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Volume 25,Issue 5,2018 Table of Contents
2018, 25(5):441-446.
DOI: 10.3872/j.issn.1007-385X.2018.05.001
Abstract:
[Abstract] EGFRvIII (epidermal growth factor receptor variant Ⅲ) is the most common mutant of epidermal growth factor receptor,which expresses in over 30% glioblastoma multiforme (GBM). EGFRvIII results from deletion of exon 2-7, leading to its constitutive activation, which is closely related to tumorigenesis, development and poor prognosis of GBM. The unique glycine site on EGFRvIII provides ideal molecular target for immunotherapy, which possess great potential value of killing GBM cell, inhibiting progress and invasion.Encouraging progress has been achieved in peptide/DC vaccine, therapeutic antibody, small molecular inhibitor and adoptive immunotherapy experimentally and clinically. The characteristics of EGFRvIII and the development in its oriented immunotherapy were summarized in this review.
[Abstract] EGFRvIII (epidermal growth factor receptor variant Ⅲ) is the most common mutant of epidermal growth factor receptor,which expresses in over 30% glioblastoma multiforme (GBM). EGFRvIII results from deletion of exon 2-7, leading to its constitutive activation, which is closely related to tumorigenesis, development and poor prognosis of GBM. The unique glycine site on EGFRvIII provides ideal molecular target for immunotherapy, which possess great potential value of killing GBM cell, inhibiting progress and invasion.Encouraging progress has been achieved in peptide/DC vaccine, therapeutic antibody, small molecular inhibitor and adoptive immunotherapy experimentally and clinically. The characteristics of EGFRvIII and the development in its oriented immunotherapy were summarized in this review.
2018, 25(5):447-454.
DOI: 10.3872/j.issn.1007-385X.2018.05.002
Abstract:
[Abstract] Objective：To study the effects of IL-34 over-expression on malignant biological behavior of acute monocytic leukemia (AMoL) cells. Methods: The lentiviral vector pCDH-GFP for over-expressing IL-34 was constructed and infected into AMoL cell lines (THP1 and MOLM-13). Then its effects on proliferation, colony forming and cell cycle as well as apoptosis were tested by the MTS,colony formation assay and Annexin-V/PI staining, respectively. The cell differentiation phenotypes were assessed by fflow cytometry.Nude mice xenograft model was established to observe the tumor size and mass as well as the macrophages recruitment. Results: qPCR analysis showed that the expression of IL-34 mRNA in THP1-IL-34 and MOLM-13-IL-34 cells was nearly 4 000 and 3 000 folds higher than their respective control cells (all P<0.01), indicating that AMoL cell lines over-expressing IL-34 were successfully established. In vitro study showed that over-expression of IL-34 in AMoL cell lines promoted their proliferation potential(72 h: [0.738 ± 0.003] vs[0.646±0.008]; [0.290±0.004] vs [0.247±0.004]; all P<0.01) and colony formation ([127.00 ± 3.37] vs [86.00±4.08]; [160.70±4.70] vs[116.70±3.93]; all P<0.01), whereas had little effect on apoptosis (all P>0.05). Over-expression of IL-34 promoted AMoL cell differentiation towards monocyte-macrophage lineage as the expressions of the monocyte-macrophage markers, CD11b and CD14, were increased whereas the expression of immature marker, CD71, was decreased in AMoL cell lines over-expressing IL-34(all P<0.05). Nude mice xenograft model showed that IL-34 over-expression stimulated macrophage recruitment in tumor tissues (P<0.01). Conclusion:Over-expression of IL-34 in human AMoL cell lines promotes their proliferation, colony forming potential and differentiation towards monocyte-macrophage lineage. Furthermore, IL-34 participates in the process of macrophages recruitment in vivo.
[Abstract] Objective：To study the effects of IL-34 over-expression on malignant biological behavior of acute monocytic leukemia (AMoL) cells. Methods: The lentiviral vector pCDH-GFP for over-expressing IL-34 was constructed and infected into AMoL cell lines (THP1 and MOLM-13). Then its effects on proliferation, colony forming and cell cycle as well as apoptosis were tested by the MTS,colony formation assay and Annexin-V/PI staining, respectively. The cell differentiation phenotypes were assessed by fflow cytometry.Nude mice xenograft model was established to observe the tumor size and mass as well as the macrophages recruitment. Results: qPCR analysis showed that the expression of IL-34 mRNA in THP1-IL-34 and MOLM-13-IL-34 cells was nearly 4 000 and 3 000 folds higher than their respective control cells (all P<0.01), indicating that AMoL cell lines over-expressing IL-34 were successfully established. In vitro study showed that over-expression of IL-34 in AMoL cell lines promoted their proliferation potential(72 h: [0.738 ± 0.003] vs[0.646±0.008]; [0.290±0.004] vs [0.247±0.004]; all P<0.01) and colony formation ([127.00 ± 3.37] vs [86.00±4.08]; [160.70±4.70] vs[116.70±3.93]; all P<0.01), whereas had little effect on apoptosis (all P>0.05). Over-expression of IL-34 promoted AMoL cell differentiation towards monocyte-macrophage lineage as the expressions of the monocyte-macrophage markers, CD11b and CD14, were increased whereas the expression of immature marker, CD71, was decreased in AMoL cell lines over-expressing IL-34(all P<0.05). Nude mice xenograft model showed that IL-34 over-expression stimulated macrophage recruitment in tumor tissues (P<0.01). Conclusion:Over-expression of IL-34 in human AMoL cell lines promotes their proliferation, colony forming potential and differentiation towards monocyte-macrophage lineage. Furthermore, IL-34 participates in the process of macrophages recruitment in vivo.
2018, 25(5):455-461.
DOI: 10.3872/j.issn.1007-385X.2018.05.003
Abstract:
[Abstract] Objective: To investigate the in vitro cytotoxicity of the chimeric antigen receptor-modified T cells and NK-92MI cells (CAR-NK-92MI cells) and CAR-CD19-T cells against mantle cell lymphoma (MCL). Methods: CAR-T cell technology, successfully obtained in clinical trial of B-lineage acute lymphoblastic leukemia (B-ALL) treatment, was used in this study. In the case of high expression of CD19 antigen in MCL, CAR- CD19-T cells and CAR- CD19-NK-92MI cells targeting CD19 antigen were generated, respectively.Then, their cytotoxicity against MCL cell lines was detected by LDH release assay and the results were verified by flow cytometry.Results: Compared with control group, both CAR-NK-92MI and CAR-CD19-T cells exhibited prominent killing effect against MCL cells（all P<0.01）; in addition, the two CAR cells exhibited high cytotoxicity against K562-CD19 cells but not on K562 cells（all P<0.01）. The death rate of MCL cells from CAR-NK-92MI group was 30%-40% more than that of control group, and the death rate ofMCL from CAR-CD19-T group was 40%-50% more than that of control group. Conclusion: Both CAR-NK-92MI and CAR-CD19-T cells exhibited potent cytotoxicity against MCL cells in vitro.
