Insights into the Molecular Pathogenesis and Targeted Treatment of Lymphedema
Identifieur interne : 001635 ( Istex/Corpus ); précédent : 001634; suivant : 001636Insights into the Molecular Pathogenesis and Targeted Treatment of Lymphedema
Auteurs : Anne Saaristo ; Marika J. Karkkainen ; Kari AlitaloSource :
- Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2002-12.
Abstract
Abstract: Abnormal function of the lymphatic vessels is associated with a variety of diseases, such as tumor metastasis and lymphedema. The development of strategies for local and controlled induction or inhibition of lymphangiogenesis would thus be of major importance for the treatment of such diseases. Two growth factors, vascular endothelial growth factor C (VEGF‐C) and D (VEGF‐D), have been found to be important in the proper formation and maintenance of the lymphatic network, through their receptor VEGFR‐3. In patients with lymphedema, heterozygous inactivation of VEGFR‐3 leads to primary lymphedema due to defective lymphatic drainage in the limbs. We have shown that VEGF‐C gene transfer to the skin of mice with lymphedema induces regeneration of the cutaneous lymphatic vessel network. However, as is the case with VEGF, high levels of VEGF‐C cause blood vessel growth and leakiness, resulting in tissue edema. Strategies to avoid these side‐effects have also been developed. This new field of reseach has important implications for the development of new therapies for human lymphedema.
Url:
DOI: 10.1111/j.1749-6632.2002.tb04871.x
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ISTEX:30933F6F32E9B52D79544104F824F52BB82DA4A5Le document en format XML
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Voice: +358‐9‐191 25511; fax: +358‐9‐191 25510; Kari.Alitalo@Helsinki.FI.</affiliation></author><idno type="istex">30933F6F32E9B52D79544104F824F52BB82DA4A5</idno><idno type="DOI">10.1111/j.1749-6632.2002.tb04871.x</idno><idno type="unit">NYAS94</idno><idno type="toTypesetVersion">file:NYAS.NYAS94.pdf</idno></analytic><monogr><title level="j" type="main">Annals of the New York Academy of Sciences</title><title level="j" type="alt">ANNALS OF NEW YORK ACADEMY SCIENCES</title><idno type="pISSN">0077-8923</idno><idno type="eISSN">1749-6632</idno><idno type="book-DOI">10.1111/(ISSN)1749-6632</idno><idno type="book-part-DOI">10.1111/nyas.2002.979.issue-1</idno><idno type="product">NYAS</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">979</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="94">94</biblScope><biblScope unit="page" to="110">110</biblScope><biblScope unit="page-count">17</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2002-12"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p><hi rend="bold">A<hi rend="smallCaps">bstract</hi>: </hi> Abnormal function of the lymphatic vessels is associated with a variety of diseases, such as tumor metastasis and lymphedema. The development of strategies for local and controlled induction or inhibition of lymphangiogenesis would thus be of major importance for the treatment of such diseases. Two growth factors, vascular endothelial growth factor C (VEGF‐C) and D (VEGF‐D), have been found to be important in the proper formation and maintenance of the lymphatic network, through their receptor VEGFR‐3. In patients with lymphedema, heterozygous inactivation of VEGFR‐3 leads to primary lymphedema due to defective lymphatic drainage in the limbs. We have shown that VEGF‐C gene transfer to the skin of mice with lymphedema induces regeneration of the cutaneous lymphatic vessel network. However, as is the case with VEGF, high levels of VEGF‐C cause blood vessel growth and leakiness, resulting in tissue edema. Strategies to avoid these side‐effects have also been developed. This new field of reseach has important implications for the development of new therapies for human lymphedema.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">gene therapy</term><term xml:id="k2">adenovirus</term><term xml:id="k3">AAV</term><term xml:id="k4">VEGFR‐3</term><term xml:id="k5">missense mutation</term><term xml:id="k6">mouse model</term></keywords><classCode scheme="tocHeading1">The Lymphatic Continuum: Lymphatic Biology and Disease: Part 3. 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Voice: +358‐9‐191 25511; fax: +358‐9‐191 25510; <email>Kari.Alitalo@Helsinki.FI</email>.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NYAS.NYAS94.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="3"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="78"></count><count type="linksCrossRef" number="84"></count></countGroup><titleGroup><title type="main">Insights into the Molecular Pathogenesis and Targeted Treatment of Lymphedema</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>ANNE</givenNames><familyName>SAARISTO</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>MARIKA J.