Linked Life Data

16322683

Source:http://linkedlifedata.com/resource/pubmed/id/16322683

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2006-2-7
pubmed:abstractText
At first glance, the antiangiogenic drug Avastin (bevacizumab) must paradoxically normalize angiogenesis, in order to potentiate chemotherapy. However, this may be only a part of the story. Here I discuss that the synergy between Avastin and chemotherapy is also consistent with the classic notion that antiangiogenic therapy actually inhibits angiogenesis. It has been previously predicted that inhibition of angiogenesis (action) will induce a reactive resistance (reaction), which is mediated by the HIF-1/VEGF pathway in cancer cells, thus allowing both endothelial and cancer cells to resist therapy. Therefore, inhibitors of the reactive resistance are needed to potentiate anti-angiogenic therapy. In the combination of chemotherapy plus Avastin, it is chemotherapy that is the principal antiangiogenic agent. This role of chemotherapy requires that something should be added to block the reaction. And this is exactly what Avastin does (by blocking VEGF). While chemotherapy inhibits angiogenesis, Avastin abrogates the reactive resistance, sensitizing both endothelial and cancer cells to therapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1538-4047
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1307-10
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
How Avastin potentiates chemotherapeutic drugs: action and reaction in antiangiogenic therapy.
pubmed:affiliation
Cancer Center, Ordway Research Institute, Albany, New York, NY 12208, USA. mblagosklonny@ordwayresearch.org
pubmed:publicationType
Journal Article, Review