[Abstract] Objective: To investigate the in vitro cytotoxicity of the chimeric antigen receptor-modified T cells and NK-92MI cells (CAR-NK-92MI cells) and CAR-CD19-T cells against mantle cell lymphoma (MCL). Methods: CAR-T cell technology, successfully obtained in clinical trial of B-lineage acute lymphoblastic leukemia (B-ALL) treatment, was used in this study. In the case of high expression of CD19 antigen in MCL, CAR- CD19-T cells and CAR- CD19-NK-92MI cells targeting CD19 antigen were generated, respectively.Then, their cytotoxicity against MCL cell lines was detected by LDH release assay and the results were verified by flow cytometry.Results: Compared with control group, both CAR-NK-92MI and CAR-CD19-T cells exhibited prominent killing effect against MCL cells（all P<0.01）; in addition, the two CAR cells exhibited high cytotoxicity against K562-CD19 cells but not on K562 cells（all P<0.01）. The death rate of MCL cells from CAR-NK-92MI group was 30%-40% more than that of control group, and the death rate ofMCL from CAR-CD19-T group was 40%-50% more than that of control group. Conclusion: Both CAR-NK-92MI and CAR-CD19-T cells exhibited potent cytotoxicity against MCL cells in vitro.
LIU Yanzhong
,
PAN Lijuan
,
TANG Qulai
,
SHI Jiangzhou
,
ZHAO Wenjing
,
HUO Lihong
,
GU Chaojiang
,
HU Guang
,
LIU Huining
,
ZHANG Tongcun
,
2018, 25(5):462-468.
DOI: 10.3872/j.issn.1007-385X.2018.05.004
Abstract:
[Abstract] Objective: To construct CD33-CAR modified NK92 cells based on CD33-scFv sequence, and to explore its killing effect on CD33+ AML (acute myeloid leukemia) cells. Methods: DNA fragment encoding CD33-CAR was synthesized by gene synthesis and molecular cloning technology and then cloned into lentiviral vector. Lentivirus were packaged and used to transfect NK92 cells. The transfection efficiency was detected by flow cytometry, and puromycin was used to screen NK92 cells stably expressing CD33-CAR(CD33-CAR-NK92). Killing effect of CD33-CAR-NK92 cells on AML cells in vitro was examined with calcein-AM release assays.IFN-γ secretions of NK92 cells and CD33-CAR-NK92 cells were measured by ELISA. Results: The pCDH-CD33-CAR lentiviral vector was successfully constructed. After lentiviral transfection, about 18.7% of NK92 cells express CD33-CAR (referred as CD33-CARNK92 cells). The percentage of CD33-CAR+ NK92 cells was about 86.3% after puromycin selection. In contrast to unmodified NK92 cells, significantly higher cytotoxic effect against CD33+ MOLM-13 cells was found in CD33-CAR-NK92 cells (P<0.01); however,there was no significant difference in cytotoxicity against CD33- JURKAT cells between NK92 cells and CD33-CAR-NK92 cells (P>0.05). After co-culture at an effect-target ratio of 2∶1 for 6 hours, the level of IFN-γ secreted by the CD33-CAR modified NK92 cells was significantly higher than that of the unmodified [190.97±11.52] vs [88.41±2.75]pg/ml, P<0.01). Conclusion: The CD33-CARNK92 cells could specifically recognize CD33 antigen and kill CD33+ AML cells in comparison with the unmodified NK92 cells, which provides experimental basis for clinical transformation of CD33-CAR-NK92 cells in treating AML.
[Abstract] Objective: To construct CD33-CAR modified NK92 cells based on CD33-scFv sequence, and to explore its killing effect on CD33+ AML (acute myeloid leukemia) cells. Methods: DNA fragment encoding CD33-CAR was synthesized by gene synthesis and molecular cloning technology and then cloned into lentiviral vector. Lentivirus were packaged and used to transfect NK92 cells. The transfection efficiency was detected by flow cytometry, and puromycin was used to screen NK92 cells stably expressing CD33-CAR(CD33-CAR-NK92). Killing effect of CD33-CAR-NK92 cells on AML cells in vitro was examined with calcein-AM release assays.IFN-γ secretions of NK92 cells and CD33-CAR-NK92 cells were measured by ELISA. Results: The pCDH-CD33-CAR lentiviral vector was successfully constructed. After lentiviral transfection, about 18.7% of NK92 cells express CD33-CAR (referred as CD33-CARNK92 cells). The percentage of CD33-CAR+ NK92 cells was about 86.3% after puromycin selection. In contrast to unmodified NK92 cells, significantly higher cytotoxic effect against CD33+ MOLM-13 cells was found in CD33-CAR-NK92 cells (P<0.01); however,there was no significant difference in cytotoxicity against CD33- JURKAT cells between NK92 cells and CD33-CAR-NK92 cells (P>0.05). After co-culture at an effect-target ratio of 2∶1 for 6 hours, the level of IFN-γ secreted by the CD33-CAR modified NK92 cells was significantly higher than that of the unmodified [190.97±11.52] vs [88.41±2.75]pg/ml, P<0.01). Conclusion: The CD33-CARNK92 cells could specifically recognize CD33 antigen and kill CD33+ AML cells in comparison with the unmodified NK92 cells, which provides experimental basis for clinical transformation of CD33-CAR-NK92 cells in treating AML.
2018, 25(5):469-474.
DOI: 10.3872/j.issn.1007-385X.2018.05.005
Abstract:
[Abstract] Objective: To explore the mechanism of glucose transport protein-1(Glut-1) promoting the migration of osteosarcoma MG63 cells through Wnt/β-catenin pathway. Methods: RNA interference recombinant adenovirus targeting Glut-1 gene (Ad-Glut-siRNA)and control recombinant adenovirus (Ad-GFP) were constructed and transfected into MG63 cells to silence Glut-1 gene expression.The cell migration ability of Blank group, Ad-AFP group, Ad-Glut-siRNA group and AZD2858 (inhibitor of GSK-3) group were detected by Transwell chamber migration assay. Immunofluorescence assay was used to detect the expression of E-cadherin and vimentin in each group and the nuclear translocation of β-catenin. The expression of MMP-2 and MMP-9 in each group and FZD7, β-catenin,Dsh protein in Blank group, Ad-AFP group, Ad-Glut-siRNA group were detected by Western blotting assay. Results: The migration ability of MG63 cells was significantly decreased (P<0.05) after Glut-1 gene silencing, which was restored after AZD2858 treatment (P<0.05). Compared with Blank group and Ad-GFP group, the E-cadherin level in MG63 cells in Ad-Glut-siRNA group was significantly increased (P<0.05), while the expressions of vimentin, MMP-2, MMP-9, FZD7, β-catenin and Dsh protein were significantly reduced (all P<0.05). Compared with Ad-Glut-siRNA group, E-cadherin expression of AZD2858 group was significantly reduced, while the expressions of vimentin, MMP-2, MMP-9 were significantly up-regulated (P<0.05). Conclusion: The high expression of Glut-1 gene is closely related to the invasion and metastasis of MG63 cells. The possible mechanism is that the high expression of Glut-1 leads to the activation of Wnt/β-catenin pathway, which leads to the decrease of EMT-related protein E-cadherin, and the increase of vimentin and MMP-2, MMP-9, and further promotes the migration of MG63 cells.
[Abstract] Objective: To explore the mechanism of glucose transport protein-1(Glut-1) promoting the migration of osteosarcoma MG63 cells through Wnt/β-catenin pathway. Methods: RNA interference recombinant adenovirus targeting Glut-1 gene (Ad-Glut-siRNA)and control recombinant adenovirus (Ad-GFP) were constructed and transfected into MG63 cells to silence Glut-1 gene expression.The cell migration ability of Blank group, Ad-AFP group, Ad-Glut-siRNA group and AZD2858 (inhibitor of GSK-3) group were detected by Transwell chamber migration assay. Immunofluorescence assay was used to detect the expression of E-cadherin and vimentin in each group and the nuclear translocation of β-catenin. The expression of MMP-2 and MMP-9 in each group and FZD7, β-catenin,Dsh protein in Blank group, Ad-AFP group, Ad-Glut-siRNA group were detected by Western blotting assay. Results: The migration ability of MG63 cells was significantly decreased (P<0.05) after Glut-1 gene silencing, which was restored after AZD2858 treatment (P<0.05). Compared with Blank group and Ad-GFP group, the E-cadherin level in MG63 cells in Ad-Glut-siRNA group was significantly increased (P<0.05), while the expressions of vimentin, MMP-2, MMP-9, FZD7, β-catenin and Dsh protein were significantly reduced (all P<0.05). Compared with Ad-Glut-siRNA group, E-cadherin expression of AZD2858 group was significantly reduced, while the expressions of vimentin, MMP-2, MMP-9 were significantly up-regulated (P<0.05). Conclusion: The high expression of Glut-1 gene is closely related to the invasion and metastasis of MG63 cells. The possible mechanism is that the high expression of Glut-1 leads to the activation of Wnt/β-catenin pathway, which leads to the decrease of EMT-related protein E-cadherin, and the increase of vimentin and MMP-2, MMP-9, and further promotes the migration of MG63 cells.
2018, 25(5):475-479.
DOI: 10.3872/j.issn.1007-385X.2018.05.006
Abstract:
[Abstract] Objective：To explore the impact of γ-chain (γc) family cytokines (IL-2, IL-7, IL-15, IL-21) on T cell phenotypes in ex vivo culture to provide experimental evidence for ex vivo cell preparation in adoptive immunotherapy. Methods: Peripheral blood mononuclear cells (PBMCs) were isolated from peripheral blood of healthy volunteers; nylon column sorting, CD3+ magnetic beads sorting,CD3- magnetic beads sorting and natural sedimentation were used to sort T cells from PBMCs. The purity, recovery rate and viability of T cells sorted by the above methods were compared. The CD3/CD28 magnetic beads-activated CD3+T cells were cultured in AIMV medium with IL-2 or mixed cytokines (IL-7, IL-15, IL-21). The expansion fold and phenotypes of T cells in ex vivo culture were detected by flow cytometry. Results：The purity of T cells sorted by CD3- magnetic beads sorting was significantly higher than that sorted by nylon column, CD3+ magnetic beads sorting and natural sedimentation ([94.06 ± 1.07]% vs [86.74 ± 1.06]%, [89.61 ± 1.40]%, [88.48 ±1.86]%, P<0.05); The recovery rate of T cells sorted by natural sedimentation was significantly higher than that by other three methods ([60.29±1.53]% vs [45.03±2.79]%, [20.15±3.41]%, [42.98±2.82]%, P<0.05). Comprehensively, the natural sedimentation method is the best option. The ex vivo expansion fold of T cells in IL-2 group was significantly higher than that in mixed group ([262.6±143.2] times vs [73.0±25.8] times, P<0.05). The proportions of early memory T cells, Tscm+Tscm-like and Tcm in the mixed group were significantly higher than those in the IL-2 group ([55.6±1.82]% vs [39.6±1.52]%,[16.6±1.82]% vs [9.8±1.30]%, [39.0±1.58]% vs [29.2±1.79]%; all P <0.05). Conclusion：Natural sedimentation sorting has advantages of low cost, high recovery and purity. Mixed cytokines of IL-7, IL-15 and IL-21 are beneficial for production of early memory T cells. This study provides an experimental data of ex vivo T cell preparation for cancer adoptive immunotherapy.
[Abstract] Objective：To explore the impact of γ-chain (γc) family cytokines (IL-2, IL-7, IL-15, IL-21) on T cell phenotypes in ex vivo culture to provide experimental evidence for ex vivo cell preparation in adoptive immunotherapy. Methods: Peripheral blood mononuclear cells (PBMCs) were isolated from peripheral blood of healthy volunteers; nylon column sorting, CD3+ magnetic beads sorting,CD3- magnetic beads sorting and natural sedimentation were used to sort T cells from PBMCs. The purity, recovery rate and viability of T cells sorted by the above methods were compared. The CD3/CD28 magnetic beads-activated CD3+T cells were cultured in AIMV medium with IL-2 or mixed cytokines (IL-7, IL-15, IL-21). The expansion fold and phenotypes of T cells in ex vivo culture were detected by flow cytometry. Results：The purity of T cells sorted by CD3- magnetic beads sorting was significantly higher than that sorted by nylon column, CD3+ magnetic beads sorting and natural sedimentation ([94.06 ± 1.07]% vs [86.74 ± 1.06]%, [89.61 ± 1.40]%, [88.48 ±1.86]%, P<0.05); The recovery rate of T cells sorted by natural sedimentation was significantly higher than that by other three methods ([60.29±1.53]% vs [45.03±2.79]%, [20.15±3.41]%, [42.98±2.82]%, P<0.05). Comprehensively, the natural sedimentation method is the best option. The ex vivo expansion fold of T cells in IL-2 group was significantly higher than that in mixed group ([262.6±143.2] times vs [73.0±25.8] times, P<0.05). The proportions of early memory T cells, Tscm+Tscm-like and Tcm in the mixed group were significantly higher than those in the IL-2 group ([55.6±1.82]% vs [39.6±1.52]%,[16.6±1.82]% vs [9.8±1.30]%, [39.0±1.58]% vs [29.2±1.79]%; all P <0.05). Conclusion：Natural sedimentation sorting has advantages of low cost, high recovery and purity. Mixed cytokines of IL-7, IL-15 and IL-21 are beneficial for production of early memory T cells. This study provides an experimental data of ex vivo T cell preparation for cancer adoptive immunotherapy.
