptide; the content of specif-ic CTL induced by peptide was detected by the method of tetramer and Flow cytometry; the in vitro cytotoxicity of EBV-CTL on both EBV + and EBV - human gastric cancer cells was detected by FITC-PI. Results: Modified cell cul-ture technique and EBV-LMP2A peptide can induce a high proportion of antigen specific CTL (EBV-LMP2A-356 specific T cells accounted for [47.1±5.2]% of CD8 + T cells）; the cytotoxicity of EBV-CTL on EBV + gastric cancer cells was significantly stronger than that of EBV - gastric cancer cells ([45.1±9.3]% vs [19.4±2.5]%，P<0.05). Con-clusion: Using the modified cell culture technique, EBV-LMP2A antigen peptide can induce a high proportion of EBV specific CTL, which has high specific cytotoxicity on EBV + gastric cancer cells.
Objective: To study the cytotoxicity of specific cytotoxic T lymphocyte (CTL) induced by EBV-LPM2A peptide on human EBV associated gastric cancer cells in vitro. Methods: The peripheral blood mononucle-ar cells (PBMC) of HLA-A2 positive gastric cancer patients from Cancer Center of Drum Tower Hospital Affiliated to Medical School of Nanjing University, human gastric adenocarcinoma cell line (AGS) and human EBV positive adenocarcinoma cell line (AGS-EBV) were selected. By modified in vitro cell culture technique, specific CTL was amplified from human PBMCs with the induction of HLA-A2 restricted EBV-LMP2A peptide; the content of specif-ic CTL induced by peptide was detected by the method of tetramer and Flow cytometry; the in vitro cytotoxicity of EBV-CTL on both EBV + and EBV - human gastric cancer cells was detected by FITC-PI. Results: Modified cell cul-ture technique and EBV-LMP2A peptide can induce a high proportion of antigen specific CTL (EBV-LMP2A-356 specific T cells accounted for [47.1±5.2]% of CD8 + T cells）; the cytotoxicity of EBV-CTL on EBV + gastric cancer cells was significantly stronger than that of EBV - gastric cancer cells ([45.1±9.3]% vs [19.4±2.5]%，P<0.05). Con-clusion: Using the modified cell culture technique, EBV-LMP2A antigen peptide can induce a high proportion of EBV specific CTL, which has high specific cytotoxicity on EBV + gastric cancer cells.
2017, 24(9):944-949.
DOI: 10.3872/j.issn.1007-385X.2017.09.003
Abstract:
Objective: To investigate the effect and mechanism of miR-223 regulating the proliferation and in vivo tumorigenesis of acute lymphoblastic leukemia (ALL) E6-1 cells. Methods: The expression of miR-223 in different ALL cell lines was detected by Real-time fluorescence quantitative PCR. Immunofluorescence was used to detect the transfection efficiency of miR-223mimic-lenitvirus transfected E6-1 cell line. Double luciferase assay was used to detect the binding between miR-223 and Lmo2. MTT assay and clone formation assay were used to detect the ef-fect of miR-223 on the proliferation and clone formation ability of E6-1 cell line. The effect of miR-223 expression on the tumorigenic ability of E6-1 cells was detected by xenograft formation in nude mice. Western blotting was used to detect the effect of miR-223 on the expressions of MAPK signal pathway related proteins. Results: The ex-pression level of miR-223 in E6-1 cell line was relatively low (P<0.05). Double luciferase assay confirmed that miR-223 could directly target the 3’UTR of Lmo2. Overexpression of miR-223 inhibited the proliferation (0.16±0.02 vs 1.15±0.21，P<0.05) and tumorigenesis ([0.56±0.08]g vs [1.69±0.22]g，P<0.05) of E6-1 cells and regulated the ac-tivity of MAPK signal pathway. Conclusion: miR-223 can regulate the proliferation, clone formation and in vivo tu-morigenesis ofALL cells through targeting Lmo2 and MAPK signal pathway.
Objective: To investigate the effect and mechanism of miR-223 regulating the proliferation and in vivo tumorigenesis of acute lymphoblastic leukemia (ALL) E6-1 cells. Methods: The expression of miR-223 in different ALL cell lines was detected by Real-time fluorescence quantitative PCR. Immunofluorescence was used to detect the transfection efficiency of miR-223mimic-lenitvirus transfected E6-1 cell line. Double luciferase assay was used to detect the binding between miR-223 and Lmo2. MTT assay and clone formation assay were used to detect the ef-fect of miR-223 on the proliferation and clone formation ability of E6-1 cell line. The effect of miR-223 expression on the tumorigenic ability of E6-1 cells was detected by xenograft formation in nude mice. Western blotting was used to detect the effect of miR-223 on the expressions of MAPK signal pathway related proteins. Results: The ex-pression level of miR-223 in E6-1 cell line was relatively low (P<0.05). Double luciferase assay confirmed that miR-223 could directly target the 3’UTR of Lmo2. Overexpression of miR-223 inhibited the proliferation (0.16±0.02 vs 1.15±0.21，P<0.05) and tumorigenesis ([0.56±0.08]g vs [1.69±0.22]g，P<0.05) of E6-1 cells and regulated the ac-tivity of MAPK signal pathway. Conclusion: miR-223 can regulate the proliferation, clone formation and in vivo tu-morigenesis ofALL cells through targeting Lmo2 and MAPK signal pathway.
2017, 24(9):950-954.
DOI: 10.3872/j.issn.1007-385X.2017.09.004
Abstract:
Objective: To investigate whether the expression of Toll like receptor-4 (TLR-4) has an effect on the phenotypes and function of dendritic cells (DCs) and the possible mechanism. Methods: pcDNA3.1 plasmid encod-ing full TLR-4 gene sequence was constructed as a template to obtain TLR-4 mRNA through in vitro transcription us-ing mMESSAGE mMACHINE T7 Kit; DCs from healthy human peripheral blood were transfected with TLR-4 mRNA by liposomal transfection. The functional molecule expression on DC surface and the ability of DC inducing cytotoxic T lymphocytes (CTLs) to secrete cytokines in vitro were detected by Flow cytometry after transfection.Results: Human TLR-4-pcDNA3.1 plasmid was successfully constructed; human TLR-4 and EGFP mRNA frag-ments were successfully amplified. The Flow cytometry results showed that the expressions of chemokine CCR7 and functional molecule HLA-DR on dendritic cell surface were significantly increased after transfection with TLR-4 mRNA compared with control mRNA transfection or pre-ransfection (CCR7: [42.4±4.93]% vs [20.1±3.09]%，[17.1±4.33]%，P<0.05; HLA-DR:[62.1±7.23]% vs [17.7±6.01]%，25.8±4.16]%，P<0.05); and the ability of secret-ing IFN-γ from CTLs induced by TLR-4 mRNA-DCS was significantly enhanced in vitro compared with control mRNA-DC，empty-DC and PBMC ([66.5±3.58]% vs [41.1±4.27]%，[37.9±2.96]%，[3.2±2.03]%，P<0.05). Conclu-sion: The function of dendritic cells could be significantly enhanced by TLR-4 mRNAtransfection. The ability of an-tigen presentation and inducing CTLs of dendritic cell were improved, which would provide an experimental basis for enhancing the anti-tumor effect of DC vaccines.
