We are analyzing https://link.springer.com/article/10.1007/s10875-012-9847-0.

Title:
Cancer-Related Inflammation | Journal of Clinical Immunology
Description:
Solid tumors consist of neoplastic cells, non-malignant stromal cells, and migratory hematopoietic cells. Complex interactions between the cell types in this microenvironment regulate tumor growth, progression, metastasis, and angiogenesis. The cells and mediators of inflammation form a major part of the epithelial tumor microenvironment. In some cancers, inflammatory conditions precede development of malignancy; in others, oncogenic change drives a tumor-promoting inflammatory milieu. Whatever its origin, this “smoldering” inflammation aids proliferation and survival of malignant cells, stimulates angiogenesis and metastasis, subverts adaptive immunity, and alters response to hormones and chemotherapy. Cytokines are major mediators of communication between cells in the inflammatory tumor microenvironment. It is known that neoplastic cells often over-express proinflammatory mediators including proteases, eicosanoids, cytokines, and chemokines. Several cytokines such as macrophage migratory inhibitory factor (MIF), TNF-α, IL-6, IL-17, IL-12, IL-23, IL-10, and TGF-β have been linked with both experimental and human cancers and can either promote or inhibit tumor development. MIF is a major cytokine in many cancers and there is evidence that the cytokine is produced by both malignant cells and infiltrating leukocytes. In this article we will discuss the role of cancer-associated inflammation and the particular role of MIF in malignant disease.
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Keywords {🔍}

google, scholar, article, pubmed, cas, cancer, factor, tumor, cells, cell, macrophage, inhibitory, migration, inflammation, necrosis, balkwill, growth, cytokine, ovarian, receptor, res, inflammatory, mif, human, med, immunol, clin, metastasis, hagemann, cytokines, nature, chemokine, promotes, interleukin, wilson, development, role, rev, pancreatic, nat, mice, expression, progression, epithelial, malignant, tumour, exp, macrophages, wang, metz,

Topics {✒️}

month download article/chapter tumor necrosis factor-alpha tumour necrosis factor autocrine tumor-promoting network colony-stimulating factor-1 pathway tumor growth-promoting response tnf-alpha receptor subtypes tnf-alpha involve tnfr1 tumor-promoting inflammatory milieu cytokine-driven compensatory proliferation bone marrow-derived cells smac-mimetic-induced apoptosis tumor-induced immune dysfunction tumor necrosis factor tumor necrosis factor oncogenic ras-induced secretion il-6-stat3 signaling pathway cell-free substances formed lymphoid cell-antigen interaction adenoma-linked barrier defects myd88-dependent il-6 production nf-kappab-dependent pathway reduced tumor growth /ebp beta-deficient mice chemokine receptor expression full article pdf promote tumor growth clinical immunology aims cell-derived il-6 epithelial tumor cells th2 cytokine interleukin-13 epithelial tumor microenvironment inflammatory tumor microenvironment blocking tnf-alpha tnf-alpha inhibitor asbestos-induced oncogenesis cytokine expression profile p53-dependent effects privacy choices/manage cookies article candido promotes chemical hepatocarcinogenesis tumor-promoting actions cxc chemokine receptors inhibit tumor development ovarian cancer therapy thorsten hagemann solid ovarian tumours il-10-activated macrophages independent prognostic factor glucocorticoid-induced modulator

Questions {❓}

Epithelial cancer cell migration: a role for chemokine receptors?
Inflammation and cancer: back to Virchow?

Schema {🗺️}

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         description:Solid tumors consist of neoplastic cells, non-malignant stromal cells, and migratory hematopoietic cells. Complex interactions between the cell types in this microenvironment regulate tumor growth, progression, metastasis, and angiogenesis. The cells and mediators of inflammation form a major part of the epithelial tumor microenvironment. In some cancers, inflammatory conditions precede development of malignancy; in others, oncogenic change drives a tumor-promoting inflammatory milieu. Whatever its origin, this “smoldering” inflammation aids proliferation and survival of malignant cells, stimulates angiogenesis and metastasis, subverts adaptive immunity, and alters response to hormones and chemotherapy. Cytokines are major mediators of communication between cells in the inflammatory tumor microenvironment. It is known that neoplastic cells often over-express proinflammatory mediators including proteases, eicosanoids, cytokines, and chemokines. Several cytokines such as macrophage migratory inhibitory factor (MIF), TNF-α, IL-6, IL-17, IL-12, IL-23, IL-10, and TGF-β have been linked with both experimental and human cancers and can either promote or inhibit tumor development. MIF is a major cytokine in many cancers and there is evidence that the cytokine is produced by both malignant cells and infiltrating leukocytes. In this article we will discuss the role of cancer-associated inflammation and the particular role of MIF in malignant disease.
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