Document Detail


Class 3 semaphorins: physiological vascular normalizing agents for anti-cancer therapy.
MedLine Citation:
PMID:  23198760     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Findings from preclinical and clinical studies show that vascular normalization represents a novel strategy to enhance the efficacy of and overcome the acquired resistance to anti-angiogenic therapies in cancer. Several mechanisms of tumour vessel normalization have been revealed. Amongst them, secreted class 3 semaphorins (Sema3), which regulate axon guidance and angiogenesis, have been recently identified as novel vascular normalizing agents that inhibit metastatic dissemination by restoring vascular function. Here, we discuss the different biological functions and mechanisms of action of Sema3 in the context of tumour vascular normalization, and their impact on the different cellular components of the tumour microenvironment.
Authors:
G Serini; F Bussolino; F Maione; E Giraudo
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Journal of internal medicine     Volume:  273     ISSN:  1365-2796     ISO Abbreviation:  J. Intern. Med.     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-01-21     Completed Date:  2013-04-03     Revised Date:  2014-03-19    
Medline Journal Info:
Nlm Unique ID:  8904841     Medline TA:  J Intern Med     Country:  England    
Other Details:
Languages:  eng     Pagination:  138-55     Citation Subset:  IM    
Copyright Information:
© 2012 The Association for the Publication of the Journal of Internal Medicine.
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MeSH Terms
Descriptor/Qualifier:
Angiogenesis Inhibitors / therapeutic use*
Clinical Trials as Topic
Humans
Neoplasms / blood supply*
Neovascularization, Pathologic / drug therapy*
Semaphorins / therapeutic use*
Grant Support
ID/Acronym/Agency:
GGP09175//Telethon
Chemical
Reg. No./Substance:
0/Angiogenesis Inhibitors; 0/Semaphorins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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