Links to Exploration step
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Lymphangiogenesis and Lymphatic Metastasis in Breast Cancer</title>
<author><name sortKey="Ran, Sophia" sort="Ran, Sophia" uniqKey="Ran S" first="Sophia" last="Ran">Sophia Ran</name>
</author>
<author><name sortKey="Volk, Lisa" sort="Volk, Lisa" uniqKey="Volk L" first="Lisa" last="Volk">Lisa Volk</name>
</author>
<author><name sortKey="Hall, Kelly" sort="Hall, Kelly" uniqKey="Hall K" first="Kelly" last="Hall">Kelly Hall</name>
</author>
<author><name sortKey="Flister, Michael J" sort="Flister, Michael J" uniqKey="Flister M" first="Michael J." last="Flister">Michael J. Flister</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">20036110</idno>
<idno type="pmc">2891887</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2891887</idno>
<idno type="RBID">PMC:2891887</idno>
<idno type="doi">10.1016/j.pathophys.2009.11.003</idno>
<date when="2009">2009</date>
<idno type="wicri:Area/Pmc/Corpus">002929</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">002929</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Lymphangiogenesis and Lymphatic Metastasis in Breast Cancer</title>
<author><name sortKey="Ran, Sophia" sort="Ran, Sophia" uniqKey="Ran S" first="Sophia" last="Ran">Sophia Ran</name>
</author>
<author><name sortKey="Volk, Lisa" sort="Volk, Lisa" uniqKey="Volk L" first="Lisa" last="Volk">Lisa Volk</name>
</author>
<author><name sortKey="Hall, Kelly" sort="Hall, Kelly" uniqKey="Hall K" first="Kelly" last="Hall">Kelly Hall</name>
</author>
<author><name sortKey="Flister, Michael J" sort="Flister, Michael J" uniqKey="Flister M" first="Michael J." last="Flister">Michael J. Flister</name>
</author>
</analytic>
<series><title level="j">Pathophysiology : the official journal of the International Society for Pathophysiology / ISP</title>
<idno type="ISSN">0928-4680</idno>
<imprint><date when="2009">2009</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p id="P1">Lymphatic metastasis is the main prognostic factor for survival of patients with breast cancer and other epithelial malignancies. Mounting clinical and experimental data suggest that migration of tumor cells into the lymph nodes is greatly facilitated by lymphangiogenesis, a process that generates new lymphatic vessels from pre-existing lymphatics with the aid of circulating lymphatic endothelial progenitor cells. The key protein that induces lymphangiogenesis is vascular endothelial growth factor receptor-3 (VEGFR-3), which is activated by vascular endothelial growth factor-C and -D (VEGF-C and VEGF-D). These lymphangiogenic factors are commonly expressed in malignant, tumor-infiltrating and stromal cells, creating a favorable environment for generation of new lymphatic vessels. Clinical evidence demonstrates that increased lymphatic vessel density in and around tumors is associated with lymphatic metastasis and reduced patient survival. Recent evidence shows that breast cancers induce remodeling of the local lymphatic vessels and the regional lymphatic network in the sentinel and distal lymph nodes. These changes include an increase in number and diameter of tumor-draining lymphatic vessels. Consequently, lymph flow away from the tumor is increased, which significantly increases tumor cell metastasis to draining lymph nodes and may contribute to systemic spread. Collectively, recent advances in the biology of tumor-induced lymphangiogenesis suggest that chemical inhibitors of this process may be an attractive target for inhibiting tumor metastasis and cancer-related death. Nevertheless, this is a relatively new field of study and much remains to be established before the concept of tumor-induced lymphangiogenesis is accepted as a viable anti-metastatic target. This review summarizes the current concepts related to breast cancer lymphangiogenesis and lymphatic metastasis while highlighting controversies and unanswered questions.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article" xml:lang="EN"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">9433813</journal-id>
<journal-id journal-id-type="pubmed-jr-id">21518</journal-id>
<journal-id journal-id-type="nlm-ta">Pathophysiology</journal-id>
<journal-title>Pathophysiology : the official journal of the International Society for Pathophysiology / ISP</journal-title>
<issn pub-type="ppub">0928-4680</issn>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">20036110</article-id>
<article-id pub-id-type="pmc">2891887</article-id>