2018, 25(5):480-484.
DOI: 10.3872/j.issn.1007-385X.2018.05.007
Abstract:
[Abstract] Objective: To study the effects of twisted gastrulation protein homolog 1 (TWSG1) gene on proliferation and apoptosis of gastric cancer MGC-803 cells. Methods: Three siRNAs for TWSG1 gene were designed.The MGC-803 cells at logarithmic phase were divided into blank control group, negative control group (siRNA-NC), siRNA1 interference group, siRNA2 interference group and siRNA3 interference group by transfecting with relevant vectors. The mRNA and protein expressions of TWSG1 in each group were identified by qPCR and Western blotting, respectively; and the stable cell line with highest interference efficiency was screened.The proliferation of cells in each group was detected by CCK-8 assay, and the apoptosis of three groups was detected by flow cytometry. Results:The results of qPCR and Western blotting showed siRNA1 exhibited highest interference efficiency. Compared with the blank control group and the negative control group, the expression of TWSG1 in siRNA interference cell group was lower (P<0.05), the cell proliferation significantly increased (P<0.05), and apoptosis significantly reduced (P<0.05). Conclusion: siRNA interfering TWSG1 expression in MGC-803 cells can promote cell proliferation, inhibit cell apoptosis.
[Abstract] Objective: To study the effects of twisted gastrulation protein homolog 1 (TWSG1) gene on proliferation and apoptosis of gastric cancer MGC-803 cells. Methods: Three siRNAs for TWSG1 gene were designed.The MGC-803 cells at logarithmic phase were divided into blank control group, negative control group (siRNA-NC), siRNA1 interference group, siRNA2 interference group and siRNA3 interference group by transfecting with relevant vectors. The mRNA and protein expressions of TWSG1 in each group were identified by qPCR and Western blotting, respectively; and the stable cell line with highest interference efficiency was screened.The proliferation of cells in each group was detected by CCK-8 assay, and the apoptosis of three groups was detected by flow cytometry. Results:The results of qPCR and Western blotting showed siRNA1 exhibited highest interference efficiency. Compared with the blank control group and the negative control group, the expression of TWSG1 in siRNA interference cell group was lower (P<0.05), the cell proliferation significantly increased (P<0.05), and apoptosis significantly reduced (P<0.05). Conclusion: siRNA interfering TWSG1 expression in MGC-803 cells can promote cell proliferation, inhibit cell apoptosis.
2018, 25(5):485-489.
DOI: 10.3872/j.issn.1007-385X.2018.05.008
Abstract:
[Abstract] Objective: To investigate the effect of Xihuang (XH) extract on the proliferation of gastric cancer SGC-7901 cells and its underlying mechanism. Methods: Gastric cancer cell line SGC-7901 was conventionally cultured. CCK-8 assay and flow cytometry were used to detect the effect of different concentrations of XH extracts (3.2, 6.4, 12.8, and 25.6 mg/ml) on proliferation and apoptosis of SGC-7901 cells after treatment for different time periods (24, 48, and 72 h); The effect of different concentrations of XH extracts on the mRNA expression of apoptosis-related genes (Bax and Bcl-2) was detected by qPCR; Western blotting was used to detect the effect of XH extracts on the expression of apoptosis-associated proteins (caspase 3, caspase 9, Bax and Bcl-2). Results: XH extracts (3.2, 6.4,12.8, and 25.6 mg/ml) could effectively inhibit proliferation of gastric cancer SGC-7901 cells (P<0.05 or P<0.01) in a concentration-depend manner (P<0.01). XH extract could significantly up-regulate Bax mRNA and down-regulate Bcl-2 mRNA expression (P<0.05 or P<0.01); Meanwhile, XH extract ouldincrease protein expressions of caspase 3, caspase 9, Bax but reduce Bcl-2 protein expression (P<0.05 or P<0.01). Conclusion: XH extract can inhibit the proliferation of gastric cancer SGC-7901 cells by triggering apoptosis, which may become a potential method of adjuvant treatment of gastric cancer.
[Abstract] Objective: To investigate the effect of Xihuang (XH) extract on the proliferation of gastric cancer SGC-7901 cells and its underlying mechanism. Methods: Gastric cancer cell line SGC-7901 was conventionally cultured. CCK-8 assay and flow cytometry were used to detect the effect of different concentrations of XH extracts (3.2, 6.4, 12.8, and 25.6 mg/ml) on proliferation and apoptosis of SGC-7901 cells after treatment for different time periods (24, 48, and 72 h); The effect of different concentrations of XH extracts on the mRNA expression of apoptosis-related genes (Bax and Bcl-2) was detected by qPCR; Western blotting was used to detect the effect of XH extracts on the expression of apoptosis-associated proteins (caspase 3, caspase 9, Bax and Bcl-2). Results: XH extracts (3.2, 6.4,12.8, and 25.6 mg/ml) could effectively inhibit proliferation of gastric cancer SGC-7901 cells (P<0.05 or P<0.01) in a concentration-depend manner (P<0.01). XH extract could significantly up-regulate Bax mRNA and down-regulate Bcl-2 mRNA expression (P<0.05 or P<0.01); Meanwhile, XH extract ouldincrease protein expressions of caspase 3, caspase 9, Bax but reduce Bcl-2 protein expression (P<0.05 or P<0.01). Conclusion: XH extract can inhibit the proliferation of gastric cancer SGC-7901 cells by triggering apoptosis, which may become a potential method of adjuvant treatment of gastric cancer.
2018, 25(5):490-496.
