Cancer and inflammation: promise for biologic therapy

Our plain-English summary of Cancer and inflammation: promise for biologic therapy, by S. Demaria, E. Pikarsky, M. Karin, et al (Journal of Immunotherapy, 2010).

The study

• Authors: S. Demaria, E. Pikarsky, M. Karin, L