Linked Life Data

15326390

Source:http://linkedlifedata.com/resource/pubmed/id/15326390

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2004-12-21
pubmed:abstractText
Through a poorly understood mechanism, tumors respond to radiation by secreting cytokines which inhibit endothelial cell apoptosis, thereby limiting treatment response by minimizing vessel damage. We have recently discovered that this pathway is governed by a major angiogenesis regulator, hypoxia-inducible factor-1 (HIF-1). We uncovered dual mechanisms initiated by radiation that both simultaneously lead to HIF-1 activation: (1) reoxygenation-induced stabilization of the HIF-1 dimer through free radical intermediates, and (2) reoxygenation-mediated depolymerization of hypoxia-induced translational suppressors known as stress granules. These findings have implications both for understanding the basic science of hypoxic signaling in tumors, and for discovering novel methods of enhancing conventional anti-tumor therapeutics in the clinic. In this article, we will highlight the apparent importance of free radical species in protecting tumor vasculature, stress granules in regulating hypoxic gene expression, and HIF-1 in regulating tumor sensitivity to ionizing radiation. The potential therapeutic utility of these findings will also be explored, with emphasis placed on putative targets in these pathways which may enhance tumor radiotherapy.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1107-10
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Raising the bar: how HIF-1 helps determine tumor radiosensitivity.
pubmed:affiliation
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural