Abstract
The possibility to inhibit tumor growth by interfering with the formation of new vessels, which most neoplasias depend on, has recently raised considerable interest. An angiogenic switch, in which proliferating cells acquire the ability to direct new vessel formation, is thought to be an early step in the natural history of solid tumors. Using a transgenic model of breast cancer, which shows many similarities to its human counterpart, including ability to metastasize, we targeted angiostatin production to an early stage of tumor formation. Liposome-delivered angiostatin considerably delayed primary tumor growth and, more importantly, inhibited the appearance of lung metastases. These findings can be relevant to the design of therapeutic intervention in humans.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Angiostatins
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Animals
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Antineoplastic Agents / administration & dosage*
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Antineoplastic Agents / therapeutic use*
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Female
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Genetic Therapy
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Humans
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Liposomes*
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Mammary Neoplasms, Experimental / drug therapy*
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Mammary Neoplasms, Experimental / pathology
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Membrane Proteins / genetics
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Mice
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Mice, Transgenic
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Neoplasm Metastasis / prevention & control*
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Peptide Fragments / administration & dosage*
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Peptide Fragments / therapeutic use*
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Plasminogen / administration & dosage*
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Plasminogen / therapeutic use*
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Receptor, ErbB-2 / genetics
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Receptors, Virus / genetics
Substances
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Antineoplastic Agents
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Fam89b protein, mouse
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Liposomes
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Membrane Proteins
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Peptide Fragments
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Receptors, Virus
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Angiostatins
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Plasminogen
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Receptor, ErbB-2