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Jaguar2feet

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Noted in atypical breast lesions [49, 50]. Our studies suggest that loss of SFRP1 in epithelial cells can enhance TGF- mediated EGR2 expression and affect TGF- induced M2 polarization of macrophages. As M2 macrophages secrete growth factors, such as Wnt ligands and EGF, this could contribute to tumor progression through a feed forward cross talk between the epithelium and the immune system. Additi
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Ated with cancer growth and proliferation. Our data reveal that mouse macrophages polarized to M1 macrophages in response to LPS exhibit a significant increase in M1 marker expression when treated with recombinant SFRP1. The fact that we did not observe similar findings when human mammary gland explants were treated with SFRP1 could be due to the fact that our murine macrophages were isolated from
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Mass consists of tumor-associated macrophages (TAMs) and poor prognosis is associated with elevated levels of TAMs [44]. Stimuli in the tumor environment polarize TAMs towards a protumor M2 rather than an anti-tumor M1 phenotype [45]. TGF- promotes tumor progression by recruiting TAMs to compete with dendritic cells by suppressing their antigen-presentation [34]. Zhang et al. provide evidence that
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Noted in atypical breast lesions [49, 50]. Our studies suggest that loss of SFRP1 in epithelial cells can enhance TGF- mediated EGR2 expression and affect TGF- induced M2 polarization of macrophages. As M2 macrophages secrete growth factors, such as Wnt ligands and EGF, this could contribute to tumor progression through a feed forward cross talk between the epithelium and the immune system. Additi
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Expression. The results shown represent experiments performed in duplicate and normalized to the amplification of ACTB mRNA. Bars represent mean ?SEM of the fold change with respect to vector transfected control cells. *p
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Expression. The results shown represent experiments performed in duplicate and normalized to the amplification of ACTB mRNA. Bars represent mean ?SEM of the fold change with respect to vector transfected control cells. *p
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Mass consists of tumor-associated macrophages (TAMs) and poor prognosis is associated with elevated levels of TAMs [44]. Stimuli in the tumor environment polarize TAMs towards a protumor M2 rather than an anti-tumor M1 phenotype [45]. TGF- promotes tumor progression by recruiting TAMs to compete with dendritic cells by suppressing their antigen-presentation [34]. Zhang et al. provide evidence that
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Stimulated M2 polarization. Moreover, human explant mammary gland cultures treated with rSFRP1 show a marked reduction in the human M2 marker, CD163. CD163 is a monocyte/macrophage-restricted scavenge receptor [47] and the mechanism by which rSFRP1 reduces CD163 expression may be due in part to repression of Wnt signaling because Bergenfelz et al. show that breast cancer CD163+ TAMs correlate with