| The shunt problem: control of functional shunting in normal and tumour vasculature. | |
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MedLine Citation:
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PMID: 20631803 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Networks of blood vessels in normal and tumour tissues have heterogeneous structures, with widely varying blood flow pathway lengths. To achieve efficient blood flow distribution, mechanisms for the structural adaptation of vessel diameters must be able to inhibit the formation of functional shunts (whereby short pathways become enlarged and flow bypasses long pathways). Such adaptation requires information about tissue metabolic status to be communicated upstream to feeding vessels, through conducted responses. We propose that impaired vascular communication in tumour microvascular networks, leading to functional shunting, is a primary cause of dysfunctional microcirculation and local hypoxia in cancer. We suggest that anti-angiogenic treatment of tumours may restore vascular communication and thereby improve or normalize flow distribution in tumour vasculature. |
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Authors:
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Axel R Pries; Michael Höpfner; Ferdinand le Noble; Mark W Dewhirst; Timothy W Secomb |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review Date: 2010-07-15 |
Journal Detail:
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Title: Nature reviews. Cancer Volume: 10 ISSN: 1474-1768 ISO Abbreviation: Nat. Rev. Cancer Publication Date: 2010 Aug |
Date Detail:
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Created Date: 2010-07-23 Completed Date: 2010-08-13 Revised Date: 2011-09-26 |
Medline Journal Info:
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Nlm Unique ID: 101124168 Medline TA: Nat Rev Cancer Country: England |
Other Details:
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Languages: eng Pagination: 587-93 Citation Subset: IM |
Affiliation:
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Department of Physiology and the Centre for Cardiovascular Research, Charité Berlin, Thielallee 71, D-14195 Berlin, Germany. axel.pries@charite.de |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adaptation, Physiological Animals Computer Simulation Gap Junctions / physiology Humans Microvessels / physiology* Models, Biological Neoplasms / blood supply* Regional Blood Flow Signal Transduction |
| Grant Support | |
ID/Acronym/Agency:
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CA040355/CA/NCI NIH HHS; HL034555/HL/NHLBI NIH HHS; R01 CA040355-28/CA/NCI NIH HHS |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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