DOI: 10.3872/j.issn.1007-385X.2018.05.009
Abstract:
[Abstract] Objective：To explore miR-103a-3p expression in the tumor tissues and the serum of breast cancer patients, and its role and mechanism in breast cancer development. Methods: Pathologically confirmed 31 cases of tumor tissues and 21 cases of para-cancerous tissues resected at Department of Oncological Surgery of the Second Affiliated Hospital of Hainan Medical University (Haikou, China)from March 1, 2017 to August 31，2017 were collected for this study; in addition, serum samples from 38 breast cancer patients and 22 healthy subjects as well as the breast cancer cell lines MCF-7 and MDA-MB-231 were used in this study. pHBLV-U6-Luc-T2A-Puro and PLL3.7 lentivirus were applied to knock down miR-103a-3p and PDK4 in MCF-7 and MDA-MB-231 cells, respectively. qPCR and Western blotting were performed to examine the mRNA and protein expressions of miR-103a-3p and PDK4 in tissues and serums of breast cancer patients as well as the in cell lines, respectively; CCK-8 assay was applied to detect the proliferation of MCF-7 and MDAMB-231 cells; Olympus AU5400 was applied to detect the glucose consumption and lactate production in indicated cell line. Results：miR-103a-3p was significantly decreased in tumor tissues compared with the paracancerous tissues (P<0.01). miR-103a-3p knockdown activated the glucos consumption and lactate production (all P<0.01), increased the PKD4 expression (P<0.01) in MCF-7 and MDAMD-231 cells, and promoted the proliferation of MCF-7 and MDA-MB-231 cells (P<0.01). Furthermore, knockdown of PDK4 suppressed the glucose consumption, lactate production and proliferation in MCF-7 and MDA-MB-231 cells with miR-103a-3p silencing (all P<0.01). Conclusion：In the breast cancer, miR-103a-3p inhibited the proliferation of breast cancer cells through down-regulation of PDK4 and PDK4-mediated aerobic glycolysis.
[Abstract] Objective：To explore miR-103a-3p expression in the tumor tissues and the serum of breast cancer patients, and its role and mechanism in breast cancer development. Methods: Pathologically confirmed 31 cases of tumor tissues and 21 cases of para-cancerous tissues resected at Department of Oncological Surgery of the Second Affiliated Hospital of Hainan Medical University (Haikou, China)from March 1, 2017 to August 31，2017 were collected for this study; in addition, serum samples from 38 breast cancer patients and 22 healthy subjects as well as the breast cancer cell lines MCF-7 and MDA-MB-231 were used in this study. pHBLV-U6-Luc-T2A-Puro and PLL3.7 lentivirus were applied to knock down miR-103a-3p and PDK4 in MCF-7 and MDA-MB-231 cells, respectively. qPCR and Western blotting were performed to examine the mRNA and protein expressions of miR-103a-3p and PDK4 in tissues and serums of breast cancer patients as well as the in cell lines, respectively; CCK-8 assay was applied to detect the proliferation of MCF-7 and MDAMB-231 cells; Olympus AU5400 was applied to detect the glucose consumption and lactate production in indicated cell line. Results：miR-103a-3p was significantly decreased in tumor tissues compared with the paracancerous tissues (P<0.01). miR-103a-3p knockdown activated the glucos consumption and lactate production (all P<0.01), increased the PKD4 expression (P<0.01) in MCF-7 and MDAMD-231 cells, and promoted the proliferation of MCF-7 and MDA-MB-231 cells (P<0.01). Furthermore, knockdown of PDK4 suppressed the glucose consumption, lactate production and proliferation in MCF-7 and MDA-MB-231 cells with miR-103a-3p silencing (all P<0.01). Conclusion：In the breast cancer, miR-103a-3p inhibited the proliferation of breast cancer cells through down-regulation of PDK4 and PDK4-mediated aerobic glycolysis.
2018, 25(5):497-502.
DOI: 10.3872/j.issn.1007-385X.2018.05.010
Abstract:
[Abstract] Objective: To explore the mRNA molecular targets for diagnosis of hepatic carcionoma and to investigate their functional roles in proliferation and cell cycle of hepatic cancer cells. Methods: Based on the statistical analysis of miRNA expression data from 377 hepatic carcionoma samples and 37 adjacent non-cancerous samples in TCGA database, a group of 33 differentially expressed miRNAs were identified. A further screen of these differentially expressed miRNAs was performed using the receiver operating characteristic curve (ROC curve) and Kaplan-Meier survival analysis; and with referring to the current publications, miR-451 was screened as the study subject. HepG2 cells were transfected with pLVX-shRNA2-miR-451 to over-express miR-451. The effect of miR-451 over-expression on the proliferation of HepG2 cell was determined by CCK-8 assay; while the effect on cell cycles was detected by flow cytometry.Results: The expression of miR-451 in the adjacent non-cancerous tissues was significantly lower than that in cancer tissues ([473.40±390.24] vs [1 990.47±2 118.04], P<0.05). MiR-451 could be used as an early diagnostic biomarker of hepatic carcionoma,with a high ROC value of 0.91 (sensitivity 0.89, specificity 0.87). The results of in vitro experiments showed that the proliferation of HepG2 cells was significantly decreased after miR-451 over-expression (48 h: [0.69±0.04] vs [1.08±0.05]; 72 h: [0.76±0.07] vs [1.52±0.02]; all P<0.01), and a large number of cells were blocked in S phase(P<0.05). Conclusion: miR-451 has the potential to be used as a biomarker for hepatic carcionoma diagnosis and prognosis; moreover, it also exhibits the inhibitory effect on proliferation of hepatic cancer cells.
[Abstract] Objective: To explore the mRNA molecular targets for diagnosis of hepatic carcionoma and to investigate their functional roles in proliferation and cell cycle of hepatic cancer cells. Methods: Based on the statistical analysis of miRNA expression data from 377 hepatic carcionoma samples and 37 adjacent non-cancerous samples in TCGA database, a group of 33 differentially expressed miRNAs were identified. A further screen of these differentially expressed miRNAs was performed using the receiver operating characteristic curve (ROC curve) and Kaplan-Meier survival analysis; and with referring to the current publications, miR-451 was screened as the study subject. HepG2 cells were transfected with pLVX-shRNA2-miR-451 to over-express miR-451. The effect of miR-451 over-expression on the proliferation of HepG2 cell was determined by CCK-8 assay; while the effect on cell cycles was detected by flow cytometry.Results: The expression of miR-451 in the adjacent non-cancerous tissues was significantly lower than that in cancer tissues ([473.40±390.24] vs [1 990.47±2 118.04], P<0.05). MiR-451 could be used as an early diagnostic biomarker of hepatic carcionoma,with a high ROC value of 0.91 (sensitivity 0.89, specificity 0.87). The results of in vitro experiments showed that the proliferation of HepG2 cells was significantly decreased after miR-451 over-expression (48 h: [0.69±0.04] vs [1.08±0.05]; 72 h: [0.76±0.07] vs [1.52±0.02]; all P<0.01), and a large number of cells were blocked in S phase(P<0.05). Conclusion: miR-451 has the potential to be used as a biomarker for hepatic carcionoma diagnosis and prognosis; moreover, it also exhibits the inhibitory effect on proliferation of hepatic cancer cells.
