Molecular regulation of the VEGF family -- inducers of angiogenesis and lymphangiogenesis.
Identifieur interne : 003E47 ( PubMed/Corpus ); précédent : 003E46; suivant : 003E48Molecular regulation of the VEGF family -- inducers of angiogenesis and lymphangiogenesis.
Auteurs : Bradley K. Mccoll ; Steven A. Stacker ; Marc G. AchenSource :
- APMIS : acta pathologica, microbiologica, et immunologica Scandinavica [ 0903-4641 ]
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
Links to Exploration step
pubmed:15563310Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><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><nlm:affiliation>Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Victoria, Australia.</nlm:affiliation></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></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></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><nlm:affiliation>Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Victoria, Australia.</nlm:affiliation></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="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" 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></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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15563310</PMID><DateCreated><Year>2004</Year><Month>11</Month><Day>25</Day></DateCreated><DateCompleted><Year>2005</Year><Month>01</Month><Day>12</Day></DateCompleted><DateRevised><Year>2008</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0903-4641</ISSN><JournalIssue CitedMedium="Print"><Volume>112</Volume><Issue>7-8</Issue><PubDate><MedlineDate>2004 Jul-Aug</MedlineDate></PubDate></JournalIssue><Title>APMIS : acta pathologica, microbiologica, et immunologica Scandinavica</Title><ISOAbbreviation>APMIS</ISOAbbreviation></Journal><ArticleTitle>Molecular regulation of the VEGF family -- inducers of angiogenesis and lymphangiogenesis.</ArticleTitle><Pagination><MedlinePgn>463-80</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>McColl</LastName><ForeName>Bradley K</ForeName><Initials>BK</Initials><AffiliationInfo><Affiliation>Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Victoria, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stacker</LastName><ForeName>Steven A</ForeName><Initials>SA</Initials></Author><Author ValidYN="Y"><LastName>Achen</LastName><ForeName>Marc G</ForeName><Initials>MG</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Denmark</Country><MedlineTA>APMIS</MedlineTA><NlmUniqueID>8803400</NlmUniqueID><ISSNLinking>0903-4641</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008565">Membrane Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C098069">PIGF protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011506">Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016760">Proto-Oncogene Proteins c-fos</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042461">Vascular Endothelial Growth Factor A</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002450" MajorTopicYN="N">Cell Communication</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002471" MajorTopicYN="N">Cell Transformation, Neoplastic</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D047108" MajorTopicYN="N">Embryonic Development</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042583" MajorTopicYN="Y">Lymphangiogenesis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008565" MajorTopicYN="N">Membrane Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009389" MajorTopicYN="N">Neovascularization, Pathologic</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018919" MajorTopicYN="Y">Neovascularization, Physiologic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011506" MajorTopicYN="N">Proteins</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016760" MajorTopicYN="N">Proto-Oncogene Proteins c-fos</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042461" MajorTopicYN="N">Vascular Endothelial Growth Factor A</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>197</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2004</Year><Month>11</Month><Day>26</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2005</Year><Month>1</Month><Day>13</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2004</Year><Month>11</Month><Day>26</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">15563310</ArticleId><ArticleId IdType="pii">APMapm11207-0807</ArticleId><ArticleId IdType="doi">10.1111/j.1600-0463.2004.apm11207-0807.x</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/LymphedemaV1/Data/PubMed/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 003E47 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 003E47 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= LymphedemaV1
|flux= PubMed
|étape= Corpus
|type= RBID
|clé= pubmed:15563310
|texte= Molecular regulation of the VEGF family -- inducers of angiogenesis and lymphangiogenesis.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:15563310" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a LymphedemaV1
| This area was generated with Dilib version V0.6.31. |  |