Inflammation-related carcinogenesis: current findings in epidemiological trends, causes and mechanisms

Our plain-English summary of Inflammation-related carcinogenesis: current findings in epidemiological trends, causes and mechanisms, by F. Okada (Yonago Acta Medica, 2014).

The study

• Author: F. Okada
• Journal: Yonago Acta Medica
• Published: 2014;57(2):65-72
• Type of article: Review
• Cited by: 98 articles, as counted by NIH iCite
• Read it: PubMed · Free full text

Abstract

Inflammation is a definite cancer-causing factor as revealed by cumulative basic, clinical and epidemiological studies. It is mostly induced by infectious agents. For instance, infection with papillomaviruses associates with anogenital cancers, especially cervical cancers; Helicobacter pylori infection of the stomach tends to increase the risk of stomach cancer; chronic hepatitis B & C viruses and fluke infections of the liver increase liver cancers; autoimmune diseases, e.g., inflammatory bowel diseases, associate with development of colorectal cancer, and aerial irritants (foreign bodies) such as asbestos or fine particulate matter (PM2.5) in outdoor air increase malignant pleural mesotheliomas or lung cancers. These are typical examples of inflammation-related carcinogenesis. It is apparent that the pathogens to induce inflammatory reactions in specific organs are not related to each other. However, the underlying pathogenesis in common is to induce and/or sustain inflammation. In this article, I would like to review the up-to-date findings of epidemiological trends, causes and mechanisms of inflammation-related carcinogenesis.

In plain English

This was a narrative review by a single author at Tottori University, Japan, about cancers linked to inflammation. It did not study any group of asbestos-exposed people. The author cited estimates that infection or inflammation accounted for around 25% of cancer deaths in sub-Saharan Africa and around 6% in Europe excluding eastern Europe. A table, based on International Agency for Research on Cancer classifications and on experimental and clinical reports, listed asbestos as a definite cause of inflammation-related cancer of the lung, lung mesothelium, larynx and ovary. It listed asbestos as a presumed cause for the pharynx, stomach, and colon and rectum. No fiber types or exposure data were given. Most of the article described the author's group's earlier mouse experiments. In them, cells that did not normally form tumors became lethal tumors when placed in an inflammation-causing gelatin sponge. Removing neutrophils, or using mice lacking the gp91phox gene, reduced this. The author concluded that inflammation, especially chronic inflammation, is a definite cause of tumor development. The author noted that the sponge model causes acute, not chronic, inflammation.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Narrative review, including a summary of the author's group's previously published mouse experiments
• Who was studied: No human study population. The review drew on published global cancer estimates. The experimental work summarized used regressive mouse fibrosarcoma cells (QR cells) implanted in normal syngeneic C57BL/6 mice, plus knockout mice.
• Exposure: In the mouse model, foreign bodies (hemostasis gelatin sponge, plastic plate) were used to cause inflammation. Asbestos appears only as an entry in a table of agents; no fiber type, product or dose is given.
• Main results:
  • Citing other sources, the review reported that the share of cancer deaths due to infection/inflammation was around 25% in sub-Saharan Africa and around 6% in Europe. Figure 1 states that this Europe figure excludes eastern Europe.
  • Table 1 listed asbestos as definitely carcinogenic for inflammation-related cancer of the lung mesothelium, with silicosis listed as presumably carcinogenic. It also listed asbestos as definite for the lung, larynx and ovary, and as presumed for the pharynx, stomach, and colon and rectum.
  • Table 1 listed asbestos as definitely carcinogenic for the ovary
  • In the author's mouse model, mice given an anti-neutrophil antibody (RB6) developed tumors that did not acquire malignant phenotypes
  • Tumor development from QR cells co-implanted with gelatin sponge was less frequent in gp91phox gene-knockout mice
  • In the mouse model, an orally active superoxide dismutase (oxykine) significantly decreased tumor formation compared with control vehicle
• The authors' conclusion: The author concluded that inflammation, especially chronic inflammation, is a definite cause of tumor development and progression. The author proposed that reactive oxygen species and nitric oxide from infiltrating inflammatory cells drive the process.
• Limitations the authors state:
  • The gelatin sponge model causes acute-phase inflammation that does not become chronic, whereas inflammation leading to cancer in people is mostly chronic
  • How chronic inflammation is induced, maintained and resolved has not been fully worked out

Topics

Medical terms in this study, explained in our Lexicon: Inflammation, Carcinogenesis, Stomach Cancer, Colorectal Cancer, Pleural Mesothelioma, Lung Cancer.

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