2018, 25(5):503-508.
DOI: 10.3872/j.issn.1007-385X.2018.05.011
Abstract:
[Abstract] Objective: To investigate the expression of galectin-3 in bladder cancer tissues and its correlation with clinicopathological characteristics of bladder cancer patients, as well as to explore its effect on the proliferation, invasion and apoptosis of bladder cancer T24 cells. Methods: A total of 104 cases of pathologically confirmed bladder cancer tissues and the corresponding adjacent tissues were collected from the patients treated at the Affiliated Hospital of North Sichuan Medical College from May 2014 to June 2016. Immunohistochemistry staining was used to determine the galectin-3 protein expression in both cancer and adjacent tissues, and the correlations between galectin-3 expression and clinical pathological features were analyzed. siRNA-Gal3 and siRNA-Control were transfected into T24 cell, respectively.The expression of galectin-3 protein was detected by Western blotting, the proliferation of cells was detected by MTT assay; the invasion of cells was detected by Transwell assay; and the cell apoptosis was determined by Flow cytometry. Results:The positive rate of galectin-3 in bladder cancer tissues was significantly higher than that in adjacent tissues (73.1% vs 9.6%, P<0.05).The expression of galectin-3 in bladder cancer was correlated with histological grade, depth of invasion, lymph node metastasis and TNM stage (all P <0.05), but not with sex and age (P>0.05). The expression of galectin-3 was down-regulated significantly by siRNAGal3 (P<0.05). After interference with galectin-3, the proliferation and invasion of T24 cells was significantly decreased (all P<0.05)but the apoptosis was significantly increased (P<0.05). Conclusion: Galectin-3 is over-expressed in bladder cancer and is closely relat-ed to the clinicopathological features of bladder cancer patients. Interference of galectin-3 protein expression can inhibit proliferation and invasion and promote cell apoptosis of bladder cancer T24 cells.
[Abstract] Objective: To investigate the expression of galectin-3 in bladder cancer tissues and its correlation with clinicopathological characteristics of bladder cancer patients, as well as to explore its effect on the proliferation, invasion and apoptosis of bladder cancer T24 cells. Methods: A total of 104 cases of pathologically confirmed bladder cancer tissues and the corresponding adjacent tissues were collected from the patients treated at the Affiliated Hospital of North Sichuan Medical College from May 2014 to June 2016. Immunohistochemistry staining was used to determine the galectin-3 protein expression in both cancer and adjacent tissues, and the correlations between galectin-3 expression and clinical pathological features were analyzed. siRNA-Gal3 and siRNA-Control were transfected into T24 cell, respectively.The expression of galectin-3 protein was detected by Western blotting, the proliferation of cells was detected by MTT assay; the invasion of cells was detected by Transwell assay; and the cell apoptosis was determined by Flow cytometry. Results:The positive rate of galectin-3 in bladder cancer tissues was significantly higher than that in adjacent tissues (73.1% vs 9.6%, P<0.05).The expression of galectin-3 in bladder cancer was correlated with histological grade, depth of invasion, lymph node metastasis and TNM stage (all P <0.05), but not with sex and age (P>0.05). The expression of galectin-3 was down-regulated significantly by siRNAGal3 (P<0.05). After interference with galectin-3, the proliferation and invasion of T24 cells was significantly decreased (all P<0.05)but the apoptosis was significantly increased (P<0.05). Conclusion: Galectin-3 is over-expressed in bladder cancer and is closely relat-ed to the clinicopathological features of bladder cancer patients. Interference of galectin-3 protein expression can inhibit proliferation and invasion and promote cell apoptosis of bladder cancer T24 cells.
2018, 25(5):509-514.
DOI: 10.3872/j.issn.1007-385X.2018.05.012
Abstract:
[Abstract] Objective: To explore the relationship between the preoperative blood indicators (platelets, monocytes, neutrophils-to-lymphocyte ratio) and clinicopathological characters and the prognosis of the early stage malignant melanoma（MM）patients. Methods:Clinicopathological data of 120 cases of stage I-III MM patients, who received initial treatment and radical operation in the Cancer Hospital of Tianjin Medical University from January 2007 to May 2012, were obtained for this study. The correlations between parameters of PLR (platelet-to-lymphocyte ratio), LMR (lymphocyte-to-monocyte ratio), NLR (neutrophil-to-lymphocyte ratio), hemoglobin, neutrophils,lymphocytes, monocytes, eosinophils, basophils, platelets, lactate dehydrogenase, age, stage as well as ulcer and the prognosis of the patients were evaluated. Results: Patients whose tumor with ulceration have higher NLR and basophilic granulocyte (all P<0.05）. Univariate analysis showed that NLR, PLR, LMR, neutrophil, lymphocyte, monocyte, lactic dehydrogenase, age, stage and ulceration were the risk factors of poor 5-year overall survival (P<0.05). The multivariate analysis identified PLR（HR=4.206，95%CI:1.654-10.696，P<0.01），stage（HR=7.670，95%CI:3.977-14.795，P<0.01）and ulceration（HR=1.931，95%CI:1.029-3.623，P<0.05）as independent risk factors for the prognosis of the MM patients. Conclusion: Higher preoperative PLR can be used as a predictive factor for poor prognosis of the early stage MM patients.
[Abstract] Objective: To explore the relationship between the preoperative blood indicators (platelets, monocytes, neutrophils-to-lymphocyte ratio) and clinicopathological characters and the prognosis of the early stage malignant melanoma（MM）patients. Methods:Clinicopathological data of 120 cases of stage I-III MM patients, who received initial treatment and radical operation in the Cancer Hospital of Tianjin Medical University from January 2007 to May 2012, were obtained for this study. The correlations between parameters of PLR (platelet-to-lymphocyte ratio), LMR (lymphocyte-to-monocyte ratio), NLR (neutrophil-to-lymphocyte ratio), hemoglobin, neutrophils,lymphocytes, monocytes, eosinophils, basophils, platelets, lactate dehydrogenase, age, stage as well as ulcer and the prognosis of the patients were evaluated. Results: Patients whose tumor with ulceration have higher NLR and basophilic granulocyte (all P<0.05）. Univariate analysis showed that NLR, PLR, LMR, neutrophil, lymphocyte, monocyte, lactic dehydrogenase, age, stage and ulceration were the risk factors of poor 5-year overall survival (P<0.05). The multivariate analysis identified PLR（HR=4.206，95%CI:1.654-10.696，P<0.01），stage（HR=7.670，95%CI:3.977-14.795，P<0.01）and ulceration（HR=1.931，95%CI:1.029-3.623，P<0.05）as independent risk factors for the prognosis of the MM patients. Conclusion: Higher preoperative PLR can be used as a predictive factor for poor prognosis of the early stage MM patients.
