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Volume 24,Issue 3,2017 Table of Contents
2017, 24(3):215-221.
DOI: 10.3872/j.issn.1007-385X.2017.03.001
Abstract:
Intestinal flora not only play an important role in human nutrition metabolism and immune homeostasis, but also was closely related with progress of malignant tumor. In recent years, intestinal flora tacking part in immune regulation of tumor has drawn much attention from researchers. Recent researches found that intestinal flora affects tumorigenesis and development of tumor via intervening negative immune regulatory network. However, most of researches on relationship between intestinal flora and immune regulation of tumor remained in correlation analysis, its molecular mechanism has not been completely elucidated. The paper expounded novel progresses of research on intestinal flora regulating mechanism of negative immune regulation and intervening malignant tumor progression from four aspects which were negative immune regulatory cells, negative immune regulatory molecules, negative immune regulatory cytokines and combined action of the multiple factors, and expected to provide new ideals and strategies for the tumor therapy.
Intestinal flora not only play an important role in human nutrition metabolism and immune homeostasis, but also was closely related with progress of malignant tumor. In recent years, intestinal flora tacking part in immune regulation of tumor has drawn much attention from researchers. Recent researches found that intestinal flora affects tumorigenesis and development of tumor via intervening negative immune regulatory network. However, most of researches on relationship between intestinal flora and immune regulation of tumor remained in correlation analysis, its molecular mechanism has not been completely elucidated. The paper expounded novel progresses of research on intestinal flora regulating mechanism of negative immune regulation and intervening malignant tumor progression from four aspects which were negative immune regulatory cells, negative immune regulatory molecules, negative immune regulatory cytokines and combined action of the multiple factors, and expected to provide new ideals and strategies for the tumor therapy.
2017, 24(3):222-229.
DOI: 10.3872/j.issn.1007-385X.2017.03.002
Abstract:
Objective:To explore effect of inhibiting Polo-like kinase 1 (PLK1) on radiosensitivity of nasopharyngeal carcinoma (NPC) CNE-1 and CNE-2 cell lines. Methods: Using small interfering RNA (siRNA) and small molecule inhibitor BI2536 to inhibit expression and phosphorylation of PLK1 in the CNE-1 and CNE-2 cells respectively. Effect of inhibiting PLK1 on proliferation ability of the NPC cells was tested by MTT assay. Flow cytometry assay was used to detect effect of the inhibition on cell cycle and apoptosis of the NPC cells and immuno fluorescence assay was used to assess the effect of damage sites of DNA in the NPC cells after radiation. Clone formation experiment and curve fitting assay were used to calculate radiation parameters and sensitization enhancement radio (SER) of the NPC cells after radiation. Results: Compared with the control group, inhibition of PLK1 in the NPC cells reduced proliferation of the NPC cells and, induced G2-M arrest and mitotic catastrophe of the NPC cells. Inhibition of PLK1 in the NPC cells combined with irradiation significantly decreased ability of cell colony formation in the NPC cells (CNE-1:P<0.05, CNE-2:P<0.05), and with increasing concentration of the B12536, the ability of cell colony formation in the NPC more pronounced declined (CNE-1:P<0.05, CNE-2:P<0.05). In addition, Inhibition of PLK1 in the NPC cells combined with irradiation reduced the cell survival fraction, increased the number of γ-H2AX loci in nucleus of the cells, and accelerated apoptosis rate of the cells obviously (all P<0.05). SER of the CNE-1 and the CEN2 cells were 1.1988 and 1.3198 respectively after transfection of them with siR-PLK1. And SER of the CNE-1 and the CEN-2 cells were 1.5508 and 1.2028 respectively after treatment of them with the B12536. After treatment of the CEN-1 and the CEN-2 cells with the B12536. Conclusion: Inhibition of PLK1 could suppress infiltration of the NPC cells, induce cell-cycle arrest and mitotic catastrophe, and significantly enhance radiosensitivity of the NPC cells.
Objective:To explore effect of inhibiting Polo-like kinase 1 (PLK1) on radiosensitivity of nasopharyngeal carcinoma (NPC) CNE-1 and CNE-2 cell lines. Methods: Using small interfering RNA (siRNA) and small molecule inhibitor BI2536 to inhibit expression and phosphorylation of PLK1 in the CNE-1 and CNE-2 cells respectively. Effect of inhibiting PLK1 on proliferation ability of the NPC cells was tested by MTT assay. Flow cytometry assay was used to detect effect of the inhibition on cell cycle and apoptosis of the NPC cells and immuno fluorescence assay was used to assess the effect of damage sites of DNA in the NPC cells after radiation. Clone formation experiment and curve fitting assay were used to calculate radiation parameters and sensitization enhancement radio (SER) of the NPC cells after radiation. Results: Compared with the control group, inhibition of PLK1 in the NPC cells reduced proliferation of the NPC cells and, induced G2-M arrest and mitotic catastrophe of the NPC cells. Inhibition of PLK1 in the NPC cells combined with irradiation significantly decreased ability of cell colony formation in the NPC cells (CNE-1:P<0.05, CNE-2:P<0.05), and with increasing concentration of the B12536, the ability of cell colony formation in the NPC more pronounced declined (CNE-1:P<0.05, CNE-2:P<0.05). In addition, Inhibition of PLK1 in the NPC cells combined with irradiation reduced the cell survival fraction, increased the number of γ-H2AX loci in nucleus of the cells, and accelerated apoptosis rate of the cells obviously (all P<0.05). SER of the CNE-1 and the CEN2 cells were 1.1988 and 1.3198 respectively after transfection of them with siR-PLK1. And SER of the CNE-1 and the CEN-2 cells were 1.5508 and 1.2028 respectively after treatment of them with the B12536. After treatment of the CEN-1 and the CEN-2 cells with the B12536. Conclusion: Inhibition of PLK1 could suppress infiltration of the NPC cells, induce cell-cycle arrest and mitotic catastrophe, and significantly enhance radiosensitivity of the NPC cells.
2017, 24(3):230-236.
DOI: 10.3872/j.issn.1007-385X.2017.03.003
Abstract:
Objective:To establish culture system of γδT cell and to explore killing activity of the γδT cells against different human hematologic neoplasms cells. Methods:Four patients with lymphoma who were hospitalized in the Department of Hematopoietic Stem Cell Transplantation, the 307th Hospital of PLA and five healthy volunteers for physical examination during January to April 2016 were selected and their peripheral blood mononuclear cell (PBMC) were isolated respectively. γδT cells were amplified in vitro with zoledronate (Zol) and IL-2, and killing activities of the γδT cells against hematologic neoplasms Jurkat, THP-1, HL-60, K562, Raji, U-937 and RPMI-8226 line cells were investigated by Flow cytometry assay. Killing effects of CIK cells, NK cells and the γδT cells on K562 cells were compared; and the expression levels of IFN-γ, TNF-α and secretion level of CD107a molecule in the γδT cells were detected. Results: The γδT cells were successfully amplified from peripheral blood in vitro. The γδT cells showed obvious killing activities against all of the Jurkat, THP-1, HL-60, K562, U-937 and RPMI-8226 cells (P<0.05). There was not a statistical difference between killing activities of the γδT and NK cells against the K562 cells (P>0.05), but killing activity of the γδT cells against K562 cells was higher than that of CIK cells (P<0.01). With extending the co-incubation time with K562 cells, level of IFN-γ secreted by the γδT cells increased as a time-dependent manner, in addition, level of TNF-α in the γδT cells gradually increased after 8 h of the co-incubation. After co-incubation of the γδT cells with the K562 or the HL-60 cells, expression level of CD107a molecule in the γδT cells was significantly up-regulated (P<0.01). Conclusion：The γδT cells amplified showed higher killing activity against hematologic neoplasms cells, which could provide experimental evidence for cellular immunotherapy of hematologic neoplasms.
