Document Detail

CSF-1R Signaling in Health and Disease: A Focus on the Mammary Gland.
MedLine Citation:
PMID:  24912655     Owner:  NLM     Status:  Publisher    
Colony-stimulating factor-1 (CSF-1), also known as macrophage-colony stimulating factor (M-CSF), is the primary growth factor regulating survival, proliferation and differentiation of macrophages. It is also a potent chemokine for macrophages and monocytes. Signaling via the CSF-1 receptor (CSF-1R) is necessary for the production of almost all tissue resident macrophage populations and these macrophages participate, via trophic mechanisms, in the normal development and homeostasis of tissues and organs in which they reside, including the mammary gland. The drawback of this close interaction between macrophages and parenchymal cells is that dysregulation of macrophage trophic functions assists in the development and progression of many cancers, including breast cancer. Furthermore, tumour cells secrete CSF-1 to attract more macrophages to the tumour microenvironment where CSF-1R signaling frequently drives the behaviour of these tumour-associated macrophages (TAMs) to promote tumour progression and metastasis. Evidence is mounting that treated tumours secrete more CSF-1 and the increased recruitment of TAMs limits treatment efficacy. Thus, therapeutic targeting of the CSF-1R to inhibit TAM function is likely to enhance tumour response and improve patient outcomes in the treatment of cancer, including breast cancer.
Amy Renee Sullivan; Fiona Jane Pixley
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-6-10
Journal Detail:
Title:  Journal of mammary gland biology and neoplasia     Volume:  -     ISSN:  1573-7039     ISO Abbreviation:  J Mammary Gland Biol Neoplasia     Publication Date:  2014 Jun 
Date Detail:
Created Date:  2014-6-10     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9601804     Medline TA:  J Mammary Gland Biol Neoplasia     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
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