Cancer-related inflammation

  title={Cancer-related inflammation},
  author={Alberto Mantovani and Paola Allavena and Antonio Sica and Frances R. Balkwill},
The mediators and cellular effectors of inflammation are important constituents of the local environment of tumours. In some types of cancer, inflammatory conditions are present before a malignant change occurs. Conversely, in other types of cancer, an oncogenic change induces an inflammatory microenvironment that promotes the development of tumours. Regardless of its origin, 'smouldering' inflammation in the tumour microenvironment has many tumour-promoting effects. It aids in the… 

Molecular pathways and targets in cancer-related inflammation

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Inflammation as target in cancer therapy.

Chronic inflammation, the tumor microenvironment and carcinogenesis.

The proposed mechanisms that lead to the recruitment of bone marrow derived cells are summarized, and the genetic and epigenetic alterations that may occur in inflammation associated cancers are explored.

Chronic inflammation, the tumor microenvironment and carcinogenesis

The proposed mechanisms that lead to the recruitment of bone marrow derived cells are summarized, and the genetic and epigenetic alterations that may occur in inflammation associated cancers are explored.

Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability.

This work surmises that CRI represents the seventh hallmark of cancer, and suggests that an additional mechanism involved in cancer-related inflammation (CRI) is induction of genetic instability by inflammatory mediators, leading to accumulation of random genetic alterations in cancer cells.

Molecular Determinants of Cancer-Related Inflammation

Tumor cells communicate with the cells of their microenvironment via a series of molecular and cellular interactions to aid their progression to a malignant state and ultimately their metastatic

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Cancer Inflammation and Cytokines.

Tumor-associated macrophages and TANs are both integrated in cancer-related inflammation and an ever better understanding of their functions can be useful to tailor the use of anticancer therapeutic approaches and patient follow-up.

Cellular and molecular pathways linking inflammation and cancer.

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Examples of how inflammation may lead to cancer formation include enhanced proliferation of initiated cells, through resistance to apoptosis, induction of genomic instability, alterations in epigenetic events and subsequent inappropriate gene expression, abnormal tumor neovascularization or angiogenesis, and the promotion of metastasis among others.



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It is shown that IL-23 is an important molecular link between tumour-promoting pro-inflammatory processes and the failure of the adaptive immune surveillance to infiltrate tumours.

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Signal transducer and activator of transcription 3 (STAT3) propagates several levels of crosstalk between tumour cells and their immunological microenvironment, leading to tumour-induced immunosuppression and has emerged as a promising target for cancer immunotherapy.

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The immune system itself represents a major pharmaceutical target and links angiogenesis inhibition to immunotherapy, and it is found that neutrophils, myeloid-derived suppressor and dendritic cells clearly have the potential for influencing tumorAngiogenesis.

NF-κB functions as a tumour promoter in inflammation-associated cancer

It is shown that the inflammatory process triggers hepatocyte NF-κB through upregulation of tumour-necrosis factor-α (TNFα) in adjacent endothelial and inflammatory cells, and is therefore a potential target for cancer prevention in chronic inflammatory diseases.

Cancer and the chemokine network

Insight is provided into host–tumour interactions, such as the role of the leukocyte infiltrate, and into the mechanisms that determine the metastatic potential and site-specific spread of cancer cells.