Objective: To investigate whether the expression of Toll like receptor-4 (TLR-4) has an effect on the phenotypes and function of dendritic cells (DCs) and the possible mechanism. Methods: pcDNA3.1 plasmid encod-ing full TLR-4 gene sequence was constructed as a template to obtain TLR-4 mRNA through in vitro transcription us-ing mMESSAGE mMACHINE T7 Kit; DCs from healthy human peripheral blood were transfected with TLR-4 mRNA by liposomal transfection. The functional molecule expression on DC surface and the ability of DC inducing cytotoxic T lymphocytes (CTLs) to secrete cytokines in vitro were detected by Flow cytometry after transfection.Results: Human TLR-4-pcDNA3.1 plasmid was successfully constructed; human TLR-4 and EGFP mRNA frag-ments were successfully amplified. The Flow cytometry results showed that the expressions of chemokine CCR7 and functional molecule HLA-DR on dendritic cell surface were significantly increased after transfection with TLR-4 mRNA compared with control mRNA transfection or pre-ransfection (CCR7: [42.4±4.93]% vs [20.1±3.09]%，[17.1±4.33]%，P<0.05; HLA-DR:[62.1±7.23]% vs [17.7±6.01]%，25.8±4.16]%，P<0.05); and the ability of secret-ing IFN-γ from CTLs induced by TLR-4 mRNA-DCS was significantly enhanced in vitro compared with control mRNA-DC，empty-DC and PBMC ([66.5±3.58]% vs [41.1±4.27]%，[37.9±2.96]%，[3.2±2.03]%，P<0.05). Conclu-sion: The function of dendritic cells could be significantly enhanced by TLR-4 mRNAtransfection. The ability of an-tigen presentation and inducing CTLs of dendritic cell were improved, which would provide an experimental basis for enhancing the anti-tumor effect of DC vaccines.
LIAO Yu
,
REN Ningchuan
,
FANG Dianliang
,
HU Yongqiang
,
HUANG Jian
,
ZENG Bo
,
HE Ping
,
YANG Tianwen
2017, 24(9):955-959.
DOI: 10.3872/j.issn.1007-385X.2017.09.005
Abstract:
Objective: To explore the effects of S100A4 on the migration and invasion capacity of gastric cancer SGC-7901 cells under hypoxia condition, and to identify the possible mechanism; Methods: The gastric cancer cell line, SGC-7901 was transfected with chemically synthesized si-S100A4 plasmidand si-control plasmid (negative control). Depend-ing on the different culture conditions, SGC-7901 cells were further divided into four groups: normoxia （Nor）+si-S100A4 group, Nor+si-Ctrl group, hypoxia(Hyp) + si-Ctrl group and Hyp+si-S100A4 group. Under the hypoxia condition, the pro-tein expressions of HIF-1 and S100A4 in SGC-7901 cells were detected using the Western blotting assay. The effects of si-S100A4 on the expression of S100A4, β-catenin and TCF-4 upon hypoxia condition were further explored. Moreover, the Transwell assay were conducted to explore the effects of hypoxia and si-S100A4 on the migration and invasion capacity of gastric cancer SGC-7901 cells. Results: Under the hypoxia condition, (1) the expression of HIF-1 and S100A4 in gas-tric cancer SGC-7901 cells were significantly up-regulated (3.12±0.23 vs 1.02±0.05，P<0.01; 2.75±0.32 vs 1.05±0.07, P<0.01), and the expressions were significantly correlated (r=0.67，P<0.01); (2) the migration and invasion capacity of SGC-7901 cells were significantly increased (223.31±35.12 vs 131.29±26.40,142.27±26.37,P<0.05]. Under hypoxia+si-S100A4 condition: (1) the promotion effect of hypoxia on the expressions of β-catenin and TCF-4 was significantly re-duced (all P<0.01); (2) the promotion effect of hypoxia on the migration and invasion ability of SGC-7901 cells was sig-nificantly decreased (161.37±31.02 vs 88.21±22.42、95.36±21.29, P<0.05). Conclusion: S100A4 promoted the migration and invasion capacity of gastric cancer SGC-7901 cells, which was possibly achieved by synergistically working with HIF-1 to regulate Wnt/β-catenin pathway.
Objective: To explore the effects of S100A4 on the migration and invasion capacity of gastric cancer SGC-7901 cells under hypoxia condition, and to identify the possible mechanism; Methods: The gastric cancer cell line, SGC-7901 was transfected with chemically synthesized si-S100A4 plasmidand si-control plasmid (negative control). Depend-ing on the different culture conditions, SGC-7901 cells were further divided into four groups: normoxia （Nor）+si-S100A4 group, Nor+si-Ctrl group, hypoxia(Hyp) + si-Ctrl group and Hyp+si-S100A4 group. Under the hypoxia condition, the pro-tein expressions of HIF-1 and S100A4 in SGC-7901 cells were detected using the Western blotting assay. The effects of si-S100A4 on the expression of S100A4, β-catenin and TCF-4 upon hypoxia condition were further explored. Moreover, the Transwell assay were conducted to explore the effects of hypoxia and si-S100A4 on the migration and invasion capacity of gastric cancer SGC-7901 cells. Results: Under the hypoxia condition, (1) the expression of HIF-1 and S100A4 in gas-tric cancer SGC-7901 cells were significantly up-regulated (3.12±0.23 vs 1.02±0.05，P<0.01; 2.75±0.32 vs 1.05±0.07, P<0.01), and the expressions were significantly correlated (r=0.67，P<0.01); (2) the migration and invasion capacity of SGC-7901 cells were significantly increased (223.31±35.12 vs 131.29±26.40,142.27±26.37,P<0.05]. Under hypoxia+si-S100A4 condition: (1) the promotion effect of hypoxia on the expressions of β-catenin and TCF-4 was significantly re-duced (all P<0.01); (2) the promotion effect of hypoxia on the migration and invasion ability of SGC-7901 cells was sig-nificantly decreased (161.37±31.02 vs 88.21±22.42、95.36±21.29, P<0.05). Conclusion: S100A4 promoted the migration and invasion capacity of gastric cancer SGC-7901 cells, which was possibly achieved by synergistically working with HIF-1 to regulate Wnt/β-catenin pathway.
2017, 24(9):960-965.
DOI: 10.3872/j.issn.1007-385X.2017.09.006
Abstract:
Objective: To investigate the effect of EZH2 (enhancer of zeste homolog 2) overexpression or knock-down on the proliferation of esophageal cancer cells. Methods: Human esophageal cancer cell lines ECA109, TE1,KYSE30 and KYSE170 were selected as the research objects. The expression of EZH2 mRNA and protein in esoph-ageal carcinoma cells were detected by Real-time fluorescence quantitative PCR (qPCR) and Western blotting, re-spectively. The mRNA expression of four esophageal cancer cells after overexpression or knockdown of EZH2 was detected by qPCR. The effects of EZH2 overexpression or knockdown as well as EZH2 inhibitor DZNep (3-deazane-planocin A) on the proliferation and clone growth rate of esophageal cancer cells were observed by CCK-8 prolifera-tion assay and clone formation assay. Results: The expression of EZH2 mRNA and protein in ECA109 and TE1 cells was significantly higher than that in KYSE30 and KYSE170 cells (P<0.05). The expression of EZH2 in esoph-ageal cancer TE1 and ECA109 cells was down-regulated after transfection with EZH2-ShRNA, and the cell prolifer-ation was decreased (1.07±0.08 vs 1.59±0.09, P<0.05; 1.05±0.11 vs 0.88±0.08, P<0.05), and the clone formation was also down-regulated (200.00±11.43 vs 480.00±13.10, P<0.05；88.00±8.16 vs 220.00±14.69, P<0.05). The ex-pression of EZH2 was increased in esophageal cancer KYSE30 and KYSE170 cells after transfection of EZH2 over-expression plasmid, and the proliferation ability (1.06±0.07 vs 0.76±0.06, P<0.05；3.36±0.30 vs 1.50±0.08, P<0.05)and clone formation (45.00±3.27 vs 18.00±1.63，P<0.05；65.00±4.08 vs 23.00±2.45，P<0.05) were significantly in-creased. After DZNep treatment, proliferation (all P<0.05) and clone formation (all P<0.05) in ECA109 and TE1 cells were decreased. Conclusion: EZH2 gene can effectively promote the proliferation and cloning ability of esoph-ageal cancer cells, which provides a basis for further study on the mechanism of EZH2 as a target in the treatment of esophageal cancer.
