Antiangiogenic gene therapy

Folkman, Judah

doi:10.1073/pnas.95.16.9064

Cited by 182 publications

(101 citation statements)

References 32 publications

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“…Since angiogenesis is required for tumor growth and metastasis, tumor can be 'starved to death' and metastasis can be prevented by EC-directed gene therapy. 1,32,36 Holmgren et al 37 and Boehm et al 38 demonstrated that systemic administration of human angiostatin potentially inhibits the growth of several human and murine primary carcinoma and promote long-term dormancy of metastasis in Lewis lung carcinoma (LLC) mouse model. Tanaka et al 13 subsequently developed angiostatin-expressing adenoviral vectors controlled by the nonspecific promoter CMV.…”

Section: Figure 7 Green Fluorescent Protein (Gfp) Gene Expression Andmentioning

confidence: 99%

Tissue-specific gene therapy directed to tumor angiogenesis

et al. 2001

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Gene therapy directed specifically to the vascular wall, particularly to angiogenic endothelial cells is a prerequisite in vascular disease treatment. Angiogenesis is a major feature in many pathological conditions including wound healing, solid tumors, developing metastases, ischemic heart diseases and diabetic retinopathy. In the present study we developed a tissue-specific gene therapy to the angiogenic blood vessels of tumor metastasis using an adeno-based vector containing the murine preproendothelin-1 (PPE-1) promoter. Genes activated by the PPE-1 promoter were highly expressed in bovine aortic endothelial cells in vitro. Systemic injection of the adenoviral vectors AdPPE-1-

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Section: Figure 7 Green Fluorescent Protein (Gfp) Gene Expression Andmentioning

confidence: 99%

Tissue-specific gene therapy directed to tumor angiogenesis

et al. 2001

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“…[11][12][13][14] Compared with protein therapy, there are several potential advantages. As a prelude to the potential clinical application of RI gene therapy, we cloned the human ri gene and inserted it in a retroviral vector pLNCX.…”

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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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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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“…Antiangiogenic gene therapy does not always require a direct, selective transduction of the gene into the cancer cells, but rather around the tumor to create an antiangiogenic environment. 36 Fortunately, the HVJopDC liposomes used in this study selectively transduced the gene into the peritoneal disseminated tumors themselves, as demonstrated in the experiment using HVJ-GFP. The exact mechanism remains unknown, but we speculate that the transduction specificity of the HVJopDC liposomes depends mainly on the electric charge of the liposomes and the mitotic activity of the cells.…”

Section: Resultsmentioning

confidence: 81%

Soluble Flt-1 gene therapy for peritoneal metastases using HVJ-cationic liposomes

et al. 2000

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Many studies have reported a close association between VEGF and tumor angiogenesis. The aim of the present study was to evaluate the effectiveness of gene therapy against cancer, including peritoneal metastasis, using a cDNA encoding a soluble type of Flt-1, one of the VEGF receptors. In a peritoneal metastasis model of MKN45 human gastric cancer cells, mice repetitively treated with intraperitoneal injections of HVJ-Fex, a type of HVJ-cationic liposome encapsulating a plasmid expressing soluble mFlt-1, exhibited smaller disseminated foci with fewer microvessels, thus resulting in a significantly longer survival period than the control mice. In

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Antiangiogenic gene therapy

Cited by 182 publications

References 32 publications

Tissue-specific gene therapy directed to tumor angiogenesis

Tissue-specific gene therapy directed to tumor angiogenesis

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

Soluble Flt-1 gene therapy for peritoneal metastases using HVJ-cationic liposomes

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