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      Inflammation and Cancer

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          Abstract

          Inflammation is often associated with the development and progression of cancer. The cells responsible for cancer-associated inflammation are genetically stable and thus are not subjected to rapid emergence of drug resistance; therefore, the targeting of inflammation represents an attractive strategy both for cancer prevention and for cancer therapy. Tumor-extrinsic inflammation is caused by many factors, including bacterial and viral infections, autoimmune diseases, obesity, tobacco smoking, asbestos exposure, and excessive alcohol consumption, all of which increase cancer risk and stimulate malignant progression. In contrast, cancer-intrinsic or cancer-elicited inflammation can be triggered by cancer-initiating mutations and can contribute to malignant progression through the recruitment and activation of inflammatory cells. Both extrinsic and intrinsic inflammations can result in immunosuppression, thereby providing a preferred background for tumor development. The current review provides a link between inflammation and cancer development.

          Résumé

          L’inflammation est souvent associée au développement et à la progression du cancer. Les cellules responsables de l’inflammation associée au cancer sont génétiquement stables et ne subissent donc pas l’émergence rapide d’une pharmacorésistance; par conséquent, le ciblage de l’inflammation représente une stratégie attrayante à la fois pour la prévention du cancer et pour le traitement du cancer. L’inflammation tumorale extrinsèque est causée par de nombreux facteurs, notamment: infections bactériennes et virales, maladies auto-immunes, obésité, tabagisme, exposition à l’amiante et consommation excessive d’alcool, le tout qui augmentent le risque de cancer et stimulent la progression maligne. En revanche, l’inflammation intrinsèque au cancer ou provoquée par le cancer peut être déclenchée par des mutations initiant un cancer et peuvent contribuer à la progression maligne par le recrutement et l’activation de cellules inflammatoires. Tous les deux les inflammations extrinsèques et intrinsèques peuvent entraîner une immunosuppression, fournissant ainsi un fond préféré pour le développement de la tumeur. le l’examen actuel établit un lien entre l’inflammation et le développement du cancer.

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          Inflammation and cancer.

          Recent data have expanded the concept that inflammation is a critical component of tumour progression. Many cancers arise from sites of infection, chronic irritation and inflammation. It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration. In addition, tumour cells have co-opted some of the signalling molecules of the innate immune system, such as selectins, chemokines and their receptors for invasion, migration and metastasis. These insights are fostering new anti-inflammatory therapeutic approaches to cancer development.
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            Cancer-related inflammation.

            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 proliferation and survival of malignant cells, promotes angiogenesis and metastasis, subverts adaptive immune responses, and alters responses to hormones and chemotherapeutic agents. The molecular pathways of this cancer-related inflammation are now being unravelled, resulting in the identification of new target molecules that could lead to improved diagnosis and treatment.
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              Inflammation and cancer: back to Virchow?

              The response of the body to a cancer is not a unique mechanism but has many parallels with inflammation and wound healing. This article reviews the links between cancer and inflammation and discusses the implications of these links for cancer prevention and treatment. We suggest that the inflammatory cells and cytokines found in tumours are more likely to contribute to tumour growth, progression, and immunosuppression than they are to mount an effective host antitumour response. Moreover cancer susceptibility and severity may be associated with functional polymorphisms of inflammatory cytokine genes, and deletion or inhibition of inflammatory cytokines inhibits development of experimental cancer. If genetic damage is the "match that lights the fire" of cancer, some types of inflammation may provide the "fuel that feeds the flames". Over the past ten years information about the cytokine and chemokine network has led to development of a range of cytokine/chemokine antagonists targeted at inflammatory and allergic diseases. The first of these to enter the clinic, tumour necrosis factor antagonists, have shown encouraging efficacy. In this article we have provided a rationale for the use of cytokine and chemokine blockade, and further investigation of non-steroidal anti-inflammatory drugs, in the chemoprevention and treatment of malignant diseases.
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                Author and article information

                Journal
                Ann Afr Med
                Ann Afr Med
                AAM
                Annals of African Medicine
                Wolters Kluwer - Medknow (India )
                1596-3519
                0975-5764
                Jul-Sep 2019
                : 18
                : 3
                : 121-126
                Affiliations
                [1]Department of Pedodontics and Preventive Dentistry, Chandra Dental College and Hospital, Safedabad, Barabanki, Uttar Pradesh, India
                [1 ]Department of Conservative and Endodontics, P.S.M Dental College and Research Centre, Akkikavu, Thrissur, Kerala, India
                [2 ]Department of Oral Pathology and Microbiology, Hi-Tech Dental College and Hospital, Bhubaneswar, Odisha, India
                [3 ]Department of Oral and Maxillofacial Surgery, School of Dental Sciences, Krishna Institute of Health Sciences Deemed to be University, Karad, Maharashtra, India
                [4 ]Department of Oral Pathology and Microbiology, Tatyasaheb Kore Dental College and Research Centre, New Pargaon, Kolhapur, Maharashtra, India
                [5 ]Department of Oral Medicine and Radiology, Tatyasaheb Kore Dental College and Research Centre, New Pargaon, Kolhapur, Maharashtra, India
                Author notes
                Address for correspondence: Dr. Nitin Singh, Chandra Dental College and Hospital, Safedabad, Barabanki, UP, India. E-mail: drsinghnitin@ 123456gmail.com
                Article
                AAM-18-121
                10.4103/aam.aam_56_18
                6704802
                31417011
                d6d3cc7b-9870-4481-b20c-ade4833d7a60
                Copyright: © 2019 Annals of African Medicine

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

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                Categories
                Review Article

                cancer,cells,inflammation,cellules
                cancer, cells, inflammation, cellules

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