Characterization of123I-vascular endothelial growth factor-binding sites expressed on human tumour cells: Possible implication for tumour scintigraphy

Li, Shuren; Peck‐Radosavljevic, Markus; Koller, Elisabeth; Koller, Franz; Kaserer, Klaus; Kreil, Anna; Kapiotis, Stylianos; Hamwi, Ahmad; Weich, Herbert A.; Valent, Peter; Angelberger, P.; Dudczak, Robert; Virgolini, Irene

doi:10.1002/1097-0215(200002)9999:9999<::aid-ijc1126>3.0.co;2-k

Cited by 63 publications

(32 citation statements)

References 27 publications

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“…The binding of VEGF 165 was completely abolished by 6 mM NaPaC. Scatchard analysis revealed in control conditions (in the absence of NaPaC), two classes of binding sites as observed by others (Soker et al, 1996;Li et al, 2001). The higher affinity class is characterised by a K d of 355 pM and the lower affinity population by a K d of 1000 pM.…”

Section: Phenylacetate Carboxymethyl Benzylamide Dextran Inhibits Thesupporting

confidence: 55%

Inhibition of epidermoid carcinoma A431 cell growth and angiogenesis in nude mice by early and late treatment with a novel dextran derivative

et al. 2003

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We investigated the effect of a new dextran derivative, phenylacetate carboxymethyl benzylamide dextran (NaPaC), on epidermoid carcinoma A431 cells secreting a large quantity of angiogenic factor, vascular endothelial growth factor (VEGF). In vitro, NaPaC inhibited the proliferation of A431 cells (IC 50 ¼ 5 mM). Also, NaPaC decreased the binding of radiolabelled VEGF 165 to endothelial cells (IC 50 ¼ 0.2 mM). In vivo, we explored the effects of NaPaC (15 mg kg À1 ) on A431 xenograft growth starting the drug administration at the time of tumour cell inoculation (early treatment) and 1 week later, when tumours were well established (late treatment). Early treatment was more efficient on tumour inhibition (70% vs control) than late treatment (50% vs control). Early and late NaPaC-treatment increased the aponecrosis in tumour by 70 and 30%, respectively. Whatever treatment, NaPaC inhibited the intratumour endothelial cell density in the same manner. In contrast, vessel area was decreased only when NaPaC was injected early (35%). These results show that NaPaC has a potent inhibitory effect, dependent on treatment outset, on epidermoid carcinoma growth associated with an intratumour microvascular network diminution and an aponecrosis increase. As this drug is nontoxic at efficient dose, it offers interesting perspectives for the therapy of malignant lesions.

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Section: Phenylacetate Carboxymethyl Benzylamide Dextran Inhibits Thesupporting

confidence: 55%

Inhibition of epidermoid carcinoma A431 cell growth and angiogenesis in nude mice by early and late treatment with a novel dextran derivative

et al. 2003

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“…These data raise concerns over the suitability of VEGF 120 as a selective tumor-targeting agent 28 -31 and possibly for scintigraphic applications, as postulated by other groups on the basis of in vitro studies. 43 Biodistribution data on scFv(L19)-VEGF 120 showed tumor: organ ratios and %ID/g values comparable to (or worse than) those obtained with scFv(L19) (Fig. 3).…”

Section: Tumor-targeting Properties Of Antibody-vegf Fusion Proteinsmentioning

confidence: 57%

Tumor‐targeting properties of antibody–vascular endothelial growth factor fusion proteins

Halin

Niesner

Villani

et al. 2002

Intl Journal of Cancer

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“…Since A431 cells produce VEGF-A and binds VEGF 165 on the surface (Li et al, 2001), we explored if CMDB7 is able to compete for VEGF 165 -specific binding (Figure 3). CMDB7 decreased the 125 I-VEGF 165 -specific binding to A431 cells at concentrations ranging from 0.1 to 50 mM with a half-maximum inhibitory effect (IC 50 ) at concentration 2 mM.…”

Section: Cmdb7 Inhibits Vegf 165 Binding To A431 Tumour Cellsmentioning

confidence: 99%

“…Such cells, xenografted in nude mice, provide a model of highly VEGFdependent (Melnyk et al, 1996) and aggressive tumour growth in an in vivo system. Since A431 cells have been recently described to express the VEGF 165 -binding sites (Li et al, 2001), we explored also the possible effect of CMDB7 on radiolabelled VEGF binding. We demonstrate that CMDB7 acts on both tumour and endothelial cells, decreasing in a potent manner the tumour growth and angiogenesis in vivo.…”

mentioning

confidence: 99%

Carboxymethyl benzylamide dextran inhibits angiogenesis and growth of VEGF-overexpressing human epidermoid carcinoma xenograft in nude mice

et al. 2003

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Vascular endothelial growth factor (VEGF) expression is elevated in a wide variety of solid tumours. Inhibition of VEGF activities is able to reduce angiogenesis and tumour growth. We have recently shown in vitro that carboxymethyl dextran benzylamide (CMDB7) prevents the binding of VEGF 165 to its cell surface receptors and thus inhibits VEGF activities on endothelial cells. In the present study, we explored the effects of CMDB7 on highly aggressive human epidermoid carcinoma A431 cells known to overexpress epidermal growth factor receptors (EGFRs) and produce a high amount of VEGF and a minor quantity of bFGF. In vitro, CMDB7 blocked the mitogenic activity of A431-conditioned medium on endothelial cells. Concerning A431 cells, CMDB7 inhibited their proliferation and the VEGF 165 binding to them. In vivo, administration of CMDB7 (10 mg kg À1 ) three times per week for 2 weeks inhibited the growth of A431 xenografts in nude mice by 73% as compared to the control group. Immunostaining of endothelial cells with mouse-specific GSL-1 lectin in tumour sections revealed that CMDB7 also inhibited the density of intratumour endothelial cells by 66%. These findings demonstrate that CMDB7 has an efficient antiangiogenic and antitumour action in vivo even when tumour cells produce a high level of VEGF and EGFRs.

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Characterization of123I-vascular endothelial growth factor-binding sites expressed on human tumour cells: Possible implication for tumour scintigraphy

Cited by 63 publications

References 27 publications

Inhibition of epidermoid carcinoma A431 cell growth and angiogenesis in nude mice by early and late treatment with a novel dextran derivative

Inhibition of epidermoid carcinoma A431 cell growth and angiogenesis in nude mice by early and late treatment with a novel dextran derivative

Tumor‐targeting properties of antibody–vascular endothelial growth factor fusion proteins

Carboxymethyl benzylamide dextran inhibits angiogenesis and growth of VEGF-overexpressing human epidermoid carcinoma xenograft in nude mice

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