Objective:To establish culture system of γδT cell and to explore killing activity of the γδT cells against different human hematologic neoplasms cells. Methods:Four patients with lymphoma who were hospitalized in the Department of Hematopoietic Stem Cell Transplantation, the 307th Hospital of PLA and five healthy volunteers for physical examination during January to April 2016 were selected and their peripheral blood mononuclear cell (PBMC) were isolated respectively. γδT cells were amplified in vitro with zoledronate (Zol) and IL-2, and killing activities of the γδT cells against hematologic neoplasms Jurkat, THP-1, HL-60, K562, Raji, U-937 and RPMI-8226 line cells were investigated by Flow cytometry assay. Killing effects of CIK cells, NK cells and the γδT cells on K562 cells were compared; and the expression levels of IFN-γ, TNF-α and secretion level of CD107a molecule in the γδT cells were detected. Results: The γδT cells were successfully amplified from peripheral blood in vitro. The γδT cells showed obvious killing activities against all of the Jurkat, THP-1, HL-60, K562, U-937 and RPMI-8226 cells (P<0.05). There was not a statistical difference between killing activities of the γδT and NK cells against the K562 cells (P>0.05), but killing activity of the γδT cells against K562 cells was higher than that of CIK cells (P<0.01). With extending the co-incubation time with K562 cells, level of IFN-γ secreted by the γδT cells increased as a time-dependent manner, in addition, level of TNF-α in the γδT cells gradually increased after 8 h of the co-incubation. After co-incubation of the γδT cells with the K562 or the HL-60 cells, expression level of CD107a molecule in the γδT cells was significantly up-regulated (P<0.01). Conclusion：The γδT cells amplified showed higher killing activity against hematologic neoplasms cells, which could provide experimental evidence for cellular immunotherapy of hematologic neoplasms.
2017, 24(3):237-241.
DOI: 10.3872/j.issn.1007-385X.2017.03.004
Abstract:
Objective:To explore effect of lysosomal associated protein transmembrane 5 (Laptm5) 3′untranslated region (3′UTR) on proliferation and apoptosis of mouse B-cell lymphoma 38B9 line cell, by means of establishing B-cell lymphoma cell line with stable overexpression of Laptm5 3′UTR. Methods:Expressions of Laptm5 miRNA and its protein in normal mouse B cell and the mouse B-cell lymphoma 38B9 line cell were respectively examined by Western blotting and fluorescence quantitative PCR. A mouse Laptm5 3′UTR and Laptm5 3′UTR mutation gene fragment containing mutated miRNA 17-3p binding sites were inserted into retrovirus expression vector pMSCV-PIG. The retrovirus was constructed and the mouse B-cell lymphoma 38B9 line cell was infected by the retrovirus. Infection rate of the retrovirus was detected by flow cytometry assay. Cell counting method and flow cytometry assay observed proliferation and apoptosis of the 38B9 cells with Laptm5 3′UTR or mutated overexpression of Laptm5 3′UTR respectively. Results: Expressions of Laptm5 miRNA and its protein in the B-cell lymphoma cell all were more significantly reduced than those in the mouse B cell (all P<0.01). The 38B9 line cell with stable overespression of Laptm5 3′UTR (mutated Laptm5 3′UTR) was succesfully constructed. Proliferation ability of the 38B9 cell with Laptm5 3′UTR was more obviously decreased than that in the 38B9 cell with the mutated Laptm5 3′UTR and apoptosis of the 38B9 cell with Laptm5 3′UTR was more significantly increased than that in the 38B9 cell with the mutated Laptm5 3′UTR （\[7.87±1.08\]% vs \[0.45±0.07\]%, P<0.01). Conclusion: Mouse Laptm5 3′UTR might have functions of inhibiting growth of B-cell lymphoma and promoting its apoptosis. The functions could be associated with regulating its effected-miRNA.
Objective:To explore effect of lysosomal associated protein transmembrane 5 (Laptm5) 3′untranslated region (3′UTR) on proliferation and apoptosis of mouse B-cell lymphoma 38B9 line cell, by means of establishing B-cell lymphoma cell line with stable overexpression of Laptm5 3′UTR. Methods:Expressions of Laptm5 miRNA and its protein in normal mouse B cell and the mouse B-cell lymphoma 38B9 line cell were respectively examined by Western blotting and fluorescence quantitative PCR. A mouse Laptm5 3′UTR and Laptm5 3′UTR mutation gene fragment containing mutated miRNA 17-3p binding sites were inserted into retrovirus expression vector pMSCV-PIG. The retrovirus was constructed and the mouse B-cell lymphoma 38B9 line cell was infected by the retrovirus. Infection rate of the retrovirus was detected by flow cytometry assay. Cell counting method and flow cytometry assay observed proliferation and apoptosis of the 38B9 cells with Laptm5 3′UTR or mutated overexpression of Laptm5 3′UTR respectively. Results: Expressions of Laptm5 miRNA and its protein in the B-cell lymphoma cell all were more significantly reduced than those in the mouse B cell (all P<0.01). The 38B9 line cell with stable overespression of Laptm5 3′UTR (mutated Laptm5 3′UTR) was succesfully constructed. Proliferation ability of the 38B9 cell with Laptm5 3′UTR was more obviously decreased than that in the 38B9 cell with the mutated Laptm5 3′UTR and apoptosis of the 38B9 cell with Laptm5 3′UTR was more significantly increased than that in the 38B9 cell with the mutated Laptm5 3′UTR （\[7.87±1.08\]% vs \[0.45±0.07\]%, P<0.01). Conclusion: Mouse Laptm5 3′UTR might have functions of inhibiting growth of B-cell lymphoma and promoting its apoptosis. The functions could be associated with regulating its effected-miRNA.
2017, 24(3):242-246.
DOI: 10.3872/j.issn.1007-385X.2017.03.005
Abstract:
Objective:To explore effect of methyl ester pyropheophorbide-a mediated photodynamic therapy (MPPa-PDT) on invasion and migration of human osteosarcoma MG-63 line cell and its possible mechanism. Methods: Using CCK8 assay, cytoactive of the MG-63 cell was detected at various time points of post-treatment with MMPa-PDT. Migration and invasion abilities of the MG-63 cell were respectively examined by Scratch and Transwell tests. Western blotting assay was used to check expression levels of E-cadherin (E-cad), matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MM-9) proteins in the MG-63 cell. Results: After treatment with MPPa-PDT, proliferation ability of the MG-63 cell at 12, 24 and 48 h in MPPa-PDT group was significantly lower than those in control, MPPa and LED groups (all P<0.05), and scratch healing ability, migration activity and invasion ability of the MG-63 cell in the MPPa-PDT group were also obviously more decline than those in the other three groups (all P<0.05). Expression of E-cad protein in the MG-63 cell of the MPPa-PDT group was evidently higher than those in the MG-63 cell of the other three groups, while expressions of MMP-2 and MMP-9 proteins in the MG-63 cell of the MPPa-PDT group were lower than those in the MG-63 cell of the other three groups (all P<0.05). Conclusion: MPPa-PDT could inhibit invasion and migration abilities of the human osteosarcoma MG-63 line cell, and could up-regulate expression of E-cad and down-regulate expressions of MMP-2 and MMP-9，which could be one of the mechanisms responsible for the above inhibition action.
