Mobile website
Volume 8,Issue 3,2001 Table of Contents
2001, 8(3):163-167.
DOI: 10.3872/j.issn.1007-385X.2001.3.001
Abstract:
异常活跃的血管发育是恶性肿瘤生长的一个重要条件。肿瘤血管有 3个要素使它成为开发抗癌药物的一个较好的靶标。第一 ,同基本处于静止状态的正常血管相比 ,肿瘤血管内皮细胞处于高度生长状态 ,因此成为突出目标。第二 ,肿瘤血管细胞是从正常组织进入肿瘤的正常细胞 ,基因组稳定 ,不象基因组极不稳定的癌细胞那样容易产生多种抗药性 ,因此可能较易控制。第三 ,尽管各种肿瘤细胞差异极大 ,其血管细胞因为是正常细胞 ,差异较小 ,因此同一药物如果针对肿瘤血管则可能对不同肿瘤均有疗效。本文对目前国际上对肿瘤血管发育机理的了解 ,常用的研究手段 ,及抗血管生长药物开发等方面的概况作一简介。
异常活跃的血管发育是恶性肿瘤生长的一个重要条件。肿瘤血管有 3个要素使它成为开发抗癌药物的一个较好的靶标。第一 ,同基本处于静止状态的正常血管相比 ,肿瘤血管内皮细胞处于高度生长状态 ,因此成为突出目标。第二 ,肿瘤血管细胞是从正常组织进入肿瘤的正常细胞 ,基因组稳定 ,不象基因组极不稳定的癌细胞那样容易产生多种抗药性 ,因此可能较易控制。第三 ,尽管各种肿瘤细胞差异极大 ,其血管细胞因为是正常细胞 ,差异较小 ,因此同一药物如果针对肿瘤血管则可能对不同肿瘤均有疗效。本文对目前国际上对肿瘤血管发育机理的了解 ,常用的研究手段 ,及抗血管生长药物开发等方面的概况作一简介。
2001, 8(3):168-172.
DOI: 10.3872/j.issn.1007-385X.2001.3.002
Abstract:
Objective: To investigate whether transfection with plasmid pCH510 after chemotherapy can improve therapeutic effect on tumor and whether linkage of two factors needs special conditions. Methods: Mice were inoculated with tumor cells. Inhibitory effect of transfection with pCH510 on murine tumor origined from different inoculative dose and inhibiting effect of immediate transfection pCH510 after chemotherapy on tumor were observed, respectively. By cell culture technique, the influence of chemotherapeutic drug to activation of marcrophages and lymphocytes after i.p. injection of drug was observed. By cell counting method, the kinetics of the change of number of peripheral blood immunocytes induced by administration of chemotherapeutic drug was observed. The inhibitory effect of transfection with pCH510 five days after chemotherapy on murine tumor was observed. Results: pCH510 had inhibitory effect on murine tumor from different inoculative dose and the effect negatively correlated with inoculative dose. Chemotherapeutic drug decreased number of immunocytes and suppressed their activation in vivo . After injection of drug, the number of immunocytes was the lowest on the third day and got back to normal level on the 10th day.The therapeutic effect was not improved by immediate 10-day transfection with plasmid pCH510 after chemotherapy, but was significantly improved by 15-day transfection with plasmid pCH510 after chemotherapy 5 days. Conclusion: Transfection with pCH510 after chemotherapy may acquire better effect for tumor therapy than using single factor. Chemotherapy not only decreases the number of immunocytes but also suppresses their function, so the immediate transfection with pCH510 after chemotherapy is not good strategy, and the time of treatment by transfection should not be too short. Comparison of the inhibitory effect of pCH510, chemotherapy and chemotherapy pCH510 showed that chemotherapy had a dual effect on tumor growth.
