We are analyzing https://link.springer.com/article/10.1186/2045-824x-5-20.

Title:
The role of tumor-associated macrophages in tumor vascularization | Vascular Cell
Description:
Tumor vascularization is a highly complex process that involves the interaction between tumors and their surrounding stroma, as well as many distinct angiogenesis-regulating factors. Tumor associated macrophages (TAMs) represent one of the most abundant cell components in the tumor environment and key contributors to cancer-related inflammation. A large body of evidence supports the notion that TAMs play a critical role in promoting the formation of an abnormal tumor vascular network and subsequent tumor progression and invasion. Clinical and experimental evidence has shown that high levels of infiltrating TAMs are associated with poor patient prognosis and tumor resistance to therapies. In addition to stimulating angiogenesis during tumor growth, TAMs enhance tumor revascularization in response to cytotoxic therapy (e.g., radiotherapy), thereby causing cancer relapse. In this review, we highlight the emerging data related to the phenotype and polarization of TAMs in the tumor microenvironment, as well as the underlying mechanisms of macrophage function in the regulation of the angiogenic switch and tumor vascularization. Additionally, we discuss the potential of targeting pro-angiogenic TAMs, or reprograming TAMs toward a tumoricidal and angiostatic phenotype, to promote normalization of the tumor vasculature to enhance the outcome of cancer therapies.
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Keywords {🔍}

pubmed, tumor, article, scholar, google, cas, cancer, tams, cells, macrophages, angiogenesis, tumors, growth, central, cell, myeloid, factor, human, macrophage, blood, proangiogenic, vascularization, phenotype, expression, tumorassociated, res, progression, role, polarization, tam, mice, factors, tme, angiogenic, monocytes, vegf, vascular, mammary, recruitment, promote, signaling, antiangiogenic, endothelial, mouse, mlike, vessel, stat, breast, receptor, nat,

Topics {✒️}

peroxisome proliferator-activated receptor-gamma fisher & xiang-yang wang enhanced pro-angiogenic/tissue-remodeling activity colony-stimulating factor-1 blockade tumor-infiltrating tie2-expressing monocytes hypoxia-inducible factor-1α article download pdf macrophage-colony stimulating factor tumor-targeted interferon-alpha delivery dna-damaging agent approved myeloid-derived suppressor cells ets2-driven transcriptional program transforming growth factor-β hif-1alpha regulates function interferon gamma-dependent induction anti-plgf inhibits growth stromal cell-derived factor-1 heparin-binding plasma protein th1 cytokine ifn-α hif-1α-dependent angiogenesis bcl-xl-dependent mechanism heme oxygenase-1-expressing macrophages thymidine phosphorylase-positive macrophages xiang-yang wang pro-angiogenic growth factors tumor-secreted soluble factors tumor cell-derived factors tumor-infiltrating myeloid cells il6-stat3-hif signaling open access license alternative pro-angiogenic programs proangiogenic tie2-expressing monocytes provoke anti-tumor responses anti-angiogenic therapies interfering hypo-perfused tumor vasculature mmtv-pymt mammary carcinomas stat3-dependent transcriptional suppression enhanced irf-3/stat1 activation high-density vessel network pro-angiogenic myeloid cells tam-related myeloid cells macrophage-induced tumor angiogenesis bm-derived myeloid cells platelet activating factor pro-angiogenic enzyme expressed monocyte/macrophage cell population tie2-expressing macrophages limit mmtv-pymt mice documented endothelial cell apoptosis small molecule inhibitor

Questions {❓}

De Bock K, Cauwenberghs S, Carmeliet P: Vessel abnormalization: another hallmark of cancer?
Fischer C, Mazzone M, Jonckx B, Carmeliet P: FLT1 and its ligands VEGFB and PlGF: drug targets for anti-angiogenic therapy?

Schema {🗺️}

WebPage:
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         headline:The role of tumor-associated macrophages in tumor vascularization
         description:Tumor vascularization is a highly complex process that involves the interaction between tumors and their surrounding stroma, as well as many distinct angiogenesis-regulating factors. Tumor associated macrophages (TAMs) represent one of the most abundant cell components in the tumor environment and key contributors to cancer-related inflammation. A large body of evidence supports the notion that TAMs play a critical role in promoting the formation of an abnormal tumor vascular network and subsequent tumor progression and invasion. Clinical and experimental evidence has shown that high levels of infiltrating TAMs are associated with poor patient prognosis and tumor resistance to therapies. In addition to stimulating angiogenesis during tumor growth, TAMs enhance tumor revascularization in response to cytotoxic therapy (e.g., radiotherapy), thereby causing cancer relapse. In this review, we highlight the emerging data related to the phenotype and polarization of TAMs in the tumor microenvironment, as well as the underlying mechanisms of macrophage function in the regulation of the angiogenic switch and tumor vascularization. Additionally, we discuss the potential of targeting pro-angiogenic TAMs, or reprograming TAMs toward a tumoricidal and angiostatic phenotype, to promote normalization of the tumor vasculature to enhance the outcome of cancer therapies.
         datePublished:2013-12-06T00:00:00Z
         dateModified:2013-12-06T00:00:00Z
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            Tumor vascularization
            Tumor-associated macrophages
            Angiology
            Cardiology
            Cancer Research
            Cell Biology
            Developmental Biology
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      headline:The role of tumor-associated macrophages in tumor vascularization
      description:Tumor vascularization is a highly complex process that involves the interaction between tumors and their surrounding stroma, as well as many distinct angiogenesis-regulating factors. Tumor associated macrophages (TAMs) represent one of the most abundant cell components in the tumor environment and key contributors to cancer-related inflammation. A large body of evidence supports the notion that TAMs play a critical role in promoting the formation of an abnormal tumor vascular network and subsequent tumor progression and invasion. Clinical and experimental evidence has shown that high levels of infiltrating TAMs are associated with poor patient prognosis and tumor resistance to therapies. In addition to stimulating angiogenesis during tumor growth, TAMs enhance tumor revascularization in response to cytotoxic therapy (e.g., radiotherapy), thereby causing cancer relapse. In this review, we highlight the emerging data related to the phenotype and polarization of TAMs in the tumor microenvironment, as well as the underlying mechanisms of macrophage function in the regulation of the angiogenic switch and tumor vascularization. Additionally, we discuss the potential of targeting pro-angiogenic TAMs, or reprograming TAMs toward a tumoricidal and angiostatic phenotype, to promote normalization of the tumor vasculature to enhance the outcome of cancer therapies.
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         Tumor vascularization
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         Cancer Research
         Cell Biology
         Developmental Biology
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      name:VCU Massey Cancer Center, Virginia Commonwealth University School of Medicine, Richmond, USA
      name:Department of Human & Molecular Genetics, Virginia Commonwealth University School of Medicine, Richmond, USA
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      name:VCU Massey Cancer Center, Virginia Commonwealth University School of Medicine, Richmond, USA
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      name:VCU Institute of Molecular Medicine, Virginia Commonwealth University School of Medicine, Richmond, USA
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