Objective:To explore effect of methyl ester pyropheophorbide-a mediated photodynamic therapy (MPPa-PDT) on invasion and migration of human osteosarcoma MG-63 line cell and its possible mechanism. Methods: Using CCK8 assay, cytoactive of the MG-63 cell was detected at various time points of post-treatment with MMPa-PDT. Migration and invasion abilities of the MG-63 cell were respectively examined by Scratch and Transwell tests. Western blotting assay was used to check expression levels of E-cadherin (E-cad), matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MM-9) proteins in the MG-63 cell. Results: After treatment with MPPa-PDT, proliferation ability of the MG-63 cell at 12, 24 and 48 h in MPPa-PDT group was significantly lower than those in control, MPPa and LED groups (all P<0.05), and scratch healing ability, migration activity and invasion ability of the MG-63 cell in the MPPa-PDT group were also obviously more decline than those in the other three groups (all P<0.05). Expression of E-cad protein in the MG-63 cell of the MPPa-PDT group was evidently higher than those in the MG-63 cell of the other three groups, while expressions of MMP-2 and MMP-9 proteins in the MG-63 cell of the MPPa-PDT group were lower than those in the MG-63 cell of the other three groups (all P<0.05). Conclusion: MPPa-PDT could inhibit invasion and migration abilities of the human osteosarcoma MG-63 line cell, and could up-regulate expression of E-cad and down-regulate expressions of MMP-2 and MMP-9，which could be one of the mechanisms responsible for the above inhibition action.
2017, 24(3):247-252.
DOI: 10.3872/j.issn.1007-385X.2017.03.006
Abstract:
Objective:To detect methylation status of Bin1 in esophageal squamous cell carcinoma (ESCC) TE13 line cell, to analyze changes of expression level of Bin1, its methylation status and bioactivity of the TE13 cell before and after demethylation with demethylation agent 5-Aza-dC, and to explore possible mechanism and therapeutical strategies of ESCC. Methods: Using qRT-PCR, expression of bridge integration factor 1 (Bin1) mRNA in the TE13 cell at pre- and post-demethylation of Bin1 was detected. Methylation status of Bin1 promoter region in the TE13 cells were detected by SDP assay. Effects of demethylation on abilities of migration and invasion of the TE13 cell were respectively tested by scratch and Transwell assays. To use Western blotting assay, expressions of Bin1, matrix metalloproteinases-2 (MMP-2) and MMP-9 proteins in the TE13 cell were detected. Results: Bin1in the TE13 cell was presented as a complete methylation. Expression of Bin1 mRNA was low, and after the treatment of 5-Aza-dC, expression of Bin1 mRNA was significantly increased (P<0.01). Results of scratch and Transwell assays showed that treatment of demethylation evidently decreased migration and invasion abilities of the TE13 cell (all P<0.01). After the treatment with 5-Aza-dC, expression of Bin1 protein was markedly increased, expressions of MMP-2 and MMP-9 proteins were significantly decreased (all P<0.01). Conclusion: DNA methylation could be one of important mechanisms for low expression or absence of Bin1, and the methylation could affected migration and invasion abilities of the TE13 cell by regulating expressions of MMP-2 and MMP-9 proteins.
Objective:To detect methylation status of Bin1 in esophageal squamous cell carcinoma (ESCC) TE13 line cell, to analyze changes of expression level of Bin1, its methylation status and bioactivity of the TE13 cell before and after demethylation with demethylation agent 5-Aza-dC, and to explore possible mechanism and therapeutical strategies of ESCC. Methods: Using qRT-PCR, expression of bridge integration factor 1 (Bin1) mRNA in the TE13 cell at pre- and post-demethylation of Bin1 was detected. Methylation status of Bin1 promoter region in the TE13 cells were detected by SDP assay. Effects of demethylation on abilities of migration and invasion of the TE13 cell were respectively tested by scratch and Transwell assays. To use Western blotting assay, expressions of Bin1, matrix metalloproteinases-2 (MMP-2) and MMP-9 proteins in the TE13 cell were detected. Results: Bin1in the TE13 cell was presented as a complete methylation. Expression of Bin1 mRNA was low, and after the treatment of 5-Aza-dC, expression of Bin1 mRNA was significantly increased (P<0.01). Results of scratch and Transwell assays showed that treatment of demethylation evidently decreased migration and invasion abilities of the TE13 cell (all P<0.01). After the treatment with 5-Aza-dC, expression of Bin1 protein was markedly increased, expressions of MMP-2 and MMP-9 proteins were significantly decreased (all P<0.01). Conclusion: DNA methylation could be one of important mechanisms for low expression or absence of Bin1, and the methylation could affected migration and invasion abilities of the TE13 cell by regulating expressions of MMP-2 and MMP-9 proteins.
LIAN Bin
,
ZHENG Nan
,
CHI Zhihong
,
ZHOU Li
,
SHENG Xinan
,
SI Lu
,
KONG Yan
,
CUI Chuanliang
,
GUO Jun
2017, 24(3):253-258.
DOI: 10.3872/j.issn.1007-385X.2017.03.007
Abstract:
Objective:To explore clinical features of the patients with advanced mucosal melanoma (MM) and effect factors on therapy and prognosis of the patients. Methods: Clinical data and regimens for the 1st line and the 2nd line therapies of 232 patients with advanced MM who were hospitalized in Department of Renal Cancer and Melanoma, Peking University Cancer Hospital during January 2008 to December 2015 were collected. Survival status of the patients were followed up, and multiple factors that effect on overall survival and prognosis of the patients were statistically analyzed. Results:There were 232 patients with advanced MM in this study (101 male, 131 female). Median age of the patients was 56 years old; anatomic sites of the primary melanoma were anorectum (29.3%), nasal cavity (25.0%), urogenital tract (20.7%), oral cavity (20.3%), esophagus (4.7%), M staging at visiting time of the patients were 17.2% as M1a, 21.6% as M1b, 61.2% as M1c; Most patients had multiple metastases, most common metastic sites of the primary melanoma were lung (504%), liver (34.9%), bone (23.3%); median progression free survival (mPFS) was 4.5 months in the patients received the 1st line therapy and 2.5 months in the patients received the 2nd line therapy; overall survival (OS) was 110 months in all of the patients, and among them, OS was 16.0 months in the patients as M1a stage, 14.0 months in the patients as M1b stage, 10.0 months in the patients as M1c stage. Prognosis analysis found that OS was significantly correlated with M staging at visiting time and serum lactate dehydrogenase (LDH) (P<0.01) and did not obviously correlated with anatomic sites of the primary melanoma, gender, age, gene mutation status of the patients. Conclusion: Nasal and oral cavities could be predilection sites of the MM. M staging at the visiting time of the patients and the serum LDH level could be dependent prognosis factor of OS.