Objective: To investigate the effect of EZH2 (enhancer of zeste homolog 2) overexpression or knock-down on the proliferation of esophageal cancer cells. Methods: Human esophageal cancer cell lines ECA109, TE1,KYSE30 and KYSE170 were selected as the research objects. The expression of EZH2 mRNA and protein in esoph-ageal carcinoma cells were detected by Real-time fluorescence quantitative PCR (qPCR) and Western blotting, re-spectively. The mRNA expression of four esophageal cancer cells after overexpression or knockdown of EZH2 was detected by qPCR. The effects of EZH2 overexpression or knockdown as well as EZH2 inhibitor DZNep (3-deazane-planocin A) on the proliferation and clone growth rate of esophageal cancer cells were observed by CCK-8 prolifera-tion assay and clone formation assay. Results: The expression of EZH2 mRNA and protein in ECA109 and TE1 cells was significantly higher than that in KYSE30 and KYSE170 cells (P<0.05). The expression of EZH2 in esoph-ageal cancer TE1 and ECA109 cells was down-regulated after transfection with EZH2-ShRNA, and the cell prolifer-ation was decreased (1.07±0.08 vs 1.59±0.09, P<0.05; 1.05±0.11 vs 0.88±0.08, P<0.05), and the clone formation was also down-regulated (200.00±11.43 vs 480.00±13.10, P<0.05；88.00±8.16 vs 220.00±14.69, P<0.05). The ex-pression of EZH2 was increased in esophageal cancer KYSE30 and KYSE170 cells after transfection of EZH2 over-expression plasmid, and the proliferation ability (1.06±0.07 vs 0.76±0.06, P<0.05；3.36±0.30 vs 1.50±0.08, P<0.05)and clone formation (45.00±3.27 vs 18.00±1.63，P<0.05；65.00±4.08 vs 23.00±2.45，P<0.05) were significantly in-creased. After DZNep treatment, proliferation (all P<0.05) and clone formation (all P<0.05) in ECA109 and TE1 cells were decreased. Conclusion: EZH2 gene can effectively promote the proliferation and cloning ability of esoph-ageal cancer cells, which provides a basis for further study on the mechanism of EZH2 as a target in the treatment of esophageal cancer.
2017, 24(9):966-971.
DOI: 10.3872/j.issn.1007-385X.2017.09.007
Abstract:
Objective: To investigate the clinical efficacy and safety of autogenous dendritic cell-cytokine induced killer (DC-CIK) cell combined with chemotherapy in treatment of locally advanced unresectable or metastatic gas-tric adenocarcinoma. Methods: In this randomized and controlled trial, 32 patients with advanced gastric adenocar-cinoma, who were hospitalized in the Department of Medical Oncology, Cancer Hospital, Chinese Academy of Med-ical Sciences during November, 2014 to July, 2016, were divided into the combined treatment group (16 cases for DC-CIK cell combined chemotherapy) and the mono-drug group (16 cases for chemotherapy alone) by the ration of 1∶1. The baseline data of two groups were comparable. Peripheral blood mononuclear cells (PBMCs) were collected from patients of both groups to obtain DC and CIK cells via in vitro culture. The mono-drug group was treated with SOX or SP chemotherapy regimen, while combined treatment group was treated with referred chemotherapy com-bined with DC-CIK cells. The adverse reactions, curative effect, peripheral blood T cell subsets and qualities of life of the patients in two groups were compared and analyzed. Results: There was no significant difference in T cell subsets in the combined treatment group compared with pre-treatment value (P>0.05); However, the post-treatment percentage of CD3 + , CD3 + CD4 + , CD3 + CD8 + and CD3 - CD56 + in peripheral blood decreased significantly in the mono-drug group(P<0.05). The disease control rate and progression free survival in combined treatment group were signif-icantly increased compared to the mono-drug group (87.5% vs 50%，8.9 months vs 4.4 months, respectively, all P<0.05). There was no significant difference in overall survival between two groups (18.0 months vs 14.0 months, P>0.05). After treatment, compared with the mono-drug group, fatigue and insomnia caused by chemotherapy or dis-ease itself in the combined treatment group was significantly improved (P<0.05). No severe toxicity was observed after infusion of DC-CIK cells. Conclusion: The treatment of DC-CIK cells combined with chemotherapy can obvi-ously optimize the immune function and improve the life quality of the patients with locally advanced unresectable or metastatic gastric adenocarcinoma; the combined treatment improved clinical efficacy and did not bring any obvi-ous adverse reactions.
Objective: To investigate the clinical efficacy and safety of autogenous dendritic cell-cytokine induced killer (DC-CIK) cell combined with chemotherapy in treatment of locally advanced unresectable or metastatic gas-tric adenocarcinoma. Methods: In this randomized and controlled trial, 32 patients with advanced gastric adenocar-cinoma, who were hospitalized in the Department of Medical Oncology, Cancer Hospital, Chinese Academy of Med-ical Sciences during November, 2014 to July, 2016, were divided into the combined treatment group (16 cases for DC-CIK cell combined chemotherapy) and the mono-drug group (16 cases for chemotherapy alone) by the ration of 1∶1. The baseline data of two groups were comparable. Peripheral blood mononuclear cells (PBMCs) were collected from patients of both groups to obtain DC and CIK cells via in vitro culture. The mono-drug group was treated with SOX or SP chemotherapy regimen, while combined treatment group was treated with referred chemotherapy com-bined with DC-CIK cells. The adverse reactions, curative effect, peripheral blood T cell subsets and qualities of life of the patients in two groups were compared and analyzed. Results: There was no significant difference in T cell subsets in the combined treatment group compared with pre-treatment value (P>0.05); However, the post-treatment percentage of CD3 + , CD3 + CD4 + , CD3 + CD8 + and CD3 - CD56 + in peripheral blood decreased significantly in the mono-drug group(P<0.05). The disease control rate and progression free survival in combined treatment group were signif-icantly increased compared to the mono-drug group (87.5% vs 50%，8.9 months vs 4.4 months, respectively, all P<0.05). There was no significant difference in overall survival between two groups (18.0 months vs 14.0 months, P>0.05). After treatment, compared with the mono-drug group, fatigue and insomnia caused by chemotherapy or dis-ease itself in the combined treatment group was significantly improved (P<0.05). No severe toxicity was observed after infusion of DC-CIK cells. Conclusion: The treatment of DC-CIK cells combined with chemotherapy can obvi-ously optimize the immune function and improve the life quality of the patients with locally advanced unresectable or metastatic gastric adenocarcinoma; the combined treatment improved clinical efficacy and did not bring any obvi-ous adverse reactions.