Objective: To investigate whether transfection with plasmid pCH510 after chemotherapy can improve therapeutic effect on tumor and whether linkage of two factors needs special conditions. Methods: Mice were inoculated with tumor cells. Inhibitory effect of transfection with pCH510 on murine tumor origined from different inoculative dose and inhibiting effect of immediate transfection pCH510 after chemotherapy on tumor were observed, respectively. By cell culture technique, the influence of chemotherapeutic drug to activation of marcrophages and lymphocytes after i.p. injection of drug was observed. By cell counting method, the kinetics of the change of number of peripheral blood immunocytes induced by administration of chemotherapeutic drug was observed. The inhibitory effect of transfection with pCH510 five days after chemotherapy on murine tumor was observed. Results: pCH510 had inhibitory effect on murine tumor from different inoculative dose and the effect negatively correlated with inoculative dose. Chemotherapeutic drug decreased number of immunocytes and suppressed their activation in vivo . After injection of drug, the number of immunocytes was the lowest on the third day and got back to normal level on the 10th day.The therapeutic effect was not improved by immediate 10-day transfection with plasmid pCH510 after chemotherapy, but was significantly improved by 15-day transfection with plasmid pCH510 after chemotherapy 5 days. Conclusion: Transfection with pCH510 after chemotherapy may acquire better effect for tumor therapy than using single factor. Chemotherapy not only decreases the number of immunocytes but also suppresses their function, so the immediate transfection with pCH510 after chemotherapy is not good strategy, and the time of treatment by transfection should not be too short. Comparison of the inhibitory effect of pCH510, chemotherapy and chemotherapy pCH510 showed that chemotherapy had a dual effect on tumor growth.
2001, 8(3):173-177.
DOI: 10.3872/j.issn.1007-385X.2001.3.003
Abstract:
克隆VEGF受体KDR基因膜外5-7区，探讨其生物学活性。方法：提取脐静脉血管内皮细胞总RNA，克隆KDR基因膜外部分5-7区，并使之在QIA表达系统进行表达；镍柱亲和层析纯化、复性、生物学活性鉴定。结果：该系统能表达KDR基因片段，表达量约占菌体蛋白总量的5%左右。经复性，可溶性蛋白具有与VEGF特异结合功能，并能抑制VEGF促使脐静脉内皮细胞增殖和鸡胚绒毛尿囊膜血管生成的作用。结论：KDR基因片段能在QIA表达系统中得到表达，复性后表达蛋白具有与VEGF结合的生物学功能。
克隆VEGF受体KDR基因膜外5-7区，探讨其生物学活性。方法：提取脐静脉血管内皮细胞总RNA，克隆KDR基因膜外部分5-7区，并使之在QIA表达系统进行表达；镍柱亲和层析纯化、复性、生物学活性鉴定。结果：该系统能表达KDR基因片段，表达量约占菌体蛋白总量的5%左右。经复性，可溶性蛋白具有与VEGF特异结合功能，并能抑制VEGF促使脐静脉内皮细胞增殖和鸡胚绒毛尿囊膜血管生成的作用。结论：KDR基因片段能在QIA表达系统中得到表达，复性后表达蛋白具有与VEGF结合的生物学功能。
2001, 8(3):178-182.
DOI: 10.3872/j.issn.1007-385X.2001.3.004
Abstract:
Objective: To study the characterization of the cultured cervical cancer cell line transfected with anti- HPV16E6-ribozyme, and to investigate the effect of ribozyme on proliferation and apoptosis of cervical cancer cell. Metliods: Anti-HPV16E6-ribozyme had been designed to cleave the HPV16E6 gene. With the method of lipofectin transfec- tion, the anti-HPVI6E6-ribozyme and empty eucaryotic expressing plasmids were transfected into CaSKi cell, which named as CaSKi-R, CaSKi-P respectively. The amounts of E6 mRNA in the three kinds of cells were detected by northern blot. Cell cycle was detemined by flow cytometry, and cell apoptosis was examined by fluorescent (Hoechst) staining and TUNEL. The expression of some genes, including c-myc, bcl-2, p53, and fas, was also detected by flow cytometry analy- sis. Results: Northern blot showed that E6 mRNA was less in CaSKi-R than in CaSKi. In CaSKi-R cells, cycle was arres- ted in G1 phase, with decreasing in percentage of S phase cells. The apoptosis rate of CaSK1-R cell was much higher than those of CaSKi and CaSK1-P. Anti-HPV16E6-ribozyme could reduce the expression of E6, c-myc, bcl-2 genes on CaSKi- R cells, and increased the expression of p53. While this phenomenon was not found on the CaSK1-P cells. The expression of fas was similar in the three kinds of cells. Conclusion: Anti-HPVE6-rivozyme induces apoptosis of human cervical cancer CaSKi cells. The mechanisms may be the decrease of E6 gene's expression, and the succedent changing of some genes'expression.