Objective:To explore clinical features of the patients with advanced mucosal melanoma (MM) and effect factors on therapy and prognosis of the patients. Methods: Clinical data and regimens for the 1st line and the 2nd line therapies of 232 patients with advanced MM who were hospitalized in Department of Renal Cancer and Melanoma, Peking University Cancer Hospital during January 2008 to December 2015 were collected. Survival status of the patients were followed up, and multiple factors that effect on overall survival and prognosis of the patients were statistically analyzed. Results:There were 232 patients with advanced MM in this study (101 male, 131 female). Median age of the patients was 56 years old; anatomic sites of the primary melanoma were anorectum (29.3%), nasal cavity (25.0%), urogenital tract (20.7%), oral cavity (20.3%), esophagus (4.7%), M staging at visiting time of the patients were 17.2% as M1a, 21.6% as M1b, 61.2% as M1c; Most patients had multiple metastases, most common metastic sites of the primary melanoma were lung (504%), liver (34.9%), bone (23.3%); median progression free survival (mPFS) was 4.5 months in the patients received the 1st line therapy and 2.5 months in the patients received the 2nd line therapy; overall survival (OS) was 110 months in all of the patients, and among them, OS was 16.0 months in the patients as M1a stage, 14.0 months in the patients as M1b stage, 10.0 months in the patients as M1c stage. Prognosis analysis found that OS was significantly correlated with M staging at visiting time and serum lactate dehydrogenase (LDH) (P<0.01) and did not obviously correlated with anatomic sites of the primary melanoma, gender, age, gene mutation status of the patients. Conclusion: Nasal and oral cavities could be predilection sites of the MM. M staging at the visiting time of the patients and the serum LDH level could be dependent prognosis factor of OS.
8 Efficacy and safety of Imatinib in the 78 patients with advanced melanoma harboring KIT mutation
MAO Lili
,
YU Sifan
,
CHEN Hanxiao
,
BAI Xue
,
WANG Xuan
,
SHENG Xinan
,
CUI Chuanliang
,
CHI Zhihong
,
TANG Bixia
,
LIAN Bin
,
YAN Xieqiao
,
LI Siming
,
GUO Jun
,
SI Lu
2017, 24(3):259-263.
DOI: 10.3872/j.issn.1007-385X.2017.03.008
Abstract:
Objective:To explore efficacy and safety of tyrosine kinase inhibitor, imatinib, in the patients with advanced melanoma haboring KIT mutation / amplification. Methods: Clinical data of 78 patients with advanced melanoma haboring KIT mutation/amplification who were hospitalized in the Department of Renal Cancer and Melanoma, Cancer Hospital of Peking University during November 2009 to September 2015 were retrospectively analyzed. All of the patients received an imatinib oral treatment (400 mg/d) until disease progression or occur of intolerable adverse reactions. Results: Curative effects of the 78 patients were evaluated. In the patients of the whole group, objective remission rate was 22.4% and disease control rate was 60.6%. Among the 17 patients who were partial remission, the 11 patients were 11 exon or 13 exon mutation. For the patients of whole group, median progression free time was 3.9 months (95% CI: 2.1~5.8 months), median overall survival time was 13.2 months (95% CI: 10.1~16.3 months), survival rate for 1 year was 57%, survival rate for 2 years was 36% and survival rate for 3 years was 19%. The most common adverse reactions included edema, fatigue, anorexia, rash and neutropenia (all incidence rate ≥10%), and no fatal drug-related adverse reactions were observed. Conclusion:Imatinib could have certain curative effect for treatment of the patients with advanced melanoma baboring KIT mutation / amplification, and good safety.
Objective:To explore efficacy and safety of tyrosine kinase inhibitor, imatinib, in the patients with advanced melanoma haboring KIT mutation / amplification. Methods: Clinical data of 78 patients with advanced melanoma haboring KIT mutation/amplification who were hospitalized in the Department of Renal Cancer and Melanoma, Cancer Hospital of Peking University during November 2009 to September 2015 were retrospectively analyzed. All of the patients received an imatinib oral treatment (400 mg/d) until disease progression or occur of intolerable adverse reactions. Results: Curative effects of the 78 patients were evaluated. In the patients of the whole group, objective remission rate was 22.4% and disease control rate was 60.6%. Among the 17 patients who were partial remission, the 11 patients were 11 exon or 13 exon mutation. For the patients of whole group, median progression free time was 3.9 months (95% CI: 2.1~5.8 months), median overall survival time was 13.2 months (95% CI: 10.1~16.3 months), survival rate for 1 year was 57%, survival rate for 2 years was 36% and survival rate for 3 years was 19%. The most common adverse reactions included edema, fatigue, anorexia, rash and neutropenia (all incidence rate ≥10%), and no fatal drug-related adverse reactions were observed. Conclusion:Imatinib could have certain curative effect for treatment of the patients with advanced melanoma baboring KIT mutation / amplification, and good safety.
2017, 24(3):264-270.
DOI: 10.3872/j.issn.1007-385X.2017.03.009
Abstract:
Objective:To explore effects of high-mobility group box 1 (HMGB1) on proliferation, apoptosis and malignant biological behaviors of bladder cancer T24 cell line as well as its potential mechanism. Methods: Twenty cases of surgically resected bladder cancer and corresponding adjacent normal tissues form the patients who were hospitalized in Department of Urinary Surgery, the 1st Hospital affiliated to Chongqing Medical University during December 2014 to January 2016 were collected. The T24 cells were treated by RNAi technique and divided into blank control group, negative control(NC) group and interfere (siHMGB1) group. Differences of HMGB1 expression between bladder cancer and adjacent normal tissues were detected by immuno chemistry assay. CCK-8 assay, flow cytometry assay, scratch test and Transwell invasion test were used to examine effect of knocking down HMGB1 on abilities of proliferation, apoptosis, cell cycle, migration and invasion of the T24 cells respectively. Western blotting assay was used to detect expression levels of HMGB1 in BIU-87 and T24 cells and effect of knocking down HMGB1 on expression of malignant biological behavior related proteins in the T24 cells. Results: Expression of HMGB1 in the bladder cancer tissues was obviously higher than that in the adjacent normal tissues (\[67.33±4.91\] vs \[12.00±3.79\], P<0.05). Comparing with the negative control and blank control groups, proliferation of the T24 cells was inhibited in the siHMGB1 group (P<0.05). Results of flow cytometry assay suggested that apoptosis rate of the T24 cells increased and its cell cycle arrested in phase of G0/G1 after knocking down HMGB1; results of scratch and Transwell invasion tests showed that after knock-down of HMGB1, abilities of migration (P<0.05) and invasion (\[16.33±1.45\] vs \[35.00±1.53\], \[34.00±2.08\]，P<0.05\] of the T24 cells decreased. Results of Western blotting assay showed that after the knock-down, expression of E-cardherin protein was up-regulated, expressions of N-cadherin, vimentin, metrix metalloproteinase（MMP)-2, MMP-9, cyclinD1, c-Myc and β-catenin proteins were down-regulated (all P<0.05). Conclusion: HMGB1 could promote epithelial-mesenchymal transition (EMT) of the bladder cancer cells and then enhance their malignant biological behaviors. The mechanism might be mediated by β-catenin signaling pathway.