2017, 24(9):972-978.
DOI: 10.3872/j.issn.1007-385X.2017.09.008
Abstract:
Objective: To investigate the expression of microRNA-6803(miR-6803) and its host gene PPP6R1 in esophageal squamous cell carcinoma (ESCC) and the role of promoter methylation status of PPP6R1 in the tumori-genisis and progression of ESCC. Methods: ESCC tissues and corresponding para-cancerous tissues from 72 cases of ESCC patients stored in the bio-specimen base of the Fourth Hospital Affiliated to Heibei Medical University dur-ing 2013 and 2014 were collected for this study.Real-time fluorescence quantitative PCR (qPCR) was used to detect the expression of miR- 6803/PPP6R1 in collected tissues and in ESCC cell lines (TE1, TE13, Eca109, T.TN,Kyse170) treated or untreated with DNA methyl-transferase inhibitor 5-aza-2’-detoxycytidine (5-Aza-dC). Methyla-tion specific PCR (MSP) method was used to detect the methylation status of PPP6R1 in esophageal cancer cell lines and collected tissues, respectively. Results: The relative expressions of miR-6803 and PPP6R1 in ESCC tis-sues were significantly reduced compared to correspondingtissues (0.318±0.156, 0.408±0.177 vs 1.000±0.001, all P<0.05), and expression of miR-6803 was associated with lymph node metastasis, TNM stage and pathological differ-entiation (all P<0.05); The expression of PPP6R1 was associated with TNM stage and pathological differentiation (all P<0.05). There was a significant correlation between the relative expression of miR-6803 and PPP6R1 in ESCC tissues (P<0.05).The promoter methylation frequency of PPP6R1 in ESCC tissues was significantly higher than that in corresponding normal tissues (56.94% vs 36.11%, P<0.05), and was also associated with TNM stage and patho-logical differentiation (all P<0.05). The low expression of miR-6803/PPP6R1 was significantly correlated with pro-moter methylation of PPP6R1 in ESCC tissues (P<0.05). The relative expression level of miR-6803 and PPP6R1 in 5 ESCC cell lines was enhanced after the treatment with 5-Aza-dC. After treatment with 5-Aza-dC, the methylation level of PPP6R1 was decreased in TE1, TE13, Kyse170 cells, while complete unmethylation of PPP6R1 was detect-ed in other two cell lines. Conclusion: Aberrant low expression of miR-6803 and its host gene PPP6R1 are closely related to the occurrence and development of ESCC, and promoter methylation may be one of the mechanisms for inactivation of miR-6803/PPP6R1 in ESCC.
Objective: To investigate the expression of microRNA-6803(miR-6803) and its host gene PPP6R1 in esophageal squamous cell carcinoma (ESCC) and the role of promoter methylation status of PPP6R1 in the tumori-genisis and progression of ESCC. Methods: ESCC tissues and corresponding para-cancerous tissues from 72 cases of ESCC patients stored in the bio-specimen base of the Fourth Hospital Affiliated to Heibei Medical University dur-ing 2013 and 2014 were collected for this study.Real-time fluorescence quantitative PCR (qPCR) was used to detect the expression of miR- 6803/PPP6R1 in collected tissues and in ESCC cell lines (TE1, TE13, Eca109, T.TN,Kyse170) treated or untreated with DNA methyl-transferase inhibitor 5-aza-2’-detoxycytidine (5-Aza-dC). Methyla-tion specific PCR (MSP) method was used to detect the methylation status of PPP6R1 in esophageal cancer cell lines and collected tissues, respectively. Results: The relative expressions of miR-6803 and PPP6R1 in ESCC tis-sues were significantly reduced compared to correspondingtissues (0.318±0.156, 0.408±0.177 vs 1.000±0.001, all P<0.05), and expression of miR-6803 was associated with lymph node metastasis, TNM stage and pathological differ-entiation (all P<0.05); The expression of PPP6R1 was associated with TNM stage and pathological differentiation (all P<0.05). There was a significant correlation between the relative expression of miR-6803 and PPP6R1 in ESCC tissues (P<0.05).The promoter methylation frequency of PPP6R1 in ESCC tissues was significantly higher than that in corresponding normal tissues (56.94% vs 36.11%, P<0.05), and was also associated with TNM stage and patho-logical differentiation (all P<0.05). The low expression of miR-6803/PPP6R1 was significantly correlated with pro-moter methylation of PPP6R1 in ESCC tissues (P<0.05). The relative expression level of miR-6803 and PPP6R1 in 5 ESCC cell lines was enhanced after the treatment with 5-Aza-dC. After treatment with 5-Aza-dC, the methylation level of PPP6R1 was decreased in TE1, TE13, Kyse170 cells, while complete unmethylation of PPP6R1 was detect-ed in other two cell lines. Conclusion: Aberrant low expression of miR-6803 and its host gene PPP6R1 are closely related to the occurrence and development of ESCC, and promoter methylation may be one of the mechanisms for inactivation of miR-6803/PPP6R1 in ESCC.
2017, 24(9):979-983.
DOI: 10.3872/j.issn.1007-385X.2017.09.009
Abstract:
Objective: To investigate lncRNA RP11-259P1.1 expression in esophageal squamous cell carcinoma (ESCC) and to explore its correlation with clinicopathological features and prognosis. Methods: 130 cases of prima-ry ESCC cancer tissues and the corresponding paracancerous tissues resected during surgery from January 1, 2012to December 31, 2016 at the Affiliated Hospital of Southwest Medical University, as well as human ESCC cell lines KYSE510, Eca109 and esophageal epithelial cell line Het-1A were collected for this study. The method of quantita-tive real-time polymerase chain reaction (qPCR) was used to measure lncRNA RP11-259P1.1 expression in speci-mens and cells, and the association between lncRNA RP11-259P1.1 expression in speciments and clinicopathologi-cal features or prognosis was analyzed. Results: The expression of lncRNA RP11-259P1.1 in esophageal cancer cells and cancer tissues was significantly higher than that in normal esophageal epithelial cells and para-cancerous tissues (all P＜0.01). High expression of lncRNA RP11-259P1.1 was significantly associated with tumor size, TNM stage, lymph node metastases and chemoradiotherapy sensitivity (CRT) (P<0.05), but not associated with ages, gen-der, tumor location, smoking (P>0.05). In 63 cases of patients receiving neoadjuvant radiochemotherapy (CRT+S),by comparing patients with high lncRNA RP11-259P1.1 expression and low expression, (1) pathological complete remission (pCR) rate in low expression patients was significantly increased (60% vs 21.21%, P<0.05); (2) the treat-ment efficacy of pre-operative CRT in patients with low expression was better (P<0.05); (3) median progress-free survival (PFS) and overall survival (OS) of patients with low expression was significantly prolonged ([28.00±2.47]months vs [17.00±1.90] months，P<0.01; [41.57±2.45] months vs [30.00±2.55] months，P<0.01). lncRNA RP11-259P1.1 can be used as a prognostic factor for patients with esophageal cancer (P<0.05). Conclusion: The expres-sion of lncRNA RP11-259P1.1 could serve as a potential molecular marker to predict the prognosis and pre-opera-tive CRT treatment efficacy of ESCC patients, and patients with low lncRNA PR11-259P1.1 expression might achieve a better treatment efficacy from pre-operative CRT.
