We are analyzing https://link.springer.com/article/10.1007/s10555-007-9072-0.

Title:
Inflammatory cell infiltration of tumors: Jekyll or Hyde | Cancer and Metastasis Reviews
Description:
Inflammatory cell infiltration of tumors contributes either positively or negatively to tumor invasion, growth, metastasis, and patient outcomes, creating a Dr. Jekyll or Mr. Hyde conundrum when examining mechanisms of action. This is due to tumor heterogeneity and the diversity of the inflammatory cell phenotypes that infiltrate primary and metastatic lesions. Tumor infiltration by macrophages is generally associated with neoangiogenesis and negative outcomes, whereas dendritic cell (DC) infiltration is typically associated with a positive clinical outcome in association with their ability to present tumor antigens (Ags) and induce Ag-specific T cell responses. Myeloid-derived suppressor cells (MDSCs) also infiltrate tumors, inhibiting immune responses and facilitating tumor growth and metastasis. In contrast, T cell infiltration of tumors provides a positive prognostic surrogate, although subset analyses suggest that not all infiltrating T cells predict a positive outcome. In general, infiltration by CD8+ T cells predicts a positive outcome, while CD4+ cells predict a negative outcome. Therefore, the analysis of cellular phenotypes and potentially spatial distribution of infiltrating cells are critical for an accurate assessment of outcome. Similarly, cellular infiltration of metastatic foci is also a critical parameter for inducing therapeutic responses, as well as establishing tumor dormancy. Current strategies for cellular, gene, and molecular therapies are focused on the manipulation of infiltrating cellular populations. Within this review, we discuss the role of tumor infiltrating, myeloid-monocytic cells, and T lymphocytes, as well as their potential for tumor control, immunosuppression, and facilitation of metastasis.
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Keywords {🔍}

scholar, google, cas, pubmed, article, cancer, journal, cells, cell, dendritic, tumor, immunology, research, human, growth, macrophages, clinical, factor, macrophage, expression, interleukin, breast, carcinoma, immune, nature, angiogenesis, infiltration, tumors, melanoma, patients, medicine, myeloid, experimental, survival, prognostic, blood, metastasis, reviews, international, suppressor, role, endothelial, national, immunity, pathology, inflammatory, biology, vascular, inhibition, immunotherapy,

Topics {✒️}

granulocyte/macrophage colony-stimulating factor tcr/mhc-tumor peptide interactions balb/cbyj methylcholanthrene-induced sarcomas gm-csf-secreting melanoma vaccines lymphocyte-endothelial cell cross-talk cd11c+cd8alpha-cd11bhigh dendritic cells macrophage colony-stimulating factor tumour-induced dendritic-cell defects murine graft-versus-host disease tumor-infiltrating foxp3-cd4+cd25+ apoptosis-inducing agents gm-csf+tnf alpha month download article/chapter tumour necrosis factor-alpha antigen-specific t-cell responses myeloid-derived suppressor cells t-cell-derived cytokine reciprocal tumor-microenvironment interactions l-2-oxothiazolidine-4-carboxylic acid hypoxia-inducible factor-2 alpha cas google scholar monocyte-mediated tumoricidal activity endothelial cell-lymphocyte network pegylated g-csf augments c-x-c- chemokine low-dose gamma-interferon tumor-induced immune dysfunction c-erbb-2 transgenic balb/ tnf-alpha dependent intratumoral cytokines/chemokines/growth factors t-cell-dependent mechanism cc chemokine mcp-1/ccl2 tumour-infiltrating mononuclear cells flt3 ligand-treated mice endogenous tnf-alpha steroidal anti-inflammatory drugs plasmacytoid dendritic cells small-cell lung cancer long-term clinical follow surface marker-bearing cells hydrogen peroxide-induced cd3zeta vivo receptor-mediated delivery interleukin-12-encapsulated biodegradable microspheres ifn-gamma stimulation lymphokine-activated killer cells granulocyte chemotactic protein-2 il-1 beta-induced neovascularization cell-dependent tumor rejection cxc chemokine-mediated angiogenesis tcr zeta-chain downregulation

Questions {❓}

Effective immunotherapy against cancer: A question of overcoming immune suppression and immune escape?
Expression of costimulatory molecules B7-1 and B7-2 by macrophages along invasive margin of colon cancer: A possible antitumor immunity?
Intratumoral cytokines/chemokines/growth factors and tumor infiltrating dendritic cells: Friends or enemies?
Partial regression in primary carcinoma of the lung: Does it occur?
Tumors and inflammatory infiltrates: Friends or foes?

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         description:Inflammatory cell infiltration of tumors contributes either positively or negatively to tumor invasion, growth, metastasis, and patient outcomes, creating a Dr. Jekyll or Mr. Hyde conundrum when examining mechanisms of action. This is due to tumor heterogeneity and the diversity of the inflammatory cell phenotypes that infiltrate primary and metastatic lesions. Tumor infiltration by macrophages is generally associated with neoangiogenesis and negative outcomes, whereas dendritic cell (DC) infiltration is typically associated with a positive clinical outcome in association with their ability to present tumor antigens (Ags) and induce Ag-specific T cell responses. Myeloid-derived suppressor cells (MDSCs) also infiltrate tumors, inhibiting immune responses and facilitating tumor growth and metastasis. In contrast, T cell infiltration of tumors provides a positive prognostic surrogate, although subset analyses suggest that not all infiltrating T cells predict a positive outcome. In general, infiltration by CD8+ T cells predicts a positive outcome, while CD4+ cells predict a negative outcome. Therefore, the analysis of cellular phenotypes and potentially spatial distribution of infiltrating cells are critical for an accurate assessment of outcome. Similarly, cellular infiltration of metastatic foci is also a critical parameter for inducing therapeutic responses, as well as establishing tumor dormancy. Current strategies for cellular, gene, and molecular therapies are focused on the manipulation of infiltrating cellular populations. Within this review, we discuss the role of tumor infiltrating, myeloid-monocytic cells, and T lymphocytes, as well as their potential for tumor control, immunosuppression, and facilitation of metastasis.
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      headline:Inflammatory cell infiltration of tumors: Jekyll or Hyde
      description:Inflammatory cell infiltration of tumors contributes either positively or negatively to tumor invasion, growth, metastasis, and patient outcomes, creating a Dr. Jekyll or Mr. Hyde conundrum when examining mechanisms of action. This is due to tumor heterogeneity and the diversity of the inflammatory cell phenotypes that infiltrate primary and metastatic lesions. Tumor infiltration by macrophages is generally associated with neoangiogenesis and negative outcomes, whereas dendritic cell (DC) infiltration is typically associated with a positive clinical outcome in association with their ability to present tumor antigens (Ags) and induce Ag-specific T cell responses. Myeloid-derived suppressor cells (MDSCs) also infiltrate tumors, inhibiting immune responses and facilitating tumor growth and metastasis. In contrast, T cell infiltration of tumors provides a positive prognostic surrogate, although subset analyses suggest that not all infiltrating T cells predict a positive outcome. In general, infiltration by CD8+ T cells predicts a positive outcome, while CD4+ cells predict a negative outcome. Therefore, the analysis of cellular phenotypes and potentially spatial distribution of infiltrating cells are critical for an accurate assessment of outcome. Similarly, cellular infiltration of metastatic foci is also a critical parameter for inducing therapeutic responses, as well as establishing tumor dormancy. Current strategies for cellular, gene, and molecular therapies are focused on the manipulation of infiltrating cellular populations. Within this review, we discuss the role of tumor infiltrating, myeloid-monocytic cells, and T lymphocytes, as well as their potential for tumor control, immunosuppression, and facilitation of metastasis.
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