Objective:To explore effects of high-mobility group box 1 (HMGB1) on proliferation, apoptosis and malignant biological behaviors of bladder cancer T24 cell line as well as its potential mechanism. Methods: Twenty cases of surgically resected bladder cancer and corresponding adjacent normal tissues form the patients who were hospitalized in Department of Urinary Surgery, the 1st Hospital affiliated to Chongqing Medical University during December 2014 to January 2016 were collected. The T24 cells were treated by RNAi technique and divided into blank control group, negative control(NC) group and interfere (siHMGB1) group. Differences of HMGB1 expression between bladder cancer and adjacent normal tissues were detected by immuno chemistry assay. CCK-8 assay, flow cytometry assay, scratch test and Transwell invasion test were used to examine effect of knocking down HMGB1 on abilities of proliferation, apoptosis, cell cycle, migration and invasion of the T24 cells respectively. Western blotting assay was used to detect expression levels of HMGB1 in BIU-87 and T24 cells and effect of knocking down HMGB1 on expression of malignant biological behavior related proteins in the T24 cells. Results: Expression of HMGB1 in the bladder cancer tissues was obviously higher than that in the adjacent normal tissues (\[67.33±4.91\] vs \[12.00±3.79\], P<0.05). Comparing with the negative control and blank control groups, proliferation of the T24 cells was inhibited in the siHMGB1 group (P<0.05). Results of flow cytometry assay suggested that apoptosis rate of the T24 cells increased and its cell cycle arrested in phase of G0/G1 after knocking down HMGB1; results of scratch and Transwell invasion tests showed that after knock-down of HMGB1, abilities of migration (P<0.05) and invasion (\[16.33±1.45\] vs \[35.00±1.53\], \[34.00±2.08\]，P<0.05\] of the T24 cells decreased. Results of Western blotting assay showed that after the knock-down, expression of E-cardherin protein was up-regulated, expressions of N-cadherin, vimentin, metrix metalloproteinase（MMP)-2, MMP-9, cyclinD1, c-Myc and β-catenin proteins were down-regulated (all P<0.05). Conclusion: HMGB1 could promote epithelial-mesenchymal transition (EMT) of the bladder cancer cells and then enhance their malignant biological behaviors. The mechanism might be mediated by β-catenin signaling pathway.
2017, 24(3):271-277.
DOI: 10.3872/j.issn.1007-385X.2017.03.010
Abstract:
Objective:To explore expression status of high mobility group B1 and N1 (HMGB1 and HMGN1) in cervical carcinoma cells and their relationship with tumor infiltrating lymphocytes (TILs). Methods:One hundred postoperative tumor tissue specimens from the patients with early cervical carcinoma who were hospitalized in Cancer Hospital of Tianjin Medical University during April 2012 to September 2015 were collected, among them stage Ⅰ and stage Ⅱ in each of 50 cases. Immune histochemical assay was used to detect expressions of HMGB1, HMGN1, CD3 and CD8 in the tumor tissues. According to overall staining intensity, HMGB1 and HMGN1 were divided into high expression group and low expression group respectively, and divided into cytoplasmic expression group and no cytoplasmic expression group based on expression of cytoplasm. Number of CD3+ and CD8+ cells in the tumor tissues were compared between the high expression group and the low expression group as well as between cytoplasmic expression group and no cytoplasmic expression group respectively. Results: Expression intensities of HMGB1 and HMGN1 in the tumor tissues as well as whether or not expression of HMGB1 and HMGN1 in cytoplasm all did not obviously correlate with age, FIGO staging and pathological grade (all P>0.05). Expressions of HMGB1 and HMGN1 in cytoplasm showed a positive correlation (P<0.05). Numbers of CD3+ and CD8+ cells in cytoplasm with expressions of HMGB1 and HMGN1 groups were significantly higher than those in cytoplasm without expressions of HMGB1 and HMGN1 groups (P<0.05).Conclusion: Cytoplasmic expressions of HMGB1 and HMGN1 in cervical carcinoma cells could correlate with high level of TILs in the tumor tissue, and this finding could be expected to provide a novel strategy for immunotherapy of cervical carcinoma.
Objective:To explore expression status of high mobility group B1 and N1 (HMGB1 and HMGN1) in cervical carcinoma cells and their relationship with tumor infiltrating lymphocytes (TILs). Methods:One hundred postoperative tumor tissue specimens from the patients with early cervical carcinoma who were hospitalized in Cancer Hospital of Tianjin Medical University during April 2012 to September 2015 were collected, among them stage Ⅰ and stage Ⅱ in each of 50 cases. Immune histochemical assay was used to detect expressions of HMGB1, HMGN1, CD3 and CD8 in the tumor tissues. According to overall staining intensity, HMGB1 and HMGN1 were divided into high expression group and low expression group respectively, and divided into cytoplasmic expression group and no cytoplasmic expression group based on expression of cytoplasm. Number of CD3+ and CD8+ cells in the tumor tissues were compared between the high expression group and the low expression group as well as between cytoplasmic expression group and no cytoplasmic expression group respectively. Results: Expression intensities of HMGB1 and HMGN1 in the tumor tissues as well as whether or not expression of HMGB1 and HMGN1 in cytoplasm all did not obviously correlate with age, FIGO staging and pathological grade (all P>0.05). Expressions of HMGB1 and HMGN1 in cytoplasm showed a positive correlation (P<0.05). Numbers of CD3+ and CD8+ cells in cytoplasm with expressions of HMGB1 and HMGN1 groups were significantly higher than those in cytoplasm without expressions of HMGB1 and HMGN1 groups (P<0.05).Conclusion: Cytoplasmic expressions of HMGB1 and HMGN1 in cervical carcinoma cells could correlate with high level of TILs in the tumor tissue, and this finding could be expected to provide a novel strategy for immunotherapy of cervical carcinoma.
2017, 24(3):278-283.
DOI: 10.3872/j.issn.1007-385X.2017.03.011
Abstract:
Objective:To explore the correlation between single nucleotide polymorphism (SNP) of Keap1 gene and clear cell renal cell carcinoma (ccRCC), and to provide an effective molecular target for the clinical diagnosis and treatment of the ccRCC. Methods: One hundred and eight carcinoma tissues from the patients with ccRCC (tumor group) and 86 normal renal tissues from the tumor-free individuals (control group) were collected. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and gene sequencing assays were used to detect NSP of the Keap1 gene and genotype of the samples of the both groups. Expression status of the Keap1 gene in the both groups were examined by real-time fluorescence quantitative PCR. Results：Distribution frequencies of the Keap1 gene rs1048289 in different genotypes and alleles were statistically different between the tumor group and the control group (P<0.05). Risk of ccRCC in the patients carraying AA genotype and A allele obviously increased, and AA genotype (OR=2.292, 95% CI:1.159-4.533, P<0.05) and A allele (OR=2.067, 95% CI:1.280-3.342, P<0.01) were risk factors of ccRCC. Expression of the 〖STBX〗Keap1 gene in the patients of the tumor group was significantly lower than that in the patients of the control group (P<0.05). But there was no obvious difference in expression of the Keap1gene among samples with different genotypes (P<0.05). Conclusion: The Keap1 gene rs1048289 could be significantly correlated with ccRCC, and could hopefully become an effective molecular target for early diagnosis and gene therapy of the patients with ccRCC.
Objective:To explore the correlation between single nucleotide polymorphism (SNP) of Keap1 gene and clear cell renal cell carcinoma (ccRCC), and to provide an effective molecular target for the clinical diagnosis and treatment of the ccRCC. Methods: One hundred and eight carcinoma tissues from the patients with ccRCC (tumor group) and 86 normal renal tissues from the tumor-free individuals (control group) were collected. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and gene sequencing assays were used to detect NSP of the Keap1 gene and genotype of the samples of the both groups. Expression status of the Keap1 gene in the both groups were examined by real-time fluorescence quantitative PCR. Results：Distribution frequencies of the Keap1 gene rs1048289 in different genotypes and alleles were statistically different between the tumor group and the control group (P<0.05). Risk of ccRCC in the patients carraying AA genotype and A allele obviously increased, and AA genotype (OR=2.292, 95% CI:1.159-4.533, P<0.05) and A allele (OR=2.067, 95% CI:1.280-3.342, P<0.01) were risk factors of ccRCC. Expression of the 〖STBX〗Keap1 gene in the patients of the tumor group was significantly lower than that in the patients of the control group (P<0.05). But there was no obvious difference in expression of the Keap1gene among samples with different genotypes (P<0.05). Conclusion: The Keap1 gene rs1048289 could be significantly correlated with ccRCC, and could hopefully become an effective molecular target for early diagnosis and gene therapy of the patients with ccRCC.
