We are analyzing https://link.springer.com/article/10.1186/s13045-019-0760-3.

Title:
Tumor-associated macrophages in tumor metastasis: biological roles and clinical therapeutic applications | Journal of Hematology & Oncology
Description:
Tumor metastasis is a major contributor to the death of cancer patients. It is driven not only by the intrinsic alterations in tumor cells, but also by the implicated cross-talk between cancer cells and their altered microenvironment components. Tumor-associated macrophages (TAMs) are the key cells that create an immunosuppressive tumor microenvironment (TME) by producing cytokines, chemokines, growth factors, and triggering the inhibitory immune checkpoint proteins release in T cells. In doing so, TAMs exhibit important functions in facilitating a metastatic cascade of cancer cells and, meanwhile, provide multiple targets of certain checkpoint blockade immunotherapies for opposing tumor progression. In this article, we summarize the regulating networks of TAM polarization and the mechanisms underlying TAM-facilitated metastasis. Based on the overview of current experimental evidence dissecting the critical roles of TAMs in tumor metastasis, we discuss and prospect the potential applications of TAM-focused therapeutic strategies in clinical cancer treatment at present and in the future.
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28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

pubmed, article, google, scholar, tumor, cancer, cas, macrophages, metastasis, cells, tams, central, macrophage, cell, clinical, polarization, tumorassociated, growth, targeting, progression, breast, patients, receptor, tme, expression, res, wang, survival, tumors, oncol, immune, factor, angiogenesis, therapy, csf, microenvironment, mechanisms, ccl, chen, phenotype, immunol, therapeutic, regulation, signaling, zhang, factors, tam, agents, fig, study,

Topics {✒️}

tgf-beta-induced epithelial-mesenchymal transition tnf alpha-tnfr1-macrophage axis anti-csf-1r antibody reveals article download pdf macrophage colony-stimulating factor-1 colony-stimulating factor-1 receptor csf-1/csf-1r signaling axis tnf-related apoptosis-inducing ligand csf-1r-positive tam accumulation tumour-induced systemic environment tissue factor-mediated coagulation mitogen-activated protein kinase myeloid-derived suppressor cells innate anti-phagocytic axis cd47/sirp alpha axis egfr/akt/creb pathway treating skeletal-related events dictate organ-specific dissemination integrin-linked kinase activity sustained anti-tumor activities facilitate breast-tumour metastasis van der touw pro-inflammatory cytokines derived signal-regulatory protein alpha monocyte-dendritic cell progenitors pro-tumoral profile tam-targeted therapeutic solutions adenoma-linked barrier defects proangiogenic tie2-expressing monocytes tumor antigen-presenting behaviors early-stage breast cancer natural killer cell-dependent play multi-functional roles tumor cell-favoring direction tam-focused therapeutic strategies m2 macrophage-targeting peptide colony-stimulating factor-1 establishing pre-metastatic niches c-kit-mutated melanoma transforming growth factor-β inflammation-induced cell migration potential anti-cancer approaches median progression-free survival csf-1r expressing tams agonist monoclonal antibody impairing pro-tumoral functions pge2-elicited macrophage infiltration anti-ccl2 mab carlumab tissue-resident macrophage stem epithelial-mesenchymal transition

Questions {❓}

Is CD47 an innate immune checkpoint for tumor evasion?
Therefore, there arises the tip of a far larger iceberg: what histology types or what cellular and molecular features in TME would benefit from TAM-targeted therapy?
Trabectedin mechanism of action: what’s new?

Schema {🗺️}

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         headline:Tumor-associated macrophages in tumor metastasis: biological roles and clinical therapeutic applications
         description:Tumor metastasis is a major contributor to the death of cancer patients. It is driven not only by the intrinsic alterations in tumor cells, but also by the implicated cross-talk between cancer cells and their altered microenvironment components. Tumor-associated macrophages (TAMs) are the key cells that create an immunosuppressive tumor microenvironment (TME) by producing cytokines, chemokines, growth factors, and triggering the inhibitory immune checkpoint proteins release in T cells. In doing so, TAMs exhibit important functions in facilitating a metastatic cascade of cancer cells and, meanwhile, provide multiple targets of certain checkpoint blockade immunotherapies for opposing tumor progression. In this article, we summarize the regulating networks of TAM polarization and the mechanisms underlying TAM-facilitated metastasis. Based on the overview of current experimental evidence dissecting the critical roles of TAMs in tumor metastasis, we discuss and prospect the potential applications of TAM-focused therapeutic strategies in clinical cancer treatment at present and in the future.
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      headline:Tumor-associated macrophages in tumor metastasis: biological roles and clinical therapeutic applications
      description:Tumor metastasis is a major contributor to the death of cancer patients. It is driven not only by the intrinsic alterations in tumor cells, but also by the implicated cross-talk between cancer cells and their altered microenvironment components. Tumor-associated macrophages (TAMs) are the key cells that create an immunosuppressive tumor microenvironment (TME) by producing cytokines, chemokines, growth factors, and triggering the inhibitory immune checkpoint proteins release in T cells. In doing so, TAMs exhibit important functions in facilitating a metastatic cascade of cancer cells and, meanwhile, provide multiple targets of certain checkpoint blockade immunotherapies for opposing tumor progression. In this article, we summarize the regulating networks of TAM polarization and the mechanisms underlying TAM-facilitated metastasis. Based on the overview of current experimental evidence dissecting the critical roles of TAMs in tumor metastasis, we discuss and prospect the potential applications of TAM-focused therapeutic strategies in clinical cancer treatment at present and in the future.
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