Objective: To investigate lncRNA RP11-259P1.1 expression in esophageal squamous cell carcinoma (ESCC) and to explore its correlation with clinicopathological features and prognosis. Methods: 130 cases of prima-ry ESCC cancer tissues and the corresponding paracancerous tissues resected during surgery from January 1, 2012to December 31, 2016 at the Affiliated Hospital of Southwest Medical University, as well as human ESCC cell lines KYSE510, Eca109 and esophageal epithelial cell line Het-1A were collected for this study. The method of quantita-tive real-time polymerase chain reaction (qPCR) was used to measure lncRNA RP11-259P1.1 expression in speci-mens and cells, and the association between lncRNA RP11-259P1.1 expression in speciments and clinicopathologi-cal features or prognosis was analyzed. Results: The expression of lncRNA RP11-259P1.1 in esophageal cancer cells and cancer tissues was significantly higher than that in normal esophageal epithelial cells and para-cancerous tissues (all P＜0.01). High expression of lncRNA RP11-259P1.1 was significantly associated with tumor size, TNM stage, lymph node metastases and chemoradiotherapy sensitivity (CRT) (P<0.05), but not associated with ages, gen-der, tumor location, smoking (P>0.05). In 63 cases of patients receiving neoadjuvant radiochemotherapy (CRT+S),by comparing patients with high lncRNA RP11-259P1.1 expression and low expression, (1) pathological complete remission (pCR) rate in low expression patients was significantly increased (60% vs 21.21%, P<0.05); (2) the treat-ment efficacy of pre-operative CRT in patients with low expression was better (P<0.05); (3) median progress-free survival (PFS) and overall survival (OS) of patients with low expression was significantly prolonged ([28.00±2.47]months vs [17.00±1.90] months，P<0.01; [41.57±2.45] months vs [30.00±2.55] months，P<0.01). lncRNA RP11-259P1.1 can be used as a prognostic factor for patients with esophageal cancer (P<0.05). Conclusion: The expres-sion of lncRNA RP11-259P1.1 could serve as a potential molecular marker to predict the prognosis and pre-opera-tive CRT treatment efficacy of ESCC patients, and patients with low lncRNA PR11-259P1.1 expression might achieve a better treatment efficacy from pre-operative CRT.
2017, 24(9):984-989.
DOI: 10.3872/j.issn.1007-385X.2017.09.010
Abstract:
Objective: To investigate the expression of Testin (TES) gene in non-small lung cancer cell (NSCLC) lines, and also to investigate its effect on cell proliferation, migration, invasion and apoptosis of human lung cancer cell line A549. Methods: Twenty-seven cases of cancer tissues and corresponding para-cancerous tissues from non-small lung cancer patients that treated in Tongji Hospital Affiliated to Tonji Medical College of Huazhong Universi-ty of Science and Technology between January 2015 and December 2015 were collected for this study; and the ex-pression of TES protein in collected tissues was examined by Western blotting. In the meanwhile,TES protein ex-pressions in six human lung cancer cell lines (A427, A549, H1299, LK2, PC9 and SW900) and lung fiberblast cell line MRC5 were also detected. shTES was transiently transfected into A549 cells to interfere the expression of TES gene; the effect of low TES expression on proliferation, migration, invasion and apoptosis of A549 were further as-sessed, and its effect on the expressions of apoptosis related proteins (Bax, Bcl-2 and Caspase-3) were also tested by Western blotting. Results: The expression of TES protein in lung cancer tissues and lung cancer cell lines was signif-icantly decreased (all P<0.05). After shTES transfection in A549 cells, the expressions of TES mRNA and protein were significantly down-regulated (P<0.05). Additionally, shTES significantly increased cell proliferation ([2.75±0.04］vs [1.79±0.06], P<0.05), migration ([52.3±2.6]% vs [19.7±1.4]%, P<0.05), and invasion ([31.2±3.89]% vs [14.5±4.1]%, P<0.05), while inhibited cell apoptosis ([8.2±1.1]% vs [23.1±1.7]%, P<0.05) of A549 cells. Moreover,TES low expression significantly decreased the expressions of Bax and Caspase-3 (P<0.05) but increased the expres-sion of Bcl-2 (P<0.05) in A549 cells. Conclusion:TES was low expressed in NSCLC tissues, and down-regulation of TES could promote cell proliferation, migration, invasion and inhibit the apoptosis of lung cancer cells, which may serve as a new target for lung cancer treatment.
Objective: To investigate the expression of Testin (TES) gene in non-small lung cancer cell (NSCLC) lines, and also to investigate its effect on cell proliferation, migration, invasion and apoptosis of human lung cancer cell line A549. Methods: Twenty-seven cases of cancer tissues and corresponding para-cancerous tissues from non-small lung cancer patients that treated in Tongji Hospital Affiliated to Tonji Medical College of Huazhong Universi-ty of Science and Technology between January 2015 and December 2015 were collected for this study; and the ex-pression of TES protein in collected tissues was examined by Western blotting. In the meanwhile,TES protein ex-pressions in six human lung cancer cell lines (A427, A549, H1299, LK2, PC9 and SW900) and lung fiberblast cell line MRC5 were also detected. shTES was transiently transfected into A549 cells to interfere the expression of TES gene; the effect of low TES expression on proliferation, migration, invasion and apoptosis of A549 were further as-sessed, and its effect on the expressions of apoptosis related proteins (Bax, Bcl-2 and Caspase-3) were also tested by Western blotting. Results: The expression of TES protein in lung cancer tissues and lung cancer cell lines was signif-icantly decreased (all P<0.05). After shTES transfection in A549 cells, the expressions of TES mRNA and protein were significantly down-regulated (P<0.05). Additionally, shTES significantly increased cell proliferation ([2.75±0.04］vs [1.79±0.06], P<0.05), migration ([52.3±2.6]% vs [19.7±1.4]%, P<0.05), and invasion ([31.2±3.89]% vs [14.5±4.1]%, P<0.05), while inhibited cell apoptosis ([8.2±1.1]% vs [23.1±1.7]%, P<0.05) of A549 cells. Moreover,TES low expression significantly decreased the expressions of Bax and Caspase-3 (P<0.05) but increased the expres-sion of Bcl-2 (P<0.05) in A549 cells. Conclusion:TES was low expressed in NSCLC tissues, and down-regulation of TES could promote cell proliferation, migration, invasion and inhibit the apoptosis of lung cancer cells, which may serve as a new target for lung cancer treatment.
ZHANG Yilin
,
ZHAO Wanhong
,
ZHANG Wanggang
,
LIU Jie
,
CHEN Yinxia
,
CAO Xingmei
,
HE Aili
,
WANG Jianli
,
YANG Nan
,
YANG Yun
,
GU Liufang
,
FAN Xiaohu
2017, 24(9):990-994.
