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Targeting Inflammation in Cancer Prevention and Therapy

Our plain-English summary of Targeting Inflammation in Cancer Prevention and Therapy, by J. Todoric, L. Antonucci, M. Karin (Cancer Prevention Research, 2016).

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The study

Abstract

Inflammation is associated with the development and malignant progression of most cancers. As most of the cell types involved in cancer-associated inflammation are genetically stable and thus are not subjected to rapid emergence of drug resistance, 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 inflammation can result in immunosuppression, thereby providing a preferred background for tumor development. In clinical trials, lifestyle modifications including healthy diet, exercise, alcohol, and smoking cessation have proven effective in ameliorating inflammation and reducing the risk of cancer-related deaths. In addition, consumption of certain anti-inflammatory drugs, including aspirin, can significantly reduce cancer risk, suggesting that common nonsteroidal anti-inflammatory drugs (NSAID) and more specific COX2 inhibitors can be used in cancer prevention. In addition to being examined for their preventative potential, both NSAIDs and more potent anti-inflammatory antibody-based drugs need to be tested for their ability to augment the efficacy of more conventional therapeutic approaches on the basis of tumor resection, radiation, and cytotoxic chemicals. Cancer Prev Res; 9(12); 895-905. ©2016 AACR.

©2016 American Association for Cancer Research.

In plain English

This article was a review, not a new study. The authors summarized published research on how inflammation is linked to cancer and how reducing inflammation might help prevent or treat cancer. It reported no new data on any group of people or animals. In the abstract, the authors listed asbestos exposure among the causes of what they called tumor-extrinsic inflammation, along with infections, autoimmune diseases, obesity, tobacco smoking and excessive alcohol consumption. The body of the article did not discuss asbestos or mesothelioma; it mentioned lung cancer, but not in connection with asbestos. It mentioned exposure to microparticles among cancer risk factors that act through inflammation, without naming asbestos. Most of the review covered obesity, alcohol, smoking, gut bacteria, exercise, anti-inflammatory and other drugs, and vaccines against cancer-causing viruses. Describing other researchers' work, the authors wrote that multiple clinical trials had linked long-term aspirin use to fewer cancer cases and deaths for several cancer types. The authors concluded that, because inflammatory changes are common across cancer types, preventing or reversing inflammation is an important approach to cancer control.

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 of published research on inflammation, cancer prevention and cancer therapy
  • Who was studied: No study population. The authors reviewed published literature and did not study any group of people or animals themselves.
  • Exposure: Asbestos exposure is named once, in the abstract, as one of several causes of tumor-extrinsic inflammation. Fiber types, jobs and doses are not discussed. The body of the article mentions exposure to microparticles among inflammation-related cancer risk factors without naming asbestos.
  • Main results:
    • In the body of the article, the authors listed exposure to microparticles among cancer risk factors whose common mechanism is inflammation. Asbestos was not named in this passage.
    • The review discussed lung cancer in contexts such as tobacco smoke exposure in mice, but not in connection with asbestos.
    • Summarizing other research (not their own data), the authors wrote that multiple clinical trials had linked long-term aspirin use to reduced incidence and mortality for several cancer types.
    • Summarizing other research, the authors described vaccination against cancer-causing viruses as a way to reduce several inflammation-related cancers.
  • The authors' conclusion: The authors concluded that, because inflammatory changes are common across cancer types, preventing or reversing inflammation is an important approach to cancer control.

Topics

Medical terms in this study, explained in our Lexicon: Inflammation, Asbestos Exposure, Clinical Trial.

Browse more research in Cancer Prevention Research, or return to medical research.

Cited on this site

How to cite it

Cite the study

J. Todoric, L. Antonucci, M. Karin. Targeting Inflammation in Cancer Prevention and Therapy. Cancer Prevention Research 2016;9(12):895-905. doi:10.1158/1940-6207.CAPR-16-0209. PMID: 27913448.

Cite our summary

“Targeting Inflammation in Cancer Prevention and Therapy.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/targeting-inflammation-in-cancer-prevention-and-therapy.

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