Colony-stimulating Factor 1 Promotes Progression of Mammary Tumors to Malignancy

Colony-stimulating Factor 1 Promotes Progression of Mammary Tumors to Malignancy

March 19, 2001 | Elaine Y. Lin, Andrew V. Nguyen, Robert G. Russell, Jeffrey W. Pollard
The study investigates the role of colony-stimulating factor 1 (CSF-1) in the progression of mammary tumors to malignancy. Overexpression of CSF-1 and its receptor (CSF-1R) is associated with poor prognosis in human breast carcinomas. The researchers used a mouse model where transgenic mice prone to mammary cancer were crossed with mice lacking the CSF-1 gene. They found that the absence of CSF-1 did not affect the incidence or growth of primary tumors but delayed their progression to invasive and metastatic carcinomas. Transgenic expression of CSF-1 in the mammary epithelium of both wild-type and null mutant mice accelerated tumor progression and increased pulmonary metastasis, associated with enhanced infiltration of macrophages into the primary tumor. These findings suggest that CSF-1 promotes tumor progression by regulating the infiltration and function of tumor-associated macrophages, and that agents targeting CSF-1/CSF-1R activity could have therapeutic potential.The study investigates the role of colony-stimulating factor 1 (CSF-1) in the progression of mammary tumors to malignancy. Overexpression of CSF-1 and its receptor (CSF-1R) is associated with poor prognosis in human breast carcinomas. The researchers used a mouse model where transgenic mice prone to mammary cancer were crossed with mice lacking the CSF-1 gene. They found that the absence of CSF-1 did not affect the incidence or growth of primary tumors but delayed their progression to invasive and metastatic carcinomas. Transgenic expression of CSF-1 in the mammary epithelium of both wild-type and null mutant mice accelerated tumor progression and increased pulmonary metastasis, associated with enhanced infiltration of macrophages into the primary tumor. These findings suggest that CSF-1 promotes tumor progression by regulating the infiltration and function of tumor-associated macrophages, and that agents targeting CSF-1/CSF-1R activity could have therapeutic potential.
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