2017, 24(3):284-289.
DOI: 10.3872/j.issn.1007-385X.2017.03.012
Abstract:
Objective:To explore the expression levels of programmed death-ligand 1 (PD-1) in cancer tissues of the patients with non-small cell lung carcinoma (NSCLC) in China and their influencing factors. Methods: Expressions of PD-L1, PD-1 and CD3+ T cell in tumor tissues from the 122 patients with NSCLC who were hospitalized in the Cancer Hospital of Tianjin Medical University during April 2008 to August 2014 were tested by Immuno histochemistry assay. χ2 and kruskal-wallis tests were used to analyze distribution difference of PD-L1 expression in clinical factors. Person and Spearman tests were to analyze correlation between expression of PD-L1 and EGFR genotype, number of CD3+T cell, expression of lymphocyte PD-1, and correlation between primary cancer focus and expression of lymphatic node PD-L1. Results: Median expression percentage of PD-L1 in cancer cells of primary tumor was 1.5% (0-93.2%) in all of the patients. Distribution of the PD-L1 expression in TNM staging had a very significant difference (P<0.01), expression of PD-L1 positively correlated with TNM staging (r=0.273, P<0.01) and did not significantly correlate with gender, age, smoking history, maximum tumor diameter, pathological type and level of CEA (P>0.05); expression level of PD-L1 did not correlate with number of CD3+ T cell and expression level of lymphocyte PD-1, negative, low and high expression of PD-L1 did not significantly correlate with EGFR gene mutation (P>0.05). There was non correlation of PD-L1 expression levels of cancer cells between primary tumor and corresponding metastasis lymph nodes in the 48 NSCLC patients with lymph node metastasis (P>0.05). Conclusion: PD-L1 expression of primary cancer cells in the patients with NSCLC could have differences in distribution of TNM staging, and don’t have correlation with number of CD3+ T cell, expression level of lymphocyte PD-1 and EGFR gene mutation. Expression of PD-L1 in cancer cells also could not have correlation between primary tumor locus and corresponding metastasis lymph nodes.
Objective:To explore the expression levels of programmed death-ligand 1 (PD-1) in cancer tissues of the patients with non-small cell lung carcinoma (NSCLC) in China and their influencing factors. Methods: Expressions of PD-L1, PD-1 and CD3+ T cell in tumor tissues from the 122 patients with NSCLC who were hospitalized in the Cancer Hospital of Tianjin Medical University during April 2008 to August 2014 were tested by Immuno histochemistry assay. χ2 and kruskal-wallis tests were used to analyze distribution difference of PD-L1 expression in clinical factors. Person and Spearman tests were to analyze correlation between expression of PD-L1 and EGFR genotype, number of CD3+T cell, expression of lymphocyte PD-1, and correlation between primary cancer focus and expression of lymphatic node PD-L1. Results: Median expression percentage of PD-L1 in cancer cells of primary tumor was 1.5% (0-93.2%) in all of the patients. Distribution of the PD-L1 expression in TNM staging had a very significant difference (P<0.01), expression of PD-L1 positively correlated with TNM staging (r=0.273, P<0.01) and did not significantly correlate with gender, age, smoking history, maximum tumor diameter, pathological type and level of CEA (P>0.05); expression level of PD-L1 did not correlate with number of CD3+ T cell and expression level of lymphocyte PD-1, negative, low and high expression of PD-L1 did not significantly correlate with EGFR gene mutation (P>0.05). There was non correlation of PD-L1 expression levels of cancer cells between primary tumor and corresponding metastasis lymph nodes in the 48 NSCLC patients with lymph node metastasis (P>0.05). Conclusion: PD-L1 expression of primary cancer cells in the patients with NSCLC could have differences in distribution of TNM staging, and don’t have correlation with number of CD3+ T cell, expression level of lymphocyte PD-1 and EGFR gene mutation. Expression of PD-L1 in cancer cells also could not have correlation between primary tumor locus and corresponding metastasis lymph nodes.
2017, 24(3):290-294.
DOI: 10.3872/j.issn.1007-385X.2017.03.013
Abstract:
Objective:To explore expression of actin filament-associated protein 1-antisense RNA1 (AFAP1-AS1), long non-coding RNA (lncRNA), in the gastric carcinoma tissues and its clinical significance. Methods: Using real-time PCR assay, expressions of AFAP1-AS1 in 274 cases of gastric carcinoma tissues and their corresponding adjacent normal gastric tissues which collected from the patients with gastric carcinoma who were hospitalized in the 2nd People Hospital of Yichang City and Renhe Hospital of Sanxia University for operative treatment during January 2010 to December 2014 were detected. And relationship between the expression of AFAP1-AS1 and clinicopathological features of the patients with gastric carcinoma was analyzed. Results: Expression of AFAP1-AS1 in the gastric carcinoma tissue was obviously higher than that in the adjaceut normal gastric tissues. Mean expression amount of AFAP1-AS1 in the early gastric carcinoma tissue was significantly lower than that in the advanced gastric carcinoma tissue (P<0.01). Among the gastric carcinoma tissues of various pathological types, expression amounts of AFAP1-AS1 were not significantly different (P>0.05). Expression amounts of AFAP1-AS1 were closely correlated with lymphatic invasion and distant metastasis of the gastric carcinoma. Expression amounts of AFAP1-AS1 in the gastric carcinoma tissue with local invasion and distant metastasis were obviously higher than those in the gastric carcinoma tissues without local invasion and distant metastasis (P<0.05). Conclusion:AFAP1-AS1 could be an important regulatory factor in the gastric carcinogenesis and development. It could be expected to become a novel marker for judging prognosis of the gastric carcinoma and used for clinical diagnosis and prognosis evaluation of the gastric carcinoma.
Objective:To explore expression of actin filament-associated protein 1-antisense RNA1 (AFAP1-AS1), long non-coding RNA (lncRNA), in the gastric carcinoma tissues and its clinical significance. Methods: Using real-time PCR assay, expressions of AFAP1-AS1 in 274 cases of gastric carcinoma tissues and their corresponding adjacent normal gastric tissues which collected from the patients with gastric carcinoma who were hospitalized in the 2nd People Hospital of Yichang City and Renhe Hospital of Sanxia University for operative treatment during January 2010 to December 2014 were detected. And relationship between the expression of AFAP1-AS1 and clinicopathological features of the patients with gastric carcinoma was analyzed. Results: Expression of AFAP1-AS1 in the gastric carcinoma tissue was obviously higher than that in the adjaceut normal gastric tissues. Mean expression amount of AFAP1-AS1 in the early gastric carcinoma tissue was significantly lower than that in the advanced gastric carcinoma tissue (P<0.01). Among the gastric carcinoma tissues of various pathological types, expression amounts of AFAP1-AS1 were not significantly different (P>0.05). Expression amounts of AFAP1-AS1 were closely correlated with lymphatic invasion and distant metastasis of the gastric carcinoma. Expression amounts of AFAP1-AS1 in the gastric carcinoma tissue with local invasion and distant metastasis were obviously higher than those in the gastric carcinoma tissues without local invasion and distant metastasis (P<0.05). Conclusion:AFAP1-AS1 could be an important regulatory factor in the gastric carcinogenesis and development. It could be expected to become a novel marker for judging prognosis of the gastric carcinoma and used for clinical diagnosis and prognosis evaluation of the gastric carcinoma.