DOI: 10.3872/j.issn.1007-385X.2017.09.011
Abstract:
Objective: To observe the therapeutic effect of tocilizumab on cytokine release syndrome (CRS) for pa-tients with relapsed or refractory multiple myeloma (MM) treated by CAR-T cell immunotherapy. Methods: From February 2016 to February 2017, 24 patients with relapsed or refractory multiple myeloma treated by CAR-T cell immunotherapy in the Department of Hematology of Second Affiliated Hospital of Medical College, Xi’an Jiaotong University were included as study subjects. Tocilizumab (4-8 mg/kg·d) was applied on MM patients with grade 2 or above , and the treatment efficacy, side effects, and the changes of hypersensitive C-reactive protein (HsCRP) etc were observed. Results: Twenty-one of the 24 patients suffered from CRS during the CAR-T treatment. According to the CRS classification criteria, 7 patients had grade 1 CRS reaction, 7 patients with grade 2, 5 patients with grade 3, and 2 patients with grade 4. The manifestations of CRS were hyperpyrexia, significant increase in cytokines and HsCRP level with the most obvious increase in IL-6. Fourteen CRS patients with grade 2 or above were treated by tocilizumab and their clinical symptoms were obviously alleviated: the temperature was rapidly decreased and cyto-kines and hypersensitive C-reactive protein dropped to normal gradually. In the process of treatment, no obvious side effects were observed. Conclusion: Tocilizumab showed a significant clinical efficacy in the treatment of CRS,which greatly guaranteed the safety of the MM patients in the CAR-T treatment.
Objective: To observe the therapeutic effect of tocilizumab on cytokine release syndrome (CRS) for pa-tients with relapsed or refractory multiple myeloma (MM) treated by CAR-T cell immunotherapy. Methods: From February 2016 to February 2017, 24 patients with relapsed or refractory multiple myeloma treated by CAR-T cell immunotherapy in the Department of Hematology of Second Affiliated Hospital of Medical College, Xi’an Jiaotong University were included as study subjects. Tocilizumab (4-8 mg/kg·d) was applied on MM patients with grade 2 or above , and the treatment efficacy, side effects, and the changes of hypersensitive C-reactive protein (HsCRP) etc were observed. Results: Twenty-one of the 24 patients suffered from CRS during the CAR-T treatment. According to the CRS classification criteria, 7 patients had grade 1 CRS reaction, 7 patients with grade 2, 5 patients with grade 3, and 2 patients with grade 4. The manifestations of CRS were hyperpyrexia, significant increase in cytokines and HsCRP level with the most obvious increase in IL-6. Fourteen CRS patients with grade 2 or above were treated by tocilizumab and their clinical symptoms were obviously alleviated: the temperature was rapidly decreased and cyto-kines and hypersensitive C-reactive protein dropped to normal gradually. In the process of treatment, no obvious side effects were observed. Conclusion: Tocilizumab showed a significant clinical efficacy in the treatment of CRS,which greatly guaranteed the safety of the MM patients in the CAR-T treatment.
2017, 24(9):995-1001.
DOI: 10.3872/j.issn.1007-385X.2017.09.012
Abstract:
Objective: To investigate the expression level of glutathione peroxidase 1（GPX1）in colorectal can-cer (CRC) tissues, and its effect on the proliferation and migration of CRC HT29 and LOVO cell lines. Methods:Colorectal cancer tissues and para-cancerous tissues that resected from 60 CRC patients at Binjiang Branch of Haik-ou People’s Hospital from June, 2015 to March, 2016 were collected for this study. Real-time fluorescence quantita-tive PCR was used to detect the expression level of GPX1 mRNA in sample tissues. HT29 cell line expressing high-er GPX1 mRNA was transfected with lentivirus shRNA to stably knock-down GPX1 expression, while LOVO cell line expressing lower GPX1 mRNA was subjected to transient transfection method to stably overexpressing GPX1,and the protein and mRNA expression level of GPX1 were verified in cells. The change in cell proliferation ability was detected by MTS assay, and the invasion and migration ability was detected by Transwell invasion assay and wound healing assay. The changes in expression of E-cadherin and vimentin were detected by Western blotting.Results: GPX1 mRNA expression was significantly lower in CRC tissues compared with para-cancerous tissues (0.051±0.044 vs 0.142±0.051, P<0.01). After knock-down of GPX1: the proliferation ability of HT29 cells was sig-nificantly improved (12.901±2.790 vs 6.617±2.462, P<0.01), the invasion and migration ability of HT29 cells were significantly enhanced (invasion: [384.7±37.9] vs [209.2± 31.2], P<0.01; migration: [0.139±0.025] mm vs [0.251±0.038] mm, P<0.01); and there was a down-regulation of E-cadherin (P<0.01) and an up-regulation of vimentin (P<0.01). After overexpression of GPX1: the proliferation ability of LOVO cell was significantly decreased (P<0.01);the invasion and migration ability of LOVO cell was significantly decreased (all P<0.01); and there was an up-regu-lation of E-cadherin (P<0.01) and a down-regulation of vimentin (P<0.01). Conclusion: GPX1 mRNA was low-ex-pressed in human colorectal cancer tissues. GPX1 may inhibit the proliferation, invasion and migration of CRC cell lines, and may play an important anti-carcinoma role in CRC.
Objective: To investigate the expression level of glutathione peroxidase 1（GPX1）in colorectal can-cer (CRC) tissues, and its effect on the proliferation and migration of CRC HT29 and LOVO cell lines. Methods:Colorectal cancer tissues and para-cancerous tissues that resected from 60 CRC patients at Binjiang Branch of Haik-ou People’s Hospital from June, 2015 to March, 2016 were collected for this study. Real-time fluorescence quantita-tive PCR was used to detect the expression level of GPX1 mRNA in sample tissues. HT29 cell line expressing high-er GPX1 mRNA was transfected with lentivirus shRNA to stably knock-down GPX1 expression, while LOVO cell line expressing lower GPX1 mRNA was subjected to transient transfection method to stably overexpressing GPX1,and the protein and mRNA expression level of GPX1 were verified in cells. The change in cell proliferation ability was detected by MTS assay, and the invasion and migration ability was detected by Transwell invasion assay and wound healing assay. The changes in expression of E-cadherin and vimentin were detected by Western blotting.Results: GPX1 mRNA expression was significantly lower in CRC tissues compared with para-cancerous tissues (0.051±0.044 vs 0.142±0.051, P<0.01). After knock-down of GPX1: the proliferation ability of HT29 cells was sig-nificantly improved (12.901±2.790 vs 6.617±2.462, P<0.01), the invasion and migration ability of HT29 cells were significantly enhanced (invasion: [384.7±37.9] vs [209.2± 31.2], P<0.01; migration: [0.139±0.025] mm vs [0.251±0.038] mm, P<0.01); and there was a down-regulation of E-cadherin (P<0.01) and an up-regulation of vimentin (P<0.01). After overexpression of GPX1: the proliferation ability of LOVO cell was significantly decreased (P<0.01);the invasion and migration ability of LOVO cell was significantly decreased (all P<0.01); and there was an up-regu-lation of E-cadherin (P<0.01) and a down-regulation of vimentin (P<0.01). Conclusion: GPX1 mRNA was low-ex-pressed in human colorectal cancer tissues. GPX1 may inhibit the proliferation, invasion and migration of CRC cell lines, and may play an important anti-carcinoma role in CRC.
2017, 24(9):1002-1005.
