Why does chronic inflammation cause cancer

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Language: English French. 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.

The presence of leukocytes within tumors, observed in the 19 th century by Rudolf Virchow, provided the first indication of a possible link between inflammation and cancer. Yet, it is only during the past decade that clear evidence has been obtained that inflammation plays a critical role in tumorigenesis.

However, when inflammation becomes chronic or lasts too long, it can prove harmful and may lead to disease. The role of pro-inflammatory cytokines, chemokines, adhesion molecules, and inflammatory enzymes has been linked with chronic inflammation [ Figure 1 ]. Chronic inflammation has been found to mediate a wide variety of diseases, including cardiovascular diseases, cancer, diabetes, arthritis, Alzheimer's disease, pulmonary diseases, and autoimmune diseases.

The current review, however, will be restricted to the role of chronic inflammation in cancer. Chronic inflammation has been linked to various steps involved in tumorgenesis, including cellular transformation, promotion, survival, proliferation, invasion, angiogenesis, and metastasis.

Many environmental causes of cancer and risk factors are associated with some form of chronic inflammation. Recent efforts have shed new light on molecular and cellular circuits linking inflammation and cancer. Two pathways have been schematically identified: in the intrinsic pathway, genetic events causing neoplasia initiate the expression of inflammation-related programs that guide the construction of an inflammatory microenvironment, and in the extrinsic pathway, inflammatory conditions facilitate cancer development.

The triggers of chronic inflammation that increase cancer risk or progression include infections e. Cancer-related inflammation, the seventh hallmark of cancer, links to genetic instability. It was in that Rudolf Virchow noted leukocytes in neoplastic tissues and made a connection between inflammation and cancer.

Over the past 10 years, our understanding of the inflammatory microenvironment of malignant tissues has supported Virchow's hypothesis, and the links between cancer and inflammation are starting to have implications for prevention and treatment.

Inflammation is the body's response to tissue damage, caused by physical injury, ischemic injury caused by an insufficient supply of blood to an organ , infection, exposure to toxins, or other types of trauma. The body's inflammatory response causes cellular changes and immune responses that result in repair of the damaged tissue and cellular proliferation growth at the site of the injured tissue. Inflammation can become chronic if the cause of the inflammation persists or certain control mechanisms in charge of shutting down the process fail.

When these inflammatory responses become chronic, cell mutation and proliferation can result, often creating an environment that is conducive to the development of cancer. This is true for the onset of cancer but also even more important for the advancement of the disease.

Various signaling pathways are key contributors in creating epigenetic changes on the outside of the cell, switching on these internal mutations. Therefore, treating the inflammatory causes is always important.

Chronic inflammation has been linked to various steps involved in tumorigenesis, including cellular transformation, promotion, survival, proliferation, invasion, angiogenesis, and metastasis. Cancer defines malignant neoplasms characterized by metastatic growth. It may occur in almost every organ and tissue relating to a variety of etiologic factors, such as genomic instability and environmental stress.

However, cancer development is still accepted as a multistep process, during which genetic alterations confer specific types of growth advantages; therefore, it drives the progressive transformation from normal cells to malignant cancer cells. Malignant growth is characterized by several key changes: self-sufficiency of growth signals, insensitivity to antigrowth signals, escaping from apoptosis, unregulated proliferation potential, enhanced angiogenesis, and metastasis.

Each of these shifts is complicated and accomplished by combined efforts of various signaling processes. In later discussion, we will find that inflammation may contribute to the formation of these cancer phenotypes. Chronic inflammation is characterized by sustained tissue damage, damage-induced cellular proliferation, and tissue repair.

The chronic inflammatory microenvironment is predominated by macrophages. Those macrophages, together with other leukocytes, generate high levels of reactive oxygen and nitrogen species to fight infection. They may produce mutagenic agents, such as peroxynitrite, which react with DNA and cause mutations in proliferating epithelial and stroma cells.

Migration inhibitory factor impairs pdependent protective responses, thus causing the accumulation of oncogenic mutations. Migration inhibitory factor also contributes to tumorigenesis by interfering Rb-E2F pathway. The bacterium H. The multistep pathogenesis of gastric cancer is the best highlighted by Correa sequence that explains the progressive pathway to gastric cancer characterized by distinct histological changes.

This model predicts that infection with H. This is followed by intestinal metaplasia which can be further classified into complete and incomplete subtypes. At this point, some patients will then proceed to gastric cancer via the intermediate stage of dysplasia [ Figure 2 ]. The improvement or elimination of atrophy and intestinal metaplasia with H. It is noteworthy to mention that gastric cancer can still develop even after successful eradication therapy. The inflammatory microenvironment of tumors is characterized by the presence of host leukocytes both in the supporting stroma and in tumor areas.

Tumor-associated macrophages TAM are a major component of the infiltrate of most, if not all tumors. TAM derives from circulating monocytic precursors and is directed into the tumor by chemoattractant cytokines called chemokines. Many tumor cells also produce cytokines called colony-stimulating factors that prolong the survival of TAM. When appropriately activated, TAM can kill tumor cells or elicit tissue destructive reactions centered on the vascular endothelium.

However, TAM also produces growth and angiogenic factors as well as protease enzymes which degrade the extracellular matrix. Hence, TAM can stimulate tumor cell proliferation, promote angiogenesis, and favor invasion and metastasis.

Dendritic cells have a crucial role in both the activation of antigen-specific immunity and the maintenance of tolerance, providing a link between innate and adaptive immunity. Tumor-associated dendritic cells TADCs usually have an immature phenotype with defective ability to stimulate T-cells. The immaturity of TADC may reflect lack of effective maturation signals, prompt migration of mature cells to lymph nodes, or the presence of maturation inhibitors.

TADC is likely to be poor inducers of effective responses to tumor antigens. Natural killer cells are rare in the tumor microenvironment. The cytokine profile of these tumor-infiltrating T-cells has not been studied systematically, but in some tumors e. Kaposi's sarcoma, Hodgkin's disease, bronchial carcinoma, and cervical carcinoma , they produce mainly interleukins ILs 4 and 5 and not interferon.

View All Events. Previous Next. Chronic inflammatory conditions associated with new or abnormal growth of tissue Pathologic condition Associated cancer Cause Asbestosis; silicosis Mesothelioma; lung carcinoma Asbestos fibers; silica particles Bronchitis Lung carcinoma Silica; asbestos; smoking Gingivitis; lichen planus Oral SCC Inflammatory bowel disease Colorectal carcinoma Skin inflammation Melanoma UV light For more comprehensive chart with more inflammatory causes.

About the Author: Morag. Morag Currin is a highly sought-after esthetic educator with more than 23 years of spa industry experience and more than eight years of training and training management experience.

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