2017, 24(3):295-299.
DOI: 10.3872/j.issn.1007-385X.2017.03.014
Abstract:
Objective:To detect expression level of ovarian tumor domain-containing protease 1 (OTUD1) in the tissue of non-small cell lung cancer (NSCLC) and to explore relationship between the expression of OTUD1 and clinical pathological features and prognosis of the patients with NSCLC. Methods: Cancer tissues from 82 patients with NSCLC, who were hospitalized in Department of Thoracic Surgery, Qilu Hospital of Shandong University during March 2008 to February 2009 for operative treatment and 40 specimens of normal lung tissues were selected, and expression levels of OTUD1 were detected by immune histochemical method. And another 25 patients with primary NSCLC who were hospitalized in Department of Thoracic Surgery, Qilu Hospital of Shandong University during March to April 2015 for operative treatment were collected and expressions of OTUD1in the NSCLC tissues and their adjacent normal lung tissues were examined by Real-time PCR assay. Results: Comparing with the normal lung tissues, expressions of OTUD1 mRNA in NSCLC tissues were distinct higher （0.620±0055 vs 0.387±0.037, P<0.01）. Expression of OTUD1 did not significantly correlated with age, gender, smoking history and pathologic type of the patients with NSCLC (all P>0.05), and significantly correlated with lymph node metastasis, differentiation grads and TNM staging of the patiewts with NSCLC (P<0.05 or P<0.01). Results of univariate and multivariate analysis showed that high expression of OTUD1 associated with poor prognosis of the patients. Conclusion: High expression of OTUD1 in the NSCLC tissues could be closely related to malignant progression and poor prognosis of NSCLC. Expression of OTUD1 could be as a reference index to evaluate biological features of NSCLC and prognosis of the patients with NSCLC.
Objective:To detect expression level of ovarian tumor domain-containing protease 1 (OTUD1) in the tissue of non-small cell lung cancer (NSCLC) and to explore relationship between the expression of OTUD1 and clinical pathological features and prognosis of the patients with NSCLC. Methods: Cancer tissues from 82 patients with NSCLC, who were hospitalized in Department of Thoracic Surgery, Qilu Hospital of Shandong University during March 2008 to February 2009 for operative treatment and 40 specimens of normal lung tissues were selected, and expression levels of OTUD1 were detected by immune histochemical method. And another 25 patients with primary NSCLC who were hospitalized in Department of Thoracic Surgery, Qilu Hospital of Shandong University during March to April 2015 for operative treatment were collected and expressions of OTUD1in the NSCLC tissues and their adjacent normal lung tissues were examined by Real-time PCR assay. Results: Comparing with the normal lung tissues, expressions of OTUD1 mRNA in NSCLC tissues were distinct higher （0.620±0055 vs 0.387±0.037, P<0.01）. Expression of OTUD1 did not significantly correlated with age, gender, smoking history and pathologic type of the patients with NSCLC (all P>0.05), and significantly correlated with lymph node metastasis, differentiation grads and TNM staging of the patiewts with NSCLC (P<0.05 or P<0.01). Results of univariate and multivariate analysis showed that high expression of OTUD1 associated with poor prognosis of the patients. Conclusion: High expression of OTUD1 in the NSCLC tissues could be closely related to malignant progression and poor prognosis of NSCLC. Expression of OTUD1 could be as a reference index to evaluate biological features of NSCLC and prognosis of the patients with NSCLC.
2017, 24(3):300-304.
DOI: 10.3872/j.issn.1007-385X.2017.03.015
Abstract:
Objective:To analyze retrospectively the clinical efficacy and safety of the cytokine induced killer (CIK) cells combined with chemotherapy for the patients with advanced pancreatic carcinoma. Methods: Twenty eight patients with advanced pancreatic carcinoma who were hospitalized in Department of biotherapy, Tumor Hospital Affiliated to Zhengzhou University during September 2010 to February 2016 were collected. All of the patients received chemical treatment with gemcitabine and/or S-1. CIK cells cultured in vitro were transfused into the patients within 1 to 3 days after the chemotherapy. Rates of progressive disease (PD), stable disease (SD), partial regression (PR) and complete regression (CR), median overall survival ( mOS), rates of survival for 6 months、12 months、18 months and 24 months, disease control rate (DCR) and adverse effects were observed. DCR included CR, PR and SD. Results: Among the 28 patients, PR rate 17.86% (5 cases), SD rate 53.57% (15 cases) and PD rate 28.57% (8 cases) respectively. DCR was 7143%. mOS was 15.41 months. Rates of survival for 6 months、12 months、18 months and 24 months respectively were 85.71%,50.00%,39.28% and 10.71%. The major adverse effects were myelo suppression，nausea and emeses, which were improved after symptomatic treatments. Conclusion: The CIK cells combined with chemotherapy could be an effective and safety treatment approach for the patients with advanced pancreatic carcinoma. The patients might have little adverse reactions and well toleration. The treatment approach could markedly prolong survival of the patients.
Objective:To analyze retrospectively the clinical efficacy and safety of the cytokine induced killer (CIK) cells combined with chemotherapy for the patients with advanced pancreatic carcinoma. Methods: Twenty eight patients with advanced pancreatic carcinoma who were hospitalized in Department of biotherapy, Tumor Hospital Affiliated to Zhengzhou University during September 2010 to February 2016 were collected. All of the patients received chemical treatment with gemcitabine and/or S-1. CIK cells cultured in vitro were transfused into the patients within 1 to 3 days after the chemotherapy. Rates of progressive disease (PD), stable disease (SD), partial regression (PR) and complete regression (CR), median overall survival ( mOS), rates of survival for 6 months、12 months、18 months and 24 months, disease control rate (DCR) and adverse effects were observed. DCR included CR, PR and SD. Results: Among the 28 patients, PR rate 17.86% (5 cases), SD rate 53.57% (15 cases) and PD rate 28.57% (8 cases) respectively. DCR was 7143%. mOS was 15.41 months. Rates of survival for 6 months、12 months、18 months and 24 months respectively were 85.71%,50.00%,39.28% and 10.71%. The major adverse effects were myelo suppression，nausea and emeses, which were improved after symptomatic treatments. Conclusion: The CIK cells combined with chemotherapy could be an effective and safety treatment approach for the patients with advanced pancreatic carcinoma. The patients might have little adverse reactions and well toleration. The treatment approach could markedly prolong survival of the patients.
2017, 24(3):305-310.