Objective: To study the characterization of the cultured cervical cancer cell line transfected with anti- HPV16E6-ribozyme, and to investigate the effect of ribozyme on proliferation and apoptosis of cervical cancer cell. Metliods: Anti-HPV16E6-ribozyme had been designed to cleave the HPV16E6 gene. With the method of lipofectin transfec- tion, the anti-HPVI6E6-ribozyme and empty eucaryotic expressing plasmids were transfected into CaSKi cell, which named as CaSKi-R, CaSKi-P respectively. The amounts of E6 mRNA in the three kinds of cells were detected by northern blot. Cell cycle was detemined by flow cytometry, and cell apoptosis was examined by fluorescent (Hoechst) staining and TUNEL. The expression of some genes, including c-myc, bcl-2, p53, and fas, was also detected by flow cytometry analy- sis. Results: Northern blot showed that E6 mRNA was less in CaSKi-R than in CaSKi. In CaSKi-R cells, cycle was arres- ted in G1 phase, with decreasing in percentage of S phase cells. The apoptosis rate of CaSK1-R cell was much higher than those of CaSKi and CaSK1-P. Anti-HPV16E6-ribozyme could reduce the expression of E6, c-myc, bcl-2 genes on CaSKi- R cells, and increased the expression of p53. While this phenomenon was not found on the CaSK1-P cells. The expression of fas was similar in the three kinds of cells. Conclusion: Anti-HPVE6-rivozyme induces apoptosis of human cervical cancer CaSKi cells. The mechanisms may be the decrease of E6 gene's expression, and the succedent changing of some genes'expression.
2001, 8(3):190-192.
DOI: 10.3872/j.issn.1007-385X.2001.3.007
Abstract:
Objective: To investigate the effects of Interlukin- 4(IL-4) on the invasiveness and the expression of several cell surface antigens related to invasive and metastatic potentials of human hepatocellular carcinoma QGY-7701 cell line in vitro. Methods: QGY-7701 cells were incubated with high concentration of IL-4 or low concentration of IL-4 in different time. The expression of ICAM-1, CD44 and HLA-I was determined by fluorescence-activated cell sorter (FACS) analysis, the tumor cell binding affinity to extracellular matrix (ECM) components was measured by cell attachment assay, the degree of homotypic aggregation was quantified by cell aggregation assay. Results: IL-4 pretreatment can enhance the expression of ICAM-1 and HLA-I, suppress the expression of CD44 on hepatocellular carcinoma cell line and decrease the binding affinity to ECM components and the degree of homotypic aggregation of hepatocellular carcinoma cells. Conclusoin: IL-4 can inhibit the invasive and metastatic potentials of hepatocellular carcinoma cells.
Objective: To investigate the effects of Interlukin- 4(IL-4) on the invasiveness and the expression of several cell surface antigens related to invasive and metastatic potentials of human hepatocellular carcinoma QGY-7701 cell line in vitro. Methods: QGY-7701 cells were incubated with high concentration of IL-4 or low concentration of IL-4 in different time. The expression of ICAM-1, CD44 and HLA-I was determined by fluorescence-activated cell sorter (FACS) analysis, the tumor cell binding affinity to extracellular matrix (ECM) components was measured by cell attachment assay, the degree of homotypic aggregation was quantified by cell aggregation assay. Results: IL-4 pretreatment can enhance the expression of ICAM-1 and HLA-I, suppress the expression of CD44 on hepatocellular carcinoma cell line and decrease the binding affinity to ECM components and the degree of homotypic aggregation of hepatocellular carcinoma cells. Conclusoin: IL-4 can inhibit the invasive and metastatic potentials of hepatocellular carcinoma cells.