DOI: 10.3872/j.issn.1007-385X.2017.09.013
Abstract:
Objective: To investigate the expression of lncRNAMALAT1 (long non-coding RNAs, metastasis-asso-ciated lung adenocarcinoma transcript 1) in the serum of DLBCL (diffuse large B-cell lymphoma) patients, and to analyze its correlation to clinical prognosis. Methods: The blood samples of 82 DLBCL patients and 32 RLH patients (lymph node reactive hyperplasia), who were diagnosed at Hematology Department of People’s Hospital of Sichuan Province from January 2010 to December 2015 with complete clinical data, were collected for this study. ln-cRNA MALAT1 expression was detected by Real-time fluorescence quantitative PCR, and the relationship between lncRNA MALAT1 expression with clinical pathological features and prognosis were analyzed. Results: Compare with RLH patients, lncRNA MALAT1 expression was significantly increased in DLBCL patients (7.48±0.27 vs 1.28±0.45, P<0.01). In addition, lncRNA MALAT1 was significantly correlated with tumor size, clinical stage, B symptoms and international prognostic index (IPI) scores. The median progression free survival time (PFS) of patients with high lncRNA MALAT1 expression was significantly shorter than those with low expression ([16.43±2.05] months vs [32.01±3.20] months, P<0.01). Cox multivariate analyses verified that lncRNA MALAT1 and IPI scores were independent predictive factors for DLBCL prognosis. Conclusion: The high expression of lncRNA MALAT1 in DLBCL patients was correlated with multiple clinicopathological parameters., and it is expected to become a new tumor marker for DLBCL prognosis.
Objective: To investigate the expression of lncRNAMALAT1 (long non-coding RNAs, metastasis-asso-ciated lung adenocarcinoma transcript 1) in the serum of DLBCL (diffuse large B-cell lymphoma) patients, and to analyze its correlation to clinical prognosis. Methods: The blood samples of 82 DLBCL patients and 32 RLH patients (lymph node reactive hyperplasia), who were diagnosed at Hematology Department of People’s Hospital of Sichuan Province from January 2010 to December 2015 with complete clinical data, were collected for this study. ln-cRNA MALAT1 expression was detected by Real-time fluorescence quantitative PCR, and the relationship between lncRNA MALAT1 expression with clinical pathological features and prognosis were analyzed. Results: Compare with RLH patients, lncRNA MALAT1 expression was significantly increased in DLBCL patients (7.48±0.27 vs 1.28±0.45, P<0.01). In addition, lncRNA MALAT1 was significantly correlated with tumor size, clinical stage, B symptoms and international prognostic index (IPI) scores. The median progression free survival time (PFS) of patients with high lncRNA MALAT1 expression was significantly shorter than those with low expression ([16.43±2.05] months vs [32.01±3.20] months, P<0.01). Cox multivariate analyses verified that lncRNA MALAT1 and IPI scores were independent predictive factors for DLBCL prognosis. Conclusion: The high expression of lncRNA MALAT1 in DLBCL patients was correlated with multiple clinicopathological parameters., and it is expected to become a new tumor marker for DLBCL prognosis.
2017, 24(9):1006-1009.
DOI: 10.3872/j.issn.1007-385X.2017.09.014
Abstract:
Objective: To compare the clinical efficacy of axitinib and sorafenib as first-line treatment for advanced renal cell carcinoma, and to explore whether axitinib could be used as a preferred first-line drug for advanced renal cell carcinoma. Methods: Sixty patients with advanced renal cell carcinoma from Haikou Municipal Hospital were enrolled in this study and divided into experimental group (n=30) and control group (n=30) according to a random number table. The experimental group received axitinib treatment and the control group received sorafenib treat-ment. Disease control rate (DCR), objective response rate (ORR), progression free survial (PFS), overall survival (OS), and adverse effects were evaluated and compared between two groups. Results: All patients in the two groups completed the experiment. There was no difference between the experimental group and the control group in DCR (83.33% vs 80.00% , P>0.05) and ORR (20.00% vs 20.00% , P>0.05). Significant difference in median PFS was found between the two groups (12.8 months of experimental group vs 10.1 months of control group, P<0.05);however, there was no significant difference in the median OS between two groups (22.2 months vs 22.8 months, P>0.05). The incidence of adverse reactions in the two groups was similar, mainly including hypertension, systemic re-actions, hand foot skin syndrome, digestive system reaction and liver function damage (P>0.05). No serious ad-verse effects were observed in both groups. Conclusion: Compared with sorafenib, axitinib significantly prolonged the median PFS in patients with advanced renal cell carcinoma, although the diseasecontrol rate, objective efficien-cy, overall survival, and adverse effects of two treatment regimen were comparable. Axitinib, the molecular targeted agent, can be used as a preferred first-line therapy for advanced renal cell carcinoma.
Objective: To compare the clinical efficacy of axitinib and sorafenib as first-line treatment for advanced renal cell carcinoma, and to explore whether axitinib could be used as a preferred first-line drug for advanced renal cell carcinoma. Methods: Sixty patients with advanced renal cell carcinoma from Haikou Municipal Hospital were enrolled in this study and divided into experimental group (n=30) and control group (n=30) according to a random number table. The experimental group received axitinib treatment and the control group received sorafenib treat-ment. Disease control rate (DCR), objective response rate (ORR), progression free survial (PFS), overall survival (OS), and adverse effects were evaluated and compared between two groups. Results: All patients in the two groups completed the experiment. There was no difference between the experimental group and the control group in DCR (83.33% vs 80.00% , P>0.05) and ORR (20.00% vs 20.00% , P>0.05). Significant difference in median PFS was found between the two groups (12.8 months of experimental group vs 10.1 months of control group, P<0.05);however, there was no significant difference in the median OS between two groups (22.2 months vs 22.8 months, P>0.05). The incidence of adverse reactions in the two groups was similar, mainly including hypertension, systemic re-actions, hand foot skin syndrome, digestive system reaction and liver function damage (P>0.05). No serious ad-verse effects were observed in both groups. Conclusion: Compared with sorafenib, axitinib significantly prolonged the median PFS in patients with advanced renal cell carcinoma, although the diseasecontrol rate, objective efficien-cy, overall survival, and adverse effects of two treatment regimen were comparable. Axitinib, the molecular targeted agent, can be used as a preferred first-line therapy for advanced renal cell carcinoma.
2017, 24(9):1010-1015.
DOI: 10.3872/j.issn.1007-385X.2017.09.015
Abstract:
Objective: To assess the association between interleukin-10 (IL-10) gene -1082A＞G polymorphism and non-Hodgkin lymphoma (NHL) susceptibility using Meta-analysis. Methods: Case-control studies about IL-10 gene -1082A＞G polymorphism and NHL susceptibility were searched in PubMed, EMBASE, Web of Science,Chinese Biomedical Literature Database, Chinese Science and Technology Academic Journal, Chinese Journal Full-text Database and Wanfang Database from their inception toJanuary 2017. Meta-analysis was performed using STA-TA 12.0 software. Results: A total of 16 case-control studies were included in this Meta-analysis, including 4 718cases and 3 877 controls. There was association between IL-10 gene -1082A＞G polymorphism and NHL suscepti-bility inallele genetic model (Avs G: OR=1.12, 95%CI=1.04-1.21)，codominant model (AA vs AG: OR=1.27, 95%CI=1.06-1.52) ，additive model (AAvsGG:OR=1.22,95%CI=1.06-1.40) and dominant model (AA vs AG+GG: OR=1.29, 95%CI=1.08-1.53)，but no association with NHL susceptibility in recessive model (GG vs AA+ AG:OR=1.11,95%CI=0.92-1.34). Conclusion: IL-10 gene -1082A＞G polymorphismmay be associated with NHL Susceptibility.
