Inhibition of human malignant glioma growthIn vivo by human recombinant plasminogen kringles 1-3

Joe, Young-Ae; Hong, Yong-Kil; Chung, Dong-Sup; Yang, Youngoo; Kang, Joon-Ki; Lee, Youn-Soo; Chang, Soo-Ik; You, Weon‐Kyoo; Lee, Hyosil; Chung, Soo‐Il

doi:10.1002/(sici)1097-0215(19990827)82:5<694::aid-ijc12>3.0.co;2-c

Cited by 49 publications

(35 citation statements)

References 21 publications

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“…1 This fundamental principle states that tumor growth beyond a few mm 3 in size strictly depends on the formation of new blood vessels. 2 Recent studies showed a direct correlation between the density of tumor vessels and an adverse prognosis in patients with a variety of solid tumors, including breast, colon, lung, kidney, bladder, and head and neck tumors.…”

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confidence: 99%

“…2 Recent studies showed a direct correlation between the density of tumor vessels and an adverse prognosis in patients with a variety of solid tumors, including breast, colon, lung, kidney, bladder, and head and neck tumors. [3][4][5] Considering the importance of vascularization in tumor progression, angiogenesis inhibition may, therefore, represent a potentially powerful new approach to cancer therapy.…”

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confidence: 99%

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Anti-tumor effect of hematopoietic cells carrying the gene of ribonuclease inhibitor

Chen

Tian

et al. 2004

Cancer Gene Ther

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Human ribonuclease inhibitor (hRI) is an acid protein with a molecular weight of 50 kDa. It can inhibit the activity of pancreatic RNase (RNase A). Angiogenin (Ang) is a member of the ribonuclease super family. It has 35% identity with RNase A and contains ribonucleolytic activity. The substrate specificity of angiogenin seems, however, to be more restricted than that of the pancreatic RNase. Since Ang is an important angiogenic factor and RI is a highly efficient inhibitor of Ang, it can be hypothesized that RI may be a latent antiangiogenic drug. This study focuses on the feasibility of transfecting the ri gene into mice hematopoietic cells and inducing the expression of the ri gene to block the angiogenesis of solid tumors. First, the cDNA gene of the ri from human placenta was cloned and inserted in a retroviral vector, pLNCX. The combined vector pLNCX-ri was transfected into retroviral packaging cells, PA317, and a clone producing a high titer of virus was obtained. Next, isolated hematopoietic cells from mice bone marrow were infected with viruses carrying the pLNCX-ri. The infected cells were then injected into lethally irradiated mice. The expression and the contribution of RI were assayed in vivo. After administration of hematopoietic cells carrying the ri gene, mice were implanted with B16 melanomas for 21 days. The results showed that tumors of control groups became large and well vascularized. In contrast, tumors from mice groups treated with hematopoietic cells carrying the ri gene were small and possessed a relatively low density of blood vessels. The inhibited growth rate of the tumors was 47%. This study demonstrated the potential utility of gene therapy for systemic delivery of a novel antiangiogenic agent -hRI.

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confidence: 99%

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confidence: 99%

Anti-tumor effect of hematopoietic cells carrying the gene of ribonuclease inhibitor

Chen

Tian

et al. 2004

Cancer Gene Ther

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“…Some studies have demonstrated that angiostatin-mediated inhibition of angiogenesis results in increased tumor cell apoptosis with no direct effect on the rate of tumor cell proliferation. 12 Endostatin may act through beta-catenin, an intracellular protein participating in cell adhesion and transcriptional regulation. 51 The inhibition of neovascularization by angiostatin or endostatin may restrict the supply of tumor cell survival factors provided either by endothelial cells or by the circulation.…”

Section: Discussionmentioning

confidence: 99%

“…[4][5][6][7][8][9] The tumor-suppressor activity of angiostatin may arise from its ability to inhibit the proliferation of endothelial cells by binding to the a/bsubunits of ATP synthase, 10 inducing apoptotic cell death, 5 by subverting adhesion plaque formation and thereby inhibiting the migration and tube formation of endothelial cells, and/or by downregulating vascular endothelial growth factor (VEGF) expression. 11,12 The latter feature of angiostatin is not retained in all tumor models, as it had no effect on VEGF expression in two reports, 13,14 and even slightly upregulated VEGF expression in EL-4 tumors. 15 On the other hand, endostatin's antitumor activity depends on its binding to the catalytic domain of matrix metalloproteinase-2, 16 blocking VEGFmediated signaling via direct interaction with KDR/Flk-1, 17 inhibiting Wnt signaling 18 and adhesion of endothelial cells to collagen I via a2b1 integrin, 19 and attenuating endothelial cell migration.…”

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confidence: 96%

Intramuscular delivery of antiangiogenic genes suppresses secondary metastases after removal of primary tumors

et al. 2004

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The success of surgery to remove primary tumors can be compromised by the subsequent outgrowth of metastases. It is recognized that primary tumors secrete antiangiogenic factors that suppress the outgrowth of their daughter metastases. In accord we show here that surgical removal of primary EL-4 lymphomas led to a marked decrease in the levels of circulating angiostatin and endostatin, and promoted the growth of distant nodular tumors. Expression vectors encoding angiostatin and endostatin, formulated with poly-N-vinyl pyrrolidone (PVP), were injected into the tibialis and gastrocnemia muscles, leading to expression of angiostatin and endostatin in muscle fibers. High levels of biologically active exogenous proteins were secreted into the circulation. Intramuscular gene therapy with angiostatin and endostatin plasmids significantly inhibited tumor vascularity and induced tumor cell apoptosis, and thereby suppressed the growth of secondary subcutaneous and disseminated metastatic tumors in the lung and liver. Simultaneous intramuscular delivery of both angiostatin and endostatin plasmids significantly prolonged the survival of mice after removal of primary tumors. These results suggest that intramuscular gene transfer of angiostatin and endostatin might serve as a prophylactic cancer-prevention strategy to combat the recurrence of cancer after surgical resection of primary tumors.

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“…Gene transfer of angiostatin represents a highly viable alternative strategy to the direct protein delivery methods of angiogenic inhibitors. 43 Previous studies using purified angiostatin protein to treat malignant glioma 19,20,24,44,45 showed its effectiveness, but also suffered drawbacks. Direct protein delivery as a pharmaceutical reagent has formidable limitations to overcome in treating malignant brain tumor.…”

Section: Discussionmentioning

confidence: 99%

Intratumoral gene therapy of malignant brain tumor in a rat model with angiostatin delivered by adeno-associated viral (AAV) vector

et al. 2002

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Inhibition of human malignant glioma growthIn vivo by human recombinant plasminogen kringles 1-3

Cited by 49 publications

References 21 publications

Anti-tumor effect of hematopoietic cells carrying the gene of ribonuclease inhibitor

Anti-tumor effect of hematopoietic cells carrying the gene of ribonuclease inhibitor

Intramuscular delivery of antiangiogenic genes suppresses secondary metastases after removal of primary tumors

Intratumoral gene therapy of malignant brain tumor in a rat model with angiostatin delivered by adeno-associated viral (AAV) vector

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