2001, 8(3):193-195.
DOI: 10.3872/j.issn.1007-385X.2001.3.008
Abstract:
Objective: To investigate the curative effects of apoptin on the multidrug-resistant model, of human osteosarcoma cell line (R-OS-732). Methods: 363 bpVP 3 gene was cloned into the vector pIRES1 and the recombinant eukaryon expression vector pIRVP3 was transfected into R-OS-732 cells with liposome. The expression of apoptin gene at transcription level was proved by RT-PCR. The pathological changes of the cells was observed by light microscope and electronmicroscope. The transfected R-OS-732 cells were collected after 48 hours. The genomic DNA extracted from the cells was observed by agarose gel electrophoresis. The apoptosis rate of the cells was analysed by flow cytometry. Results: The expression of apoptin gene at transcription level had been proved by RT-PCR. The construction changes of the two groups were obviously different under light microscope: most of R-OS-732 cells in the transfected group existed in form of being away from the bottom of the culture dish after 24 hours, in form of apoptosis after 48 hours and in form of necrosis after 72 hours; but those cells in the controlled group grow luxuriantly. And under electronmicroscope there was much change of cell nucleus between the two groups. DNA ladder of the transfected cells was observed through agarose gel electrophoresis only one band was observed in the controlled group; but bands of fragmented DNA observed in ositive control group. Flow cytometry analysis showed that the apoptosis rate of the cells in the transfected group was relatively higher than that of the controlls( P <0.01).Conclusion: Apoptin can induce apoptosis in the multidrug-resistant model of human osteosarcoma cell line(R-OS-732) .
Objective: To investigate the curative effects of apoptin on the multidrug-resistant model, of human osteosarcoma cell line (R-OS-732). Methods: 363 bpVP 3 gene was cloned into the vector pIRES1 and the recombinant eukaryon expression vector pIRVP3 was transfected into R-OS-732 cells with liposome. The expression of apoptin gene at transcription level was proved by RT-PCR. The pathological changes of the cells was observed by light microscope and electronmicroscope. The transfected R-OS-732 cells were collected after 48 hours. The genomic DNA extracted from the cells was observed by agarose gel electrophoresis. The apoptosis rate of the cells was analysed by flow cytometry. Results: The expression of apoptin gene at transcription level had been proved by RT-PCR. The construction changes of the two groups were obviously different under light microscope: most of R-OS-732 cells in the transfected group existed in form of being away from the bottom of the culture dish after 24 hours, in form of apoptosis after 48 hours and in form of necrosis after 72 hours; but those cells in the controlled group grow luxuriantly. And under electronmicroscope there was much change of cell nucleus between the two groups. DNA ladder of the transfected cells was observed through agarose gel electrophoresis only one band was observed in the controlled group; but bands of fragmented DNA observed in ositive control group. Flow cytometry analysis showed that the apoptosis rate of the cells in the transfected group was relatively higher than that of the controlls( P <0.01).Conclusion: Apoptin can induce apoptosis in the multidrug-resistant model of human osteosarcoma cell line(R-OS-732) .
2001, 8(3):196-200.
DOI: 10.3872/j.issn.1007-385X.2001.3.009
Abstract:
Objective: Using phage display randem peptide library to generate peptides as small molecular weight vec tors for tumor-targeting therapy. Methods: MUC1/Y extracellular domain was used as a target molecule to biopan Ph. D. 12 TM phage randem peptide library. Two protocols using affinity gel and cell culture plates respectively were carried out. Positive phage clones were identified by ELISA. ssDNA sequencing was done on 16 positive phage clones to get the amino acid sequences of MUC1/Y-binding peptides. Immunohistochemistry was done to show the capacity and specificity of positive phage clones to bind the tumor cell lines. Results: After 4 rounds biopanning, three MUC1/Y-binding peptides were generated including HHWHSRSQLSWF, HLKHUKNYLPPTP and GNWYRHPHYLQP. HXXHS may be the key motif for binding to MUCI/Y. The positive phage clones tested showed the ability to bind MCF, OVCA3 cell lines while no binding to normal peripheral blood lymphocytes( PBLs) was observed. Conclusion: The peptides generated by biopanning phage library showed some affinity and tumor-specificity and may be potential candidates as ligands for tumor-targeting therapy.
