Document Detail

Premetastatic lung "niche": is vascular endothelial growth factor receptor 1 activation required?
MedLine Citation:
PMID:  20587530     Owner:  NLM     Status:  MEDLINE    
Inflammatory pathways may mediate preparation of the "metastatic soil" in the lungs. Some of these pathways--activation and/or the recruitment of certain inflammatory cells--might depend on vascular endothelial growth factor receptor 1 (VEGFR1) activity. Thus, blocking the activity of VEGFR1 (or the interaction with its ligands) has emerged as a potential antimetastasis strategy to target not only angiogenesis and cancer cell survival and migration, but also the recruitment of tumor growth-promoting bone marrow-derived cells (BMDC). However, inhibition of VEGFR1 activity by blocking antibodies or by genetic deletion of the tyrosine kinase domain neither prevented nor changed the rate of spontaneous metastasis formation after surgical removal of primary tumors. Thus, development of VEGFR1-targeted agents should be pursued in selected tumors (e.g., by identifying cancers that depend on VEGFR1 signaling for survival) or in specific combination therapies. Preventing metastasis will likely require identification and blockade of additional or alternative proinflammatory pathways that mediate the priming of the metastatic soil and the growth of micrometastases.
Dan G Duda; Rakesh K Jain
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2010-06-29
Journal Detail:
Title:  Cancer research     Volume:  70     ISSN:  1538-7445     ISO Abbreviation:  Cancer Res.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-07-16     Completed Date:  2010-08-24     Revised Date:  2014-09-24    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5670-3     Citation Subset:  IM    
Copyright Information:
(c)2010 AACR.
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MeSH Terms
Lung / blood supply,  metabolism*
Lung Neoplasms / secondary*
Vascular Endothelial Growth Factor Receptor-1 / metabolism*
Grant Support
P01 CA080124/CA/NCI NIH HHS; P01 CA080124-01A1/CA/NCI NIH HHS; P01 CA080124-05/CA/NCI NIH HHS; P01 CA080124-05S1/CA/NCI NIH HHS; P01 CA080124-06A2/CA/NCI NIH HHS; P01 CA080124-07/CA/NCI NIH HHS; P01 CA080124-08/CA/NCI NIH HHS; P01 CA080124-09/CA/NCI NIH HHS; P01-CA80124/CA/NCI NIH HHS; R01 CA085140/CA/NCI NIH HHS; R01 CA085140-06/CA/NCI NIH HHS; R01 CA085140-07/CA/NCI NIH HHS; R01 CA085140-08/CA/NCI NIH HHS; R01 CA085140-09/CA/NCI NIH HHS; R01 CA115767/CA/NCI NIH HHS; R01 CA115767-01A1/CA/NCI NIH HHS; R01 CA115767-02/CA/NCI NIH HHS; R01 CA115767-03/CA/NCI NIH HHS; R01 CA115767-04/CA/NCI NIH HHS; R01 CA126642/CA/NCI NIH HHS; R01 CA126642-01A1/CA/NCI NIH HHS; R01 CA126642-02/CA/NCI NIH HHS; R01 CA126642-02S1/CA/NCI NIH HHS; R01 CA159258/CA/NCI NIH HHS; R01-CA115767/CA/NCI NIH HHS; R01-CA126642/CA/NCI NIH HHS; R01-CA85140/CA/NCI NIH HHS; R21 CA139168/CA/NCI NIH HHS; R21 CA139168-01A1/CA/NCI NIH HHS; R21-CA139168/CA/NCI NIH HHS; R24 CA085140/CA/NCI NIH HHS; R24 CA085140-05/CA/NCI NIH HHS; T32 CA073479/CA/NCI NIH HHS; T32 CA073479-08/CA/NCI NIH HHS; T32 CA073479-09/CA/NCI NIH HHS; T32 CA073479-10/CA/NCI NIH HHS; T32 CA073479-11/CA/NCI NIH HHS; T32 CA073479-12/CA/NCI NIH HHS; T32-CA73479/CA/NCI NIH HHS
Reg. No./Substance:
EC Endothelial Growth Factor Receptor-1

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