</givenNames><familyName>KARKKAINEN</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1" corresponding="yes"><personName><givenNames>KARI</givenNames><familyName>ALITALO</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="FI"><unparsedAffiliation>Molecular/Cancer Biology Laboratory, Biomedicum, University of Helsinki, Helsinki, Finland</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">gene therapy</keyword><keyword xml:id="k2">adenovirus</keyword><keyword xml:id="k3">AAV</keyword><keyword xml:id="k4">VEGFR‐3</keyword><keyword xml:id="k5">missense mutation</keyword><keyword xml:id="k6">mouse model</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>A<sc>bstract</sc>: </b> Abnormal function of the lymphatic vessels is associated with a variety of diseases, such as tumor metastasis and lymphedema. 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This new field of reseach has important implications for the development of new therapies for human lymphedema.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Insights into the Molecular Pathogenesis and Targeted Treatment of Lymphedema</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Insights into the Molecular Pathogenesis and Targeted Treatment of Lymphedema</title></titleInfo><name type="personal"><namePart type="given">ANNE</namePart><namePart type="family">SAARISTO</namePart><affiliation>Molecular/Cancer Biology Laboratory, Biomedicum, University of Helsinki, Helsinki, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MARIKA J.</namePart><namePart type="family">KARKKAINEN</namePart><affiliation>Molecular/Cancer Biology Laboratory, Biomedicum, University of Helsinki, Helsinki, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KARI</namePart><namePart type="family">ALITALO</namePart><affiliation>Molecular/Cancer Biology Laboratory, Biomedicum, University of Helsinki, Helsinki, Finland</affiliation><affiliation>E-mail: Kari.Alitalo@Helsinki.FI</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2002-12</dateIssued><copyrightDate encoding="w3cdtf">2002</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">4</extent><extent unit="tables">3</extent><extent unit="references">78</extent></physicalDescription><abstract>Abstract: Abnormal function of the lymphatic vessels is associated with a variety of diseases, such as tumor metastasis and lymphedema. The development of strategies for local and controlled induction or inhibition of lymphangiogenesis would thus be of major importance for the treatment of such diseases. Two growth factors, vascular endothelial growth factor C (VEGF‐C) and D (VEGF‐D), have been found to be important in the proper formation and maintenance of the lymphatic network, through their receptor VEGFR‐3. In patients with lymphedema, heterozygous inactivation of VEGFR‐3 leads to primary lymphedema due to defective lymphatic drainage in the limbs. We have shown that VEGF‐C gene transfer to the skin of mice with lymphedema induces regeneration of the cutaneous lymphatic vessel network. However, as is the case with VEGF, high levels of VEGF‐C cause blood vessel growth and leakiness, resulting in tissue edema. Strategies to avoid these side‐effects have also been developed. This new field of reseach has important implications for the development of new therapies for human lymphedema.</abstract><subject lang="en"><genre>keywords</genre><topic>gene therapy</topic><topic>adenovirus</topic><topic>AAV</topic><topic>VEGFR‐3</topic><topic>missense mutation</topic><topic>mouse model</topic></subject><relatedItem type="host"><titleInfo><title>Annals of the New York Academy of Sciences</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0077-8923</identifier><identifier type="eISSN">1749-6632</identifier><identifier type="DOI">10.1111/(ISSN)1749-6632</identifier><identifier type="PublisherID">NYAS</identifier><part><date>2002</date><detail type="title"><title>THE LYMPHATIC CONTINUUM: Lymphatic Biology and Disease</title></detail><detail type="volume"><caption>vol.</caption><number>979</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>94</start><end>110</end><total>17</total></extent></part></relatedItem><identifier type="istex">30933F6F32E9B52D79544104F824F52BB82DA4A5</identifier><identifier type="DOI">10.1111/j.1749-6632.2002.tb04871.x</identifier><identifier type="ArticleID">NYAS94</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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