Objective: To assess the association between interleukin-10 (IL-10) gene -1082A＞G polymorphism and non-Hodgkin lymphoma (NHL) susceptibility using Meta-analysis. Methods: Case-control studies about IL-10 gene -1082A＞G polymorphism and NHL susceptibility were searched in PubMed, EMBASE, Web of Science,Chinese Biomedical Literature Database, Chinese Science and Technology Academic Journal, Chinese Journal Full-text Database and Wanfang Database from their inception toJanuary 2017. Meta-analysis was performed using STA-TA 12.0 software. Results: A total of 16 case-control studies were included in this Meta-analysis, including 4 718cases and 3 877 controls. There was association between IL-10 gene -1082A＞G polymorphism and NHL suscepti-bility inallele genetic model (Avs G: OR=1.12, 95%CI=1.04-1.21)，codominant model (AA vs AG: OR=1.27, 95%CI=1.06-1.52) ，additive model (AAvsGG:OR=1.22,95%CI=1.06-1.40) and dominant model (AA vs AG+GG: OR=1.29, 95%CI=1.08-1.53)，but no association with NHL susceptibility in recessive model (GG vs AA+ AG:OR=1.11,95%CI=0.92-1.34). Conclusion: IL-10 gene -1082A＞G polymorphismmay be associated with NHL Susceptibility.
2017, 24(9):1016-1021.
DOI: 10.3872/j.issn.1007-385X.2017.09.016
Abstract:
外泌体（exosome）是一类直径30~100 nm的囊泡样小体，其含有蛋白质、mRNA、微小RNA（miRNA）、DNA片段等，是细胞间物质和信息转导的重要媒介。外泌体参与肿瘤的发生、发展、侵袭和转移等各个过程，其在肿瘤免疫中发挥双向调控功能。本文重点阐述外泌体在肿瘤负向免疫调控中的作用，如肿瘤来源外泌体（tumor-derived exosome，TEX）能够阻碍DC的分化和成熟，促进巨噬细胞极化，减弱B细胞功能及诱导调节性B细胞（regulatory B cell，Breg）产生，促骨髓前体细胞分化为髓系抑制性细胞（myeloid-derived suppressor cell，MDSC），减弱NK及T淋巴细胞的杀伤功能，诱导调节性T细胞（regulatory T cell，Treg）等；又如免疫细胞来源外泌体（immunocyte-derived exosome，IEX），主要为Treg、CD8 + T细胞来源的外泌体，同样具有免疫抑制功能。
外泌体（exosome）是一类直径30~100 nm的囊泡样小体，其含有蛋白质、mRNA、微小RNA（miRNA）、DNA片段等，是细胞间物质和信息转导的重要媒介。外泌体参与肿瘤的发生、发展、侵袭和转移等各个过程，其在肿瘤免疫中发挥双向调控功能。本文重点阐述外泌体在肿瘤负向免疫调控中的作用，如肿瘤来源外泌体（tumor-derived exosome，TEX）能够阻碍DC的分化和成熟，促进巨噬细胞极化，减弱B细胞功能及诱导调节性B细胞（regulatory B cell，Breg）产生，促骨髓前体细胞分化为髓系抑制性细胞（myeloid-derived suppressor cell，MDSC），减弱NK及T淋巴细胞的杀伤功能，诱导调节性T细胞（regulatory T cell，Treg）等；又如免疫细胞来源外泌体（immunocyte-derived exosome，IEX），主要为Treg、CD8 + T细胞来源的外泌体，同样具有免疫抑制功能。
2017, 24(9):1022-1031.
DOI: 10.3872/j.issn.1007-385X.2017.09.017
Abstract:
蛋白磷酸酶2A癌性抑制因子（cancerous inhibitor of protein phosphatase 2A，CIP2A）在绝大多数肿瘤中高表达。CIP2A能够与转录因子Myc和蛋白磷酸酶2A（protein phosphatase 2A，PP2A）直接相互作用，抑制PP2A对Myc第62位丝氨酸的磷酸化作用，进而阻止Myc蛋白降解，该功能是CIP2A促癌作用的重要体现。CIP2A在肿瘤细胞增殖、凋亡、侵袭、迁移、上皮间充质转化（epithelial-mesenchymal transition，EMT）、细胞周期及抗药性等方面发挥着重要的作用；同时，CIP2A也是一些肿瘤诊断和预后的潜在生物标志物。本文就近年来CIP2A在肿瘤中的表达、调控以及其在肿瘤细胞中的作用和其作为潜在抗肿瘤药物靶标的研究作一综述。
蛋白磷酸酶2A癌性抑制因子（cancerous inhibitor of protein phosphatase 2A，CIP2A）在绝大多数肿瘤中高表达。CIP2A能够与转录因子Myc和蛋白磷酸酶2A（protein phosphatase 2A，PP2A）直接相互作用，抑制PP2A对Myc第62位丝氨酸的磷酸化作用，进而阻止Myc蛋白降解，该功能是CIP2A促癌作用的重要体现。CIP2A在肿瘤细胞增殖、凋亡、侵袭、迁移、上皮间充质转化（epithelial-mesenchymal transition，EMT）、细胞周期及抗药性等方面发挥着重要的作用；同时，CIP2A也是一些肿瘤诊断和预后的潜在生物标志物。本文就近年来CIP2A在肿瘤中的表达、调控以及其在肿瘤细胞中的作用和其作为潜在抗肿瘤药物靶标的研究作一综述。
2017, 24(9):1032-1036.
DOI: 10.3872/j.issn.1007-385X.2017.09.018
Abstract:
骨髓增生异常综合征（myelodysplastic syndrome, MDS）是以骨髓无效造血并伴有向急性髓系白血病转化风险为特点的一组造血系统肿瘤性疾病。肿瘤细胞的识别并清除，不仅需要肿瘤特异性T细胞的产生，还需要免疫细胞能够在肿瘤微环境中增殖以增加免疫细胞的数量从而控制肿瘤细胞。肿瘤细胞免于T细胞的清除说明MDS肿瘤细胞周围存在免疫抑制性微环境，其中,间充质干细胞(mesenchymal stem cell, MSC)促进MDS免疫抑制性微环境的形成，若能克服MSC对T细胞的抑制，将能促进免疫治疗改善MDS的治疗效果。笔者对近年来MSC（MDS-MSC）抑制T细胞在骨髓微环境中的增殖和效应功能、促进调节T细胞分化的研究进展进行回顾。
骨髓增生异常综合征（myelodysplastic syndrome, MDS）是以骨髓无效造血并伴有向急性髓系白血病转化风险为特点的一组造血系统肿瘤性疾病。肿瘤细胞的识别并清除，不仅需要肿瘤特异性T细胞的产生，还需要免疫细胞能够在肿瘤微环境中增殖以增加免疫细胞的数量从而控制肿瘤细胞。肿瘤细胞免于T细胞的清除说明MDS肿瘤细胞周围存在免疫抑制性微环境，其中,间充质干细胞(mesenchymal stem cell, MSC)促进MDS免疫抑制性微环境的形成，若能克服MSC对T细胞的抑制，将能促进免疫治疗改善MDS的治疗效果。笔者对近年来MSC（MDS-MSC）抑制T细胞在骨髓微环境中的增殖和效应功能、促进调节T细胞分化的研究进展进行回顾。
2017, 24(9):1037-1040.
DOI: 10.3872/j.issn.1007-385X.2017.09.019
Abstract:
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- 《中国肿瘤生物治疗杂志》
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.