DOI: 10.3872/j.issn.1007-385X.2017.03.016
Abstract:
近年来在非小细胞肺癌（non-small cell lung cancer,NSCLC）治疗领域里程碑式的改变是采用EGFR-酪氨酸激酶抑制剂（tyrosine kinase inhibitor, TKI）治疗表皮生长因子受体（epidermal growth factor receptor, EGFR）基因突变阳性的晚期患者。但大部分患者在使用该药治疗9~11个月后陆续出现耐药现象。研究发现EGFR基因20号外显子T790M基因突变是导致EGFR TKI耐药的最主要因素，因此特异性靶向T790M抗药性突变的EGFR抑制剂AZD9291受到了极大的关注。本文对AZD9291治疗非小细胞肺癌的临床转化进行了综述。
近年来在非小细胞肺癌（non-small cell lung cancer,NSCLC）治疗领域里程碑式的改变是采用EGFR-酪氨酸激酶抑制剂（tyrosine kinase inhibitor, TKI）治疗表皮生长因子受体（epidermal growth factor receptor, EGFR）基因突变阳性的晚期患者。但大部分患者在使用该药治疗9~11个月后陆续出现耐药现象。研究发现EGFR基因20号外显子T790M基因突变是导致EGFR TKI耐药的最主要因素，因此特异性靶向T790M抗药性突变的EGFR抑制剂AZD9291受到了极大的关注。本文对AZD9291治疗非小细胞肺癌的临床转化进行了综述。
2017, 24(3):311-316.
DOI: 10.3872/j.issn.1007-385X.2017.03.017
Abstract:
多发性骨髓瘤（multiple myeloma，MM）是一种浆细胞恶性肿瘤，约占血液系统恶性肿瘤的10%。传统大剂量化疗及自体干细胞移植提高了患者的生存率，近十年来新型药物的出现也极大地延长了患者的OS；然而，化疗毒性作用及移植相关死亡率也不容忽视。在现有的治疗手段下，大部分MM患者最终会复发耐药而死亡，因此亟需寻找新的治疗方法。肿瘤免疫治疗在控制骨髓瘤方面有极好的前景，可能为MM患者提供除传统化疗之外的新的治疗选择。治疗性疫苗可通过诱导免疫应答以清除骨髓瘤细胞，大量研究着眼于研发可产生骨髓瘤特异性免疫的肿瘤疫苗，目前许多疫苗正处于临床试验阶段，并已经开始呈现出令人欣喜的结果。本文就MM疫苗的最新主要研究进展进行综述。
多发性骨髓瘤（multiple myeloma，MM）是一种浆细胞恶性肿瘤，约占血液系统恶性肿瘤的10%。传统大剂量化疗及自体干细胞移植提高了患者的生存率，近十年来新型药物的出现也极大地延长了患者的OS；然而，化疗毒性作用及移植相关死亡率也不容忽视。在现有的治疗手段下，大部分MM患者最终会复发耐药而死亡，因此亟需寻找新的治疗方法。肿瘤免疫治疗在控制骨髓瘤方面有极好的前景，可能为MM患者提供除传统化疗之外的新的治疗选择。治疗性疫苗可通过诱导免疫应答以清除骨髓瘤细胞，大量研究着眼于研发可产生骨髓瘤特异性免疫的肿瘤疫苗，目前许多疫苗正处于临床试验阶段，并已经开始呈现出令人欣喜的结果。本文就MM疫苗的最新主要研究进展进行综述。
2017, 24(3):317-322.
DOI: 10.3872/j.issn.1007-385X.2017.03.018
Abstract:
嵌合抗原受体(chimeric antigen receptor ，CAR)是单链抗体的可变区（single-chain variable fragments, scFv）和T细胞信号分子的重组融合蛋白，它使T细胞可以通过非MHC限制性方式识别特异性抗原。最近的临床研究证明，CAR-T细胞在治疗B细胞肿瘤中取得了显著效果。但在目前的临床应用中存在诸多限制，尤其是当肿瘤抗原在正常组织中表达时会造成脱靶效应。本文就靶抗原的选择、脱靶效应及相应的预防策略作一综述，期望这些策略的实施，将会提高CAR-T细胞治疗的安全性及有效性，使更多肿瘤患者从中获益。
嵌合抗原受体(chimeric antigen receptor ，CAR)是单链抗体的可变区（single-chain variable fragments, scFv）和T细胞信号分子的重组融合蛋白，它使T细胞可以通过非MHC限制性方式识别特异性抗原。最近的临床研究证明，CAR-T细胞在治疗B细胞肿瘤中取得了显著效果。但在目前的临床应用中存在诸多限制，尤其是当肿瘤抗原在正常组织中表达时会造成脱靶效应。本文就靶抗原的选择、脱靶效应及相应的预防策略作一综述，期望这些策略的实施，将会提高CAR-T细胞治疗的安全性及有效性，使更多肿瘤患者从中获益。
2017, 24(3):323-327.
DOI: 10.3872/j.issn.1007-385X.2017.03.019
Abstract:
组成核糖体相关复合物的MPP11和HSPA14，因其能够辅助“伴侣分子”完成新生肽链在核糖体从最初合成的线性结构到组装、正确折叠成三维构象的过程，又被称为“辅助伴侣”分子。近年来的研究表明，MPP11和HSPA14不仅能够发挥其“辅助伴侣”分子作用，也与细胞分化发育以及肿瘤发生发展存在紧密联系。本文通过就MPP11和HSPA14分子的结构、细胞内定位、生物学功能以及它们之间的相互作用、相互调控等方面进行综述，进一步揭示MPP11和HSPA14在肿瘤中的高表达，介导了肿瘤的发生发展过程，为后续肿瘤免疫治疗提供了新的方向。
组成核糖体相关复合物的MPP11和HSPA14，因其能够辅助“伴侣分子”完成新生肽链在核糖体从最初合成的线性结构到组装、正确折叠成三维构象的过程，又被称为“辅助伴侣”分子。近年来的研究表明，MPP11和HSPA14不仅能够发挥其“辅助伴侣”分子作用，也与细胞分化发育以及肿瘤发生发展存在紧密联系。本文通过就MPP11和HSPA14分子的结构、细胞内定位、生物学功能以及它们之间的相互作用、相互调控等方面进行综述，进一步揭示MPP11和HSPA14在肿瘤中的高表达，介导了肿瘤的发生发展过程，为后续肿瘤免疫治疗提供了新的方向。
2017, 24(3):328-331.
DOI: 10.3872/j.issn.1007-385X.2017.03.020
Abstract:
随着医学分子生物学技术的发展和对大肠癌分子发病机制的深入研究，以表皮生长因子受体( epidermal growth factor receptor, EGFR)为靶点的分子靶向治疗在大肠癌的治疗中作用显著。其中，以西妥昔单抗和帕尼单抗为代表的抗EGFR单抗为大肠癌患者带来了福音，EGFR过表达的患者对EGFR单抗治疗敏感、疗效显著，但无论近期疗效如何，患者最终都不可避免的产生耐药性及病情进展。因此，了解抗EGFR单抗耐药机制有利于指导大肠癌患者的临床治疗。
随着医学分子生物学技术的发展和对大肠癌分子发病机制的深入研究，以表皮生长因子受体( epidermal growth factor receptor, EGFR)为靶点的分子靶向治疗在大肠癌的治疗中作用显著。其中，以西妥昔单抗和帕尼单抗为代表的抗EGFR单抗为大肠癌患者带来了福音，EGFR过表达的患者对EGFR单抗治疗敏感、疗效显著，但无论近期疗效如何，患者最终都不可避免的产生耐药性及病情进展。因此，了解抗EGFR单抗耐药机制有利于指导大肠癌患者的临床治疗。
联系方式
- 《中国肿瘤生物治疗杂志》
- 1994年创刊
- 主办单位：Chinese Society of Immunology, Chinese Anti-cancer Association
- 邮编：200433
- 电话：021-81871002-22
- 电子邮箱：cjcb@biother.cn
- 网址:http://www.biother.cn
- 刊号：ISSN 1007-385X
- CN 31-1725/R
- 国内定价： ￥20元/册
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.
Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.