Literature DB >> 17476345

Altered macrophage differentiation and immune dysfunction in tumor development.

Antonio Sica1, Vincenzo Bronte.   

Abstract

Tumors require a constant influx of myelomonocytic cells to support the angiogenesis and stroma remodeling needed for their growth. This is mediated by tumor-derived factors, which cause sustained myelopoiesis and the accumulation and functional differentiation of myelomonocytic cells, most of which are macrophages, at the tumor site. An important side effect of the accumulation and functional differentiation of these cells is that they can induce lymphocyte dysfunction. A complete understanding of the complex interplay between neoplastic and myelomonocytic cells might offer novel targets for therapeutic intervention aimed at depriving tumor cells of important growth support and enhancing the antitumor immune response.

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Year:  2007        PMID: 17476345      PMCID: PMC1857267          DOI: 10.1172/JCI31422

Source DB:  PubMed          Journal:  J Clin Invest        ISSN: 0021-9738            Impact factor:   14.808


  124 in total

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Review 3.  The IFN gamma receptor: a paradigm for cytokine receptor signaling.

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4.  Alternative metabolic states in murine macrophages reflected by the nitric oxide synthase/arginase balance: competitive regulation by CD4+ T cells correlates with Th1/Th2 phenotype.

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Journal:  Proc Natl Acad Sci U S A       Date:  1998-06-23       Impact factor: 11.205

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Journal:  J Immunol       Date:  1995-08-15       Impact factor: 5.422

10.  A hypoxia-responsive element mediates a novel pathway of activation of the inducible nitric oxide synthase promoter.

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Journal:  J Exp Med       Date:  1995-12-01       Impact factor: 14.307

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  479 in total

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Review 7.  Pancreatic ductal adenocarcinoma: a review of immunologic aspects.

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8.  Absence of host NF-κB p50 induces murine glioblastoma tumor regression, increases survival, and decreases T-cell induction of tumor-associated macrophage M2 polarization.

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Review 9.  Regulation of macrophage function in tumors: the multifaceted role of NF-kappaB.

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