Document Detail


Cytokine regulation of angiogenesis in breast cancer: the role of tumor-associated macrophages.
MedLine Citation:
PMID:  7539028     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Studies over the past 20 years have established that the development of new capillaries from an existing vascular network (a process called angiogenesis) is an essential component of tumor growth. Malignant tumors do not grow beyond 2-3 mm3 in size unless they stimulate the formation of new blood vessels and thus provide a route for the increased inflow of nutrients and oxygen and outflow of waste products. Tumor angiogenesis also provides an essential exit route for metastasizing tumor cells from the tumor to the bloodstream. Indeed, extensive neovascularization is a poor prognostic factor in several forms of human cancer. Angiogenesis is a complex, multistep process driven by many local signals within the tumor. This involves the degradation of the extracellular matrix around a local venule after the release of collagenases and proteases, the proliferation and migration of capillary endothelial cells, and their differentiation into functioning capillaries. Cytokines produced by various cell types present within the microenvironment of solid tumors form a complex, dynamic network in which they have multiple effects on tumor progression. Herein we review our work on the presence, and possible regulatory influence on tumor angiogenesis, of a number of these cytokines within invasive breast carcinomas. We have combined immunocytochemistry with a single cell cytokine release assay called the reverse hemolytic plaque assay to investigate the cellular sources of the key angiogenic cytokines, vascular endothelial growth factor, basic fibroblast growth factor, and tumor necrosis factor-alpha. Tumor-associated macrophages in the stromal compartment of these tumors and/or malignant epithelial cells were seen to be a major producer cell for these cytokines, whereas tumor necrosis factor-alpha receptors were expressed by leukocytes, malignant cells, and endothelial cells in tumor blood vessels.
Authors:
C E Lewis; R Leek; A Harris; J O McGee
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Journal of leukocyte biology     Volume:  57     ISSN:  0741-5400     ISO Abbreviation:  J. Leukoc. Biol.     Publication Date:  1995 May 
Date Detail:
Created Date:  1995-06-28     Completed Date:  1995-06-28     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  8405628     Medline TA:  J Leukoc Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  747-51     Citation Subset:  IM    
Affiliation:
Nuffield Department of Pathology and Bacteriology, University of Oxford, John Radcliffe Hospital, Headington, UK.
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MeSH Terms
Descriptor/Qualifier:
Antigens, CD / metabolism
Antigens, CD31
Antigens, Differentiation, Myelomonocytic / metabolism
Breast Neoplasms / blood supply*
Cell Adhesion Molecules / metabolism
Cytokines / physiology*
Endothelial Growth Factors / physiology
Fibroblast Growth Factor 2 / physiology
Humans
Lymphokines / physiology
Macrophages / physiology*
Neovascularization, Pathologic*
Tumor Necrosis Factor-alpha / physiology
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
Chemical
Reg. No./Substance:
0/Antigens, CD; 0/Antigens, CD31; 0/Antigens, Differentiation, Myelomonocytic; 0/CD68 antigen, human; 0/Cell Adhesion Molecules; 0/Cytokines; 0/Endothelial Growth Factors; 0/Lymphokines; 0/Tumor Necrosis Factor-alpha; 0/Vascular Endothelial Growth Factor A; 0/Vascular Endothelial Growth Factors; 103107-01-3/Fibroblast Growth Factor 2

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


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