<article-id pub-id-type="doi">10.1016/j.pathophys.2009.11.003</article-id>
<article-id pub-id-type="manuscript">NIHMS160279</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Lymphangiogenesis and Lymphatic Metastasis in Breast Cancer</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Ran</surname>
<given-names>Sophia</given-names>
</name>
<xref ref-type="corresp" rid="cor1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Volk</surname>
<given-names>Lisa</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Hall</surname>
<given-names>Kelly</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Flister</surname>
<given-names>Michael J.</given-names>
</name>
</contrib>
<aff id="A1"><bold>Authors’ Affiliations:</bold>
Department of Medical Microbiology, Immunology and Cell Biology, Southern Illinois University School of Medicine, 801 N. Rutledge, Springfield, IL, 62794-9678, USA</aff>
</contrib-group>
<author-notes><corresp id="cor1"><label>1</label>
<bold>Corresponding author at:</bold>
Department of Medical Microbiology, Immunology and Cell Biology, Southern Illinois University School of Medicine, Springfield, IL, 62794-9626 USA. Phone: (217) 545-7026; Fax: (217) 545-7333; <email>sran@siumed.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>11</day>
<month>12</month>
<year>2009</year>
</pub-date>
<pub-date pub-type="epub"><day>24</day>
<month>12</month>
<year>2009</year>
</pub-date>
<pub-date pub-type="ppub"><month>9</month>
<year>2010</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>1</day>
<month>9</month>
<year>2011</year>
</pub-date>
<volume>17</volume>
<issue>4</issue>
<fpage>229</fpage>
<lpage>251</lpage>
<permissions><copyright-statement>© 2009 Elsevier Ireland Ltd. All rights reserved.</copyright-statement>
<copyright-year>2009</copyright-year>
</permissions>
<abstract><p id="P1">Lymphatic metastasis is the main prognostic factor for survival of patients with breast cancer and other epithelial malignancies. Mounting clinical and experimental data suggest that migration of tumor cells into the lymph nodes is greatly facilitated by lymphangiogenesis, a process that generates new lymphatic vessels from pre-existing lymphatics with the aid of circulating lymphatic endothelial progenitor cells. The key protein that induces lymphangiogenesis is vascular endothelial growth factor receptor-3 (VEGFR-3), which is activated by vascular endothelial growth factor-C and -D (VEGF-C and VEGF-D). These lymphangiogenic factors are commonly expressed in malignant, tumor-infiltrating and stromal cells, creating a favorable environment for generation of new lymphatic vessels. Clinical evidence demonstrates that increased lymphatic vessel density in and around tumors is associated with lymphatic metastasis and reduced patient survival. Recent evidence shows that breast cancers induce remodeling of the local lymphatic vessels and the regional lymphatic network in the sentinel and distal lymph nodes. These changes include an increase in number and diameter of tumor-draining lymphatic vessels. Consequently, lymph flow away from the tumor is increased, which significantly increases tumor cell metastasis to draining lymph nodes and may contribute to systemic spread. Collectively, recent advances in the biology of tumor-induced lymphangiogenesis suggest that chemical inhibitors of this process may be an attractive target for inhibiting tumor metastasis and cancer-related death. Nevertheless, this is a relatively new field of study and much remains to be established before the concept of tumor-induced lymphangiogenesis is accepted as a viable anti-metastatic target. This review summarizes the current concepts related to breast cancer lymphangiogenesis and lymphatic metastasis while highlighting controversies and unanswered questions.</p>
</abstract>
<kwd-group><kwd>lymphangiogenesis</kwd>
<kwd>VEGF-C•VEGFR-3 axis</kwd>
<kwd>breast cancer</kwd>
<kwd>lymph nodes</kwd>
<kwd>lymphatic metastasis</kwd>
</kwd-group>
<contract-num rid="CA1">R15 CA125682-01
||CA</contract-num>
<contract-sponsor id="CA1">National Cancer Institute : NCI</contract-sponsor>
</article-meta>
</front>
</pmc>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/LymphedemaV1/Data/Pmc/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002929 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Pmc/Corpus/biblio.hfd -nk 002929 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Sante |area= LymphedemaV1 |flux= Pmc |étape= Corpus |type= RBID |clé= |texte= }}
![]() | This area was generated with Dilib version V0.6.31. | ![]() |