56 research outputs found
Extending the Marketing Dialog on Poverty
We appreciate Professor Aneel Karnani’s contributions to the marketing dialog on poverty and our article “Marketing’s Lost Frontier: The Poor” (Achrol and Kotler 2016). We do not necessarily disagree with some of his criticisms but rather see them as an opportunity for expanding the discussion of marketing’s role in reducing world poverty. In this response, we revisit and elaborate on Social Marketing for the bottom-of-the-pyramid (BOP) and Distributed Production-Consumption view presented in the original article. These new marketing models – focused on distributing economic opportunity, income and standards of life to local communities – can substantially displace the giant centralized manufacturing systems and urban based services economy, and usher in a new era of diminished poverty and industrial renewal
Network Organization and Systems Competition: A Marketing Analysis
Network organization and systems competition challenge competition policy and antitrust law. Networks can be powerful engines of marketing and innovation, but they can also function in ways that raise competition questions and antitrust concerns. Drawing on the marketing literature, the authors explain the nature and competitive behavior of firms operating in and competing through networks. Key questions for understanding and analyzing marketing networks in competition policy and antitrust law are discussed. The article adds marketing insights to the growing dialogue on network forms of business organization and systems competition. It also demonstrates the benefits of including knowledge from marketing and related disciplines in competition policy and antitrust analysis
Network Organization and Systems Competition: A Marketing Analysis
Network organization and systems competition challenge competition policy and antitrust law. Networks can be powerful engines of marketing and innovation, but they can also function in ways that raise competition questions and antitrust concerns. Drawing on the marketing literature, the authors explain the nature and competitive behavior of firms operating in and competing through networks. Key questions for understanding and analyzing marketing networks in competition policy and antitrust law are discussed. The article adds marketing insights to the growing dialogue on network forms of business organization and systems competition. It also demonstrates the benefits of including knowledge from marketing and related disciplines in competition policy and antitrust analysis
Anti-CD47 Treatment Stimulates Phagocytosis of Glioblastoma by M1 and M2 Polarized Macrophages and Promotes M1 Polarized Macrophages In Vivo.
Tumor-associated macrophages (TAMs) represent an important cellular subset within the glioblastoma (WHO grade IV) microenvironment and are a potential therapeutic target. TAMs display a continuum of different polarization states between antitumorigenic M1 and protumorigenic M2 phenotypes, with a lower M1/M2 ratio correlating with worse prognosis. Here, we investigated the effect of macrophage polarization on anti-CD47 antibody-mediated phagocytosis of human glioblastoma cells in vitro, as well as the effect of anti-CD47 on the distribution of M1 versus M2 macrophages within human glioblastoma cells grown in mouse xenografts. Bone marrow-derived mouse macrophages and peripheral blood-derived human macrophages were polarized in vitro toward M1 or M2 phenotypes and verified by flow cytometry. Primary human glioblastoma cell lines were offered as targets to mouse and human M1 or M2 polarized macrophages in vitro. The addition of an anti-CD47 monoclonal antibody led to enhanced tumor-cell phagocytosis by mouse and human M1 and M2 macrophages. In both cases, the anti-CD47-induced phagocytosis by M1 was more prominent than that for M2. Dissected tumors from human glioblastoma xenografted within NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ mice and treated with anti-CD47 showed a significant increase of M1 macrophages within the tumor. These data show that anti-CD47 treatment leads to enhanced tumor cell phagocytosis by both M1 and M2 macrophage subtypes with a higher phagocytosis rate by M1 macrophages. Furthermore, these data demonstrate that anti-CD47 treatment alone can shift the phenotype of macrophages toward the M1 subtype in vivo
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