2018, 25(5):515-521.
DOI: 10.3872/j.issn.1007-385X.2018.05.013
Abstract:
[Abstract] Objective: To systematically evaluate the efficacy and safety of ramcircumab in the treatment of advanced non-small cell lung cancer (NSCLC) by a Meta-analysis. Methods: The randomized controlled clinical trials of ramcircumab in the treatment of advanced non-small cell lung cancer were retrieved from Cochrane Library (2017, Issue 8), Web of Science, Pubmed, EMbase, Wanfang Database, CNKI, CBM, Chinese Science and Technology Academic Journal and ASCO, ESMO main conference database, with the enddate of September 1, 2017. Two independent reviewers selected the literatures, extracted the data, and assessed the quality of the included studies. The progression-free survival (PFS), overall survival (OS), objective response rate (ORR), and adverse reactions in NSCLC patients of ramcircumab group and control group were analyzed by RevMan5.3 software. Results: Three RCTs were finally included in this meta-analysis. A total of 1 545 NSCLC patients were enrolled, including 777 in ramcircumab group and 768 in control group. The PFS and OS of NSCLC patients in the ramcircumab group were all better than those of the control group (HR=0.77,95%CI[0.69-0.85],P<0.01; HR=0.88, 95%CI[0.78-0.99], P<0.05). However, there was no statistically significant difference in the ORR between the ramcircumab group and the control group (RR=1.33, 95%CI[0.68-2.61], P>0.05). Compared with docetaxel single-agent second-line treatment,Ramcircumab combined with docetaxel can prolong PFS and OS of advanced NSCLC patients (HR=0.77, 95%CI[0.69-0.86], P<0.01; HR=0.86, 95%CI [0.76-0.98], P<0.05). The most serious adverse reaction in the ramcircumab group was hypertension (RR=3.33,95%CI[1.83-6.05], P<0.01); whereas the incidences of nausea, vomiting, diarrhea, loss of appetite, fatigue, proteinuria, neutropenia,leukopenia, thrombocytopenia, and bleeding etc. showed no significant differences between the two groups (all P>0.05). Conclusion:Ramcircumab can prolong PFS and OS of patients with advanced NSCLC. The main adverse reaction is hypertension.
[Abstract] Objective: To systematically evaluate the efficacy and safety of ramcircumab in the treatment of advanced non-small cell lung cancer (NSCLC) by a Meta-analysis. Methods: The randomized controlled clinical trials of ramcircumab in the treatment of advanced non-small cell lung cancer were retrieved from Cochrane Library (2017, Issue 8), Web of Science, Pubmed, EMbase, Wanfang Database, CNKI, CBM, Chinese Science and Technology Academic Journal and ASCO, ESMO main conference database, with the enddate of September 1, 2017. Two independent reviewers selected the literatures, extracted the data, and assessed the quality of the included studies. The progression-free survival (PFS), overall survival (OS), objective response rate (ORR), and adverse reactions in NSCLC patients of ramcircumab group and control group were analyzed by RevMan5.3 software. Results: Three RCTs were finally included in this meta-analysis. A total of 1 545 NSCLC patients were enrolled, including 777 in ramcircumab group and 768 in control group. The PFS and OS of NSCLC patients in the ramcircumab group were all better than those of the control group (HR=0.77,95%CI[0.69-0.85],P<0.01; HR=0.88, 95%CI[0.78-0.99], P<0.05). However, there was no statistically significant difference in the ORR between the ramcircumab group and the control group (RR=1.33, 95%CI[0.68-2.61], P>0.05). Compared with docetaxel single-agent second-line treatment,Ramcircumab combined with docetaxel can prolong PFS and OS of advanced NSCLC patients (HR=0.77, 95%CI[0.69-0.86], P<0.01; HR=0.86, 95%CI [0.76-0.98], P<0.05). The most serious adverse reaction in the ramcircumab group was hypertension (RR=3.33,95%CI[1.83-6.05], P<0.01); whereas the incidences of nausea, vomiting, diarrhea, loss of appetite, fatigue, proteinuria, neutropenia,leukopenia, thrombocytopenia, and bleeding etc. showed no significant differences between the two groups (all P>0.05). Conclusion:Ramcircumab can prolong PFS and OS of patients with advanced NSCLC. The main adverse reaction is hypertension.
14 Research progress on relationship between tumor chemotherapy and damageassociated molecular patterns
2018, 25(5):522-527.
DOI: 10.3872/j.issn.1007-385X.2018.05.014
Abstract:
[摘要] 传统化疗药物及治疗方案在非特异性杀伤肿瘤细胞的同时不可避免地损伤免疫细胞，不利于机体免疫系统的抗肿瘤作用。近期研究表明，特定化疗，如蒽环类药物或调整化疗药物剂量或调整部分化疗药物配伍，在非特异性杀伤肿瘤细胞时可以通过多种机制增强肿瘤细胞的免疫原性，肿瘤细胞在发生死亡的同时，由非免疫原性转化为免疫原性而介导抗肿瘤免疫应答，此现象被称之为免疫原性细胞死亡（immunogenic cell death, ICD）。肿瘤细胞发生ICD时，一系列信号分子和细胞因子参与其中，包括细胞膜表面信号分子表达水平的改变，促免疫效应因子的合成与释放，此类物质被称为损伤相关分子模式(damage-associated molecular patterns, DAMP)。DAMP主要包括细胞死亡早期钙网蛋白、热激蛋白的分子释放，以及细胞死亡晚期三磷酸腺苷和高迁移率蛋白B1 的分子释放等。本文就DAMP对免疫细胞的调控作用、引发DAMP的常见化疗药物、化疗与免疫治疗的协调作用等近年来的研究进展进行综述
[摘要] 传统化疗药物及治疗方案在非特异性杀伤肿瘤细胞的同时不可避免地损伤免疫细胞，不利于机体免疫系统的抗肿瘤作用。近期研究表明，特定化疗，如蒽环类药物或调整化疗药物剂量或调整部分化疗药物配伍，在非特异性杀伤肿瘤细胞时可以通过多种机制增强肿瘤细胞的免疫原性，肿瘤细胞在发生死亡的同时，由非免疫原性转化为免疫原性而介导抗肿瘤免疫应答，此现象被称之为免疫原性细胞死亡（immunogenic cell death, ICD）。肿瘤细胞发生ICD时，一系列信号分子和细胞因子参与其中，包括细胞膜表面信号分子表达水平的改变，促免疫效应因子的合成与释放，此类物质被称为损伤相关分子模式(damage-associated molecular patterns, DAMP)。DAMP主要包括细胞死亡早期钙网蛋白、热激蛋白的分子释放，以及细胞死亡晚期三磷酸腺苷和高迁移率蛋白B1 的分子释放等。本文就DAMP对免疫细胞的调控作用、引发DAMP的常见化疗药物、化疗与免疫治疗的协调作用等近年来的研究进展进行综述
2018, 25(5):528-532.
