Journal
ONCOGENE
Volume 30, Issue 6, Pages 679-689Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2010.439
Keywords
erbB2/HER2; mammary; microenvironment; regeneration; suppression of tumorigenesis
Funding
- Center for Cancer Research, NCI
- NIH
- Institute for Biological Interfaces of Engineering of Clemson University
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The microenvironment of the mammary gland has been shown to exert a deterministic control over cells from different normal organs during murine mammary gland regeneration in transplantation studies. When mouse mammary tumor virus (MMTV)-neu-induced tumor cells were mixed with normal mammary epithelial cells (MECs) in a dilution series and inoculated into epithelium-free mammary fat pads, they were redirected to noncarcinogenic cell fates by interaction with untransformed MECs during regenerative growth. In the presence of non-transformed MECs (50:1), tumor cells interacted with MECs to generate functional chimeric outgrowths. When injected alone, tumor cells invariably produced tumors. Here, the normal microenvironment redirects MMTV-neu-transformed tumorigenic cells to participate in the regeneration of a normal, functional mammary gland. In addition, the redirected tumor cells show the capacity to differentiate into normal mammary cell types, including luminal, myoepithelial and secretory. The results indicate that signals emanating from a normal mammary microenvironment, comprised of stromal, epithelial and host-mediated signals, combine to suppress the cancer phenotype during glandular regeneration. Clarification of these signals offers improved therapeutic possibilities for the control of mammary cancer growth. Oncogene (2011) 30, 679-689; doi:10.1038/onc.2010.439; published online 4 October 2010
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