Molecular regulation of the VEGF family -- inducers of angiogenesis and lymphangiogenesis.
Identifieur interne : 001C21 ( Ncbi/Curation ); précédent : 001C20; suivant : 001C22Molecular regulation of the VEGF family -- inducers of angiogenesis and lymphangiogenesis.
Auteurs : Bradley K. Mccoll [Australie] ; Steven A. Stacker ; Marc G. AchenSource :
- APMIS : acta pathologica, microbiologica, et immunologica Scandinavica [ 0903-4641 ]
Descripteurs français
- KwdFr :
- Animaux, Communication cellulaire, Développement embryonnaire, Facteur de croissance endothéliale vasculaire de type A (physiologie), Humains, Lymphangiogenèse, Néovascularisation pathologique (étiologie), Néovascularisation physiologique, Protéines (physiologie), Protéines membranaires, Protéines proto-oncogènes c-fos (physiologie), Transformation cellulaire néoplasique (génétique).
- MESH :
- génétique : Transformation cellulaire néoplasique.
- physiologie : Facteur de croissance endothéliale vasculaire de type A, Protéines, Protéines proto-oncogènes c-fos.
- étiologie : Néovascularisation pathologique.
- Animaux, Communication cellulaire, Développement embryonnaire, Humains, Lymphangiogenèse, Néovascularisation physiologique, Protéines membranaires.
English descriptors
- KwdEn :
- Animals, Cell Communication, Cell Transformation, Neoplastic (genetics), Embryonic Development, Humans, Lymphangiogenesis, Membrane Proteins, Neovascularization, Pathologic (etiology), Neovascularization, Physiologic, Proteins (physiology), Proto-Oncogene Proteins c-fos (physiology), Vascular Endothelial Growth Factor A (physiology).
- MESH :
- chemical , physiology : Proteins, Proto-Oncogene Proteins c-fos, Vascular Endothelial Growth Factor A.
- chemical : Membrane Proteins.
- etiology : Neovascularization, Pathologic.
- genetics : Cell Transformation, Neoplastic.
- Animals, Cell Communication, Embryonic Development, Humans, Lymphangiogenesis, Neovascularization, Physiologic.
Abstract
The vascular endothelial growth factor (VEGF) family of secreted glycoproteins are critical inducers of angiogenesis (growth of blood vessels) and lymphangiogenesis (growth of lymphatic vessels). These proteins are attractive therapeutic targets for blocking growth of blood vessels and lymphatics in tumors and thereby inhibiting the growth and spread of cancer -- in fact, the first VEGF inhibitor has recently entered the clinic for treatment of cancer. In addition, the VEGFs are being considered for stimulation of angiogenesis in the context of ischemic disease and lymphangiogenesis for treatment of lymphedema. These therapeutic possibilities have focused great interest on the molecular regulation of VEGF family members. Much has been learned in the past five years about the mechanisms controlling the action of the VEGFs, including the importance of hypoxia, proteolysis, transcription factors and RNA splicing. An understanding of these mechanisms offers broader opportunities to manipulate expression and activity of the VEGFs for treatment of disease.
DOI: 10.1111/j.1600-0463.2004.apm11207-0807.x
PubMed: 15563310
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pubmed:15563310Le document en format XML
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Achen</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="????"><PubDate><MedlineDate>2004 Jul-Aug</MedlineDate></PubDate></date><idno type="RBID">pubmed:15563310</idno><idno type="pmid">15563310</idno><idno type="doi">10.1111/j.1600-0463.2004.apm11207-0807.x</idno><idno type="wicri:Area/PubMed/Corpus">003E47</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">003E47</idno><idno type="wicri:Area/PubMed/Curation">003E47</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">003E47</idno><idno type="wicri:Area/PubMed/Checkpoint">003E47</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">003E47</idno><idno type="wicri:Area/Ncbi/Merge">001C21</idno><idno type="wicri:Area/Ncbi/Curation">001C21</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Molecular regulation of the VEGF family -- inducers of angiogenesis and lymphangiogenesis.</title><author><name sortKey="Mccoll, Bradley K" sort="Mccoll, Bradley K" uniqKey="Mccoll B" first="Bradley K" last="Mccoll">Bradley K. Mccoll</name><affiliation wicri:level="1"><nlm:affiliation>Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Victoria, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Victoria</wicri:regionArea><wicri:noRegion>Victoria</wicri:noRegion></affiliation></author><author><name sortKey="Stacker, Steven A" sort="Stacker, Steven A" uniqKey="Stacker S" first="Steven A" last="Stacker">Steven A. Stacker</name></author><author><name sortKey="Achen, Marc G" sort="Achen, Marc G" uniqKey="Achen M" first="Marc G" last="Achen">Marc G. Achen</name></author></analytic><series><title level="j">APMIS : acta pathologica, microbiologica, et immunologica Scandinavica</title><idno type="ISSN">0903-4641</idno></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Communication</term><term>Cell Transformation, Neoplastic (genetics)</term><term>Embryonic Development</term><term>Humans</term><term>Lymphangiogenesis</term><term>Membrane Proteins</term><term>Neovascularization, Pathologic (etiology)</term><term>Neovascularization, Physiologic</term><term>Proteins (physiology)</term><term>Proto-Oncogene Proteins c-fos (physiology)</term><term>Vascular Endothelial Growth Factor A (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Communication cellulaire</term><term>Développement embryonnaire</term><term>Facteur de croissance endothéliale vasculaire de type A (physiologie)</term><term>Humains</term><term>Lymphangiogenèse</term><term>Néovascularisation pathologique (étiologie)</term><term>Néovascularisation physiologique</term><term>Protéines (physiologie)</term><term>Protéines membranaires</term><term>Protéines proto-oncogènes c-fos (physiologie)</term><term>Transformation cellulaire néoplasique (génétique)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Proteins</term><term>Proto-Oncogene Proteins c-fos</term><term>Vascular Endothelial Growth Factor A</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Membrane Proteins</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Neovascularization, Pathologic</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Transformation, Neoplastic</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Transformation cellulaire néoplasique</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Facteur de croissance endothéliale vasculaire de type A</term><term>Protéines</term><term>Protéines proto-oncogènes c-fos</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Néovascularisation pathologique</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Communication</term><term>Embryonic Development</term><term>Humans</term><term>Lymphangiogenesis</term><term>Neovascularization, Physiologic</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Communication cellulaire</term><term>Développement embryonnaire</term><term>Humains</term><term>Lymphangiogenèse</term><term>Néovascularisation physiologique</term><term>Protéines membranaires</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The vascular endothelial growth factor (VEGF) family of secreted glycoproteins are critical inducers of angiogenesis (growth of blood vessels) and lymphangiogenesis (growth of lymphatic vessels). These proteins are attractive therapeutic targets for blocking growth of blood vessels and lymphatics in tumors and thereby inhibiting the growth and spread of cancer -- in fact, the first VEGF inhibitor has recently entered the clinic for treatment of cancer. In addition, the VEGFs are being considered for stimulation of angiogenesis in the context of ischemic disease and lymphangiogenesis for treatment of lymphedema. These therapeutic possibilities have focused great interest on the molecular regulation of VEGF family members. Much has been learned in the past five years about the mechanisms controlling the action of the VEGFs, including the importance of hypoxia, proteolysis, transcription factors and RNA splicing. An understanding of these mechanisms offers broader opportunities to manipulate expression and activity of the VEGFs for treatment of disease.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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