DOI: 10.3872/j.issn.1007-385X.2018.05.015
Abstract:
[摘要] 环状RNA（circular RNA, circRNA），作为非编码RNA（non-coding RNA）的重要成员，广泛存在于包括人类在内的多种原核及真核生物体内，对生命活动具有重要的调控作用，已成为非编码RNA研究领域的热点。与线性RNA相比，circRNA 呈共价闭合环状结构，具有结构稳定、序列保守、组织特异性、时空特异性等特点，在包括消化道肿瘤在内的多种疾病中发挥重要作用。circRNA 可通过竞争性吸附miRNA、调控基因表达、参与蛋白质翻译等多种途径，参与肿瘤的发生发展，在肿瘤早期诊断、疗效监测、分期分型、预后、耐药逆转等方面具有一定的潜能，有望成为消化道肿瘤诊断和治疗的新靶点。本文就circRNA 的结构特点、调控机制及其在消化道肿瘤的相关研究进展进行综述。
[摘要] 环状RNA（circular RNA, circRNA），作为非编码RNA（non-coding RNA）的重要成员，广泛存在于包括人类在内的多种原核及真核生物体内，对生命活动具有重要的调控作用，已成为非编码RNA研究领域的热点。与线性RNA相比，circRNA 呈共价闭合环状结构，具有结构稳定、序列保守、组织特异性、时空特异性等特点，在包括消化道肿瘤在内的多种疾病中发挥重要作用。circRNA 可通过竞争性吸附miRNA、调控基因表达、参与蛋白质翻译等多种途径，参与肿瘤的发生发展，在肿瘤早期诊断、疗效监测、分期分型、预后、耐药逆转等方面具有一定的潜能，有望成为消化道肿瘤诊断和治疗的新靶点。本文就circRNA 的结构特点、调控机制及其在消化道肿瘤的相关研究进展进行综述。
2018, 25(5):533-537.
DOI: 10.3872/j.issn.1007-385X.2018.05.016
Abstract:
[摘要] 蛋白质精氨酸甲基转移酶5（protein arginine methyltransferase 5，PRMT5）是一种Ⅱ型蛋白质精氨酸甲基转移酶，在胃癌、肝癌、结直肠癌、肺癌和乳腺癌等多种肿瘤中异常表达。异常表达的PRMT5 通过调节细胞周期蛋白、PI3K细胞信号通路等途径影响肿瘤细胞，通过对相关肿瘤抑制基因的调控进而影响肿瘤的发生和发展。本文围绕近年来肿瘤中PRMT5 的最新研究进展，包括对雄激素受体、免疫细胞、E2F-1-Bcl-2 途径、PTEN和P16 等的作用及其机制，并结合目前相关抑制剂的研究，讨论如何在未来临床治疗中靶向PRMT5达到治疗肿瘤的目的。
[摘要] 蛋白质精氨酸甲基转移酶5（protein arginine methyltransferase 5，PRMT5）是一种Ⅱ型蛋白质精氨酸甲基转移酶，在胃癌、肝癌、结直肠癌、肺癌和乳腺癌等多种肿瘤中异常表达。异常表达的PRMT5 通过调节细胞周期蛋白、PI3K细胞信号通路等途径影响肿瘤细胞，通过对相关肿瘤抑制基因的调控进而影响肿瘤的发生和发展。本文围绕近年来肿瘤中PRMT5 的最新研究进展，包括对雄激素受体、免疫细胞、E2F-1-Bcl-2 途径、PTEN和P16 等的作用及其机制，并结合目前相关抑制剂的研究，讨论如何在未来临床治疗中靶向PRMT5达到治疗肿瘤的目的。
2018, 25(5):539-542.
DOI: 10.3872/j.issn.1007-385X.2018.05.017
Abstract:
[摘要] 小细胞肺癌（small cell lung cancer，SCLC）具有生长分数高、倍增时间短、侵袭性极高的特点，往往在诊断该病的时候就已发生远处转移，若不对其病情进行及时有效的治疗，患者将在2~3 个月内死亡。如果SCLC能够在局限期得到诊断，那么将有20%～25%的患者在接受联合化疗与放疗后，可以获得一个较长生存期。因此，寻找特异性和敏感性高的血液肿瘤标志物，为SCLC早期诊断提供可靠、简便、安全、耐受性好等依据对治疗SCLC极其重要。本文就近年来SCLC神经内分泌起源标志物嗜铬粒蛋白A、神经特异性烯醇化酶、促胃泌素释放肽、脑型肌酸激酶同工酶BB、神经细胞黏附分子、突触素等的研究进展进行综述。
[摘要] 小细胞肺癌（small cell lung cancer，SCLC）具有生长分数高、倍增时间短、侵袭性极高的特点，往往在诊断该病的时候就已发生远处转移，若不对其病情进行及时有效的治疗，患者将在2~3 个月内死亡。如果SCLC能够在局限期得到诊断，那么将有20%～25%的患者在接受联合化疗与放疗后，可以获得一个较长生存期。因此，寻找特异性和敏感性高的血液肿瘤标志物，为SCLC早期诊断提供可靠、简便、安全、耐受性好等依据对治疗SCLC极其重要。本文就近年来SCLC神经内分泌起源标志物嗜铬粒蛋白A、神经特异性烯醇化酶、促胃泌素释放肽、脑型肌酸激酶同工酶BB、神经细胞黏附分子、突触素等的研究进展进行综述。
2018, 25(5):543-544.
DOI: 10.3872/j.issn.1007-385X.2018.05.018
Abstract:
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.