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Macrophage-based immunotherapy for the treatment of pancreatic ductal adenocarcinoma

Article: e26837 | Received 10 Oct 2013, Accepted 16 Oct 2013, Published online: 22 Oct 2013

Figures & data

Figure 1. Re-directing the phenotype of tumor-infiltrating macrophages induces the regression of pancreatic adenocarcinoma lesions. Peripheral blood monocytes are routinely recruited to neoplastic lesions, where they can support tumor growth and development. The systemic administration of an agonist CD40 antibody shifts the phenotype of tumor-infiltrating macrophages from pro-tumor to anti-tumor. Anti-tumor macrophages induce the regression of some malignant lesions by eliminating cancer cells and degrading the extracellular matrix (ECM) that generally surrounds tumors. Tumor response is associated with changes in glucose metabolism as measured by [18F]-fluorodeoxyglucose (FDG) uptake detected on positron emission tomography/CT (PET/CT) imaging.

Figure 1. Re-directing the phenotype of tumor-infiltrating macrophages induces the regression of pancreatic adenocarcinoma lesions. Peripheral blood monocytes are routinely recruited to neoplastic lesions, where they can support tumor growth and development. The systemic administration of an agonist CD40 antibody shifts the phenotype of tumor-infiltrating macrophages from pro-tumor to anti-tumor. Anti-tumor macrophages induce the regression of some malignant lesions by eliminating cancer cells and degrading the extracellular matrix (ECM) that generally surrounds tumors. Tumor response is associated with changes in glucose metabolism as measured by [18F]-fluorodeoxyglucose (FDG) uptake detected on positron emission tomography/CT (PET/CT) imaging.