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Tion, and additional tumor initiating pathways promote mammary carcinogenesis. We have previously shown that activated ERK1/2 levels and the migratory action of TERT-siSFRP1 cells are drastically reduced in response to TGF-R inhibition which is consistent with work described by Imamichi et al. showing that TGF- signaling mediates the cellular migration of breast cancer cells by ERK1/2 activation [
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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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Tegy was consequently, paradoxically, intrinsic to caring for future generations. McAdams (1993 230) likens this to the notion of the `hero's gift' (Becker, 1973), which entails caring to get a programme sufficiently to let it go, the `care and letting go signal[ling] a extra communal aspect of generativit.Tegy was as a result, paradoxically, intrinsic to caring for future generations. McAdams (19
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Tegy was consequently, paradoxically, intrinsic to caring for future generations. McAdams (1993 230) likens this to the notion of the `hero's gift' (Becker, 1973), which entails caring to get a programme sufficiently to let it go, the `care and letting go signal[ling] a extra communal aspect of generativit.Tegy was as a result, paradoxically, intrinsic to caring for future generations. McAdams (19
1
Tegy was consequently, paradoxically, intrinsic to caring for future generations. McAdams (1993 230) likens this to the notion of the `hero's gift' (Becker, 1973), which entails caring to get a programme sufficiently to let it go, the `care and letting go signal[ling] a extra communal aspect of generativit.Tegy was as a result, paradoxically, intrinsic to caring for future generations. McAdams (19
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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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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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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