Objective: Using phage display randem peptide library to generate peptides as small molecular weight vec tors for tumor-targeting therapy. Methods: MUC1/Y extracellular domain was used as a target molecule to biopan Ph. D. 12 TM phage randem peptide library. Two protocols using affinity gel and cell culture plates respectively were carried out. Positive phage clones were identified by ELISA. ssDNA sequencing was done on 16 positive phage clones to get the amino acid sequences of MUC1/Y-binding peptides. Immunohistochemistry was done to show the capacity and specificity of positive phage clones to bind the tumor cell lines. Results: After 4 rounds biopanning, three MUC1/Y-binding peptides were generated including HHWHSRSQLSWF, HLKHUKNYLPPTP and GNWYRHPHYLQP. HXXHS may be the key motif for binding to MUCI/Y. The positive phage clones tested showed the ability to bind MCF, OVCA3 cell lines while no binding to normal peripheral blood lymphocytes( PBLs) was observed. Conclusion: The peptides generated by biopanning phage library showed some affinity and tumor-specificity and may be potential candidates as ligands for tumor-targeting therapy.
2001, 8(3):201-204.
DOI: 10.3872/j.issn.1007-385X.2001.3.010
Abstract:
Objective: To isolate small molecular polypeptides which bind to KDR specifically using C7 and 12 peptide libraries. Methods: KDR/IgGFc was coated directly on plates, C7 and 12 peptide libraries are then applied, followed by vigorous washings in washing buffers to remove most non-specifically bound phage and to select specific phage particals by VEGF suspension and elution in acid buffers. The positive phage clones were detected by ELISA, cell-ELISA and competitive binding ELISA. Results: After three washes, 12 positive phage clones were selected and sequenced. Conclusion: A conserved peptide motif was not found in these sequences. The peptide binding to KDR specifically may be helpful for lead drug to improve selectivity and decrease the side effect of anti cancer drug in clinical treatment.
Objective: To isolate small molecular polypeptides which bind to KDR specifically using C7 and 12 peptide libraries. Methods: KDR/IgGFc was coated directly on plates, C7 and 12 peptide libraries are then applied, followed by vigorous washings in washing buffers to remove most non-specifically bound phage and to select specific phage particals by VEGF suspension and elution in acid buffers. The positive phage clones were detected by ELISA, cell-ELISA and competitive binding ELISA. Results: After three washes, 12 positive phage clones were selected and sequenced. Conclusion: A conserved peptide motif was not found in these sequences. The peptide binding to KDR specifically may be helpful for lead drug to improve selectivity and decrease the side effect of anti cancer drug in clinical treatment.
2001, 8(3):205-207.
DOI: 10.3872/j.issn.1007-385X.2001.3.011
Abstract:
建立效价测定用的重组人粒细胞巨噬细胞集落刺激因子(GM-CSF)国家标准品.方法标准品按WHO有关要求进行制备、分装、冻干、检测,用GM-CSF国际标准品为标准进行协作标定.结果冻干重组GM-CSF标准品经检测外观,无菌实验合格,水分为0.93%,加速热稳定实验表明其生物学活性在温度为-20℃,4℃和25℃,37℃条件下23个月保持稳定.该标准品经3家实验室协作标定共21次测定,几何平均效价为1.77×105IU/支.实验均数的95%可信区间为(1.64～1.90)×105IU/支,单次实验的95%参考值范围为(1.23～2.34)×105IU/支,平均可信限率为6.962%.结论该批重组GM-CSF国家标准品各项指标均符合要求,可作为国家标准品使用,效价定为1.8×105IU/支,编号为98/01.
建立效价测定用的重组人粒细胞巨噬细胞集落刺激因子(GM-CSF)国家标准品.方法标准品按WHO有关要求进行制备、分装、冻干、检测,用GM-CSF国际标准品为标准进行协作标定.结果冻干重组GM-CSF标准品经检测外观,无菌实验合格,水分为0.93%,加速热稳定实验表明其生物学活性在温度为-20℃,4℃和25℃,37℃条件下23个月保持稳定.该标准品经3家实验室协作标定共21次测定,几何平均效价为1.77×105IU/支.实验均数的95%可信区间为(1.64～1.90)×105IU/支,单次实验的95%参考值范围为(1.23～2.34)×105IU/支,平均可信限率为6.962%.结论该批重组GM-CSF国家标准品各项指标均符合要求,可作为国家标准品使用,效价定为1.8×105IU/支,编号为98/01.
2001, 8(3):219-221.
DOI: 10.3872/j.issn.1007-385X.2001.3.016
Abstract:
不同类型的肿瘤细胞对化学药物、放射治疗、TNF α治疗都表现出不同的敏感性。NF κB作为Rel家族的一个成员 ,能够被电离辐射、细胞因子和化学因子激活。NF κB活化后启动转录合成一些细胞因子和保护蛋白 ,能对细胞提供有益保护 ,增加其应激耐受性。在肿瘤治疗中 ,NF κB活化影响肿瘤细胞对治疗的敏感性。通过抑制NF κB活化 ,可提高放疗、化疗和TNF α治疗肿瘤的疗效 ,用作肿瘤治疗的有效辅助手段。
不同类型的肿瘤细胞对化学药物、放射治疗、TNF α治疗都表现出不同的敏感性。NF κB作为Rel家族的一个成员 ,能够被电离辐射、细胞因子和化学因子激活。NF κB活化后启动转录合成一些细胞因子和保护蛋白 ,能对细胞提供有益保护 ,增加其应激耐受性。在肿瘤治疗中 ,NF κB活化影响肿瘤细胞对治疗的敏感性。通过抑制NF κB活化 ,可提高放疗、化疗和TNF α治疗肿瘤的疗效 ,用作肿瘤治疗的有效辅助手段。
2001, 8(3):222-224.
DOI: 10.3872/j.issn.1007-385X.2001.3.017
Abstract:
双特异性抗体是改善抗体治疗效果的发展方向之一，现已成为抗体工程研究领域的热点。随着分子生物学技术的迅速发展，出现了基因工程双特异性抗体的多种构建模式，并且有多种基因工程双特异性抗体制剂已经用于肿瘤的临床诊断和治疗试验。本文仅就这两方面的研究进展进行综述。
双特异性抗体是改善抗体治疗效果的发展方向之一，现已成为抗体工程研究领域的热点。随着分子生物学技术的迅速发展，出现了基因工程双特异性抗体的多种构建模式，并且有多种基因工程双特异性抗体制剂已经用于肿瘤的临床诊断和治疗试验。本文仅就这两方面的研究进展进行综述。
2001, 8(3):225-227.
DOI: 10.3872/j.issn.1007-385X.2001.3.018
Abstract:
热休克蛋白（HSP）gp96是一种高度保守的呈单态性的蛋白质。它具有分子伴侣功能，能与细胞内大量多肽非共价结合而不受细胞单倍型和MHC分子的影响。gp96-肽复合物也可在体外形成，并具有与体内相似的免疫活性。gp96参与MHC1类抗原的提呈。用肿瘤gp96-肽复合物免疫小鼠可诱发抗相应肿瘤细胞的MHC I类限制性CD8^ 细胞毒性T细胞免疫应答，并能产生记忆性T细胞应答，具备了作为疫苗的一个关键重要，为肿瘤免疫治疗开辟了一个新的途径。
热休克蛋白（HSP）gp96是一种高度保守的呈单态性的蛋白质。它具有分子伴侣功能，能与细胞内大量多肽非共价结合而不受细胞单倍型和MHC分子的影响。gp96-肽复合物也可在体外形成，并具有与体内相似的免疫活性。gp96参与MHC1类抗原的提呈。用肿瘤gp96-肽复合物免疫小鼠可诱发抗相应肿瘤细胞的MHC I类限制性CD8^ 细胞毒性T细胞免疫应答，并能产生记忆性T细胞应答，具备了作为疫苗的一个关键重要，为肿瘤免疫治疗开辟了一个新的途径。
2001, 8(3):227-230.
DOI: 10.3872/j.issn.1007-385X.2001.3.019
Abstract:
TRAIL是近年来发现的凋亡分子之一 ,其最显著的特征就是能够选择性的诱导肿瘤细胞或转化细胞的凋亡 ,而对正常组织没有明显的毒性作用。目前发现TRAIL分子在体内有 4个膜结合型受体 ,和一个分泌型受体。这些受体在体内不同组织的选择性表达参与调控不同组织对TRAIL诱导凋亡的敏感性。因此 ,本文从TRAIL和TRAILR的发现、分子结构、表达调控、和诱导凋亡的分子机制 4个方面详细介绍了TRAIL与凋亡的关系。
TRAIL是近年来发现的凋亡分子之一 ,其最显著的特征就是能够选择性的诱导肿瘤细胞或转化细胞的凋亡 ,而对正常组织没有明显的毒性作用。目前发现TRAIL分子在体内有 4个膜结合型受体 ,和一个分泌型受体。这些受体在体内不同组织的选择性表达参与调控不同组织对TRAIL诱导凋亡的敏感性。因此 ,本文从TRAIL和TRAILR的发现、分子结构、表达调控、和诱导凋亡的分子机制 4个方面详细介绍了TRAIL与凋亡的关系。
2001, 8(3):231-233.
DOI: 10.3872/j.issn.1007-385X.2001.3.020
Abstract:
在自杀基因治疗中，旁观者效应表现为转染细胞对临近未转染细胞的毒性作用，是决定自杀基因疗效的关键因素。研究证实：细胞缝隙连接（gap-junctions,GJs）是旁观者效应的主要机制；检测这种连接的基本组成元件一接合素，可供筛选肿瘤细胞对自杀基因的敏感性；通过生化或基因转移的方法诱导细胞GJs，可增强GJs功能缺陷细胞自杀基因的旁观者效应。
在自杀基因治疗中，旁观者效应表现为转染细胞对临近未转染细胞的毒性作用，是决定自杀基因疗效的关键因素。研究证实：细胞缝隙连接（gap-junctions,GJs）是旁观者效应的主要机制；检测这种连接的基本组成元件一接合素，可供筛选肿瘤细胞对自杀基因的敏感性；通过生化或基因转移的方法诱导细胞GJs，可增强GJs功能缺陷细胞自杀基因的旁观者效应。
2001, 8(3):236-238.
DOI: 10.3872/j.issn.1007-385X.2001.3.022
Abstract:
结直肠癌浸润、转移常影响临床治疗效果 ,也是患者死亡的主要原因。浸润、转移涉及一系列多机制、多步骤的复杂过程 ,如原发肿瘤组织中具有转移潜能的细胞亚群的异常增生、黏附分子介导癌细胞间或癌细胞与细胞基质间的黏附与脱黏附、水解酶对细胞外基质的降解、癌细胞的迁移运动、新生血管的形成、癌细胞逃逸机体免疫系统的攻击等。针对癌细胞浸润、转移的各步骤 ,从分子水平进行阻断治疗 ,将会大大提高结直肠癌现有治疗效果 ,提高患者的生存率。
结直肠癌浸润、转移常影响临床治疗效果 ,也是患者死亡的主要原因。浸润、转移涉及一系列多机制、多步骤的复杂过程 ,如原发肿瘤组织中具有转移潜能的细胞亚群的异常增生、黏附分子介导癌细胞间或癌细胞与细胞基质间的黏附与脱黏附、水解酶对细胞外基质的降解、癌细胞的迁移运动、新生血管的形成、癌细胞逃逸机体免疫系统的攻击等。针对癌细胞浸润、转移的各步骤 ,从分子水平进行阻断治疗 ,将会大大提高结直肠癌现有治疗效果 ,提高患者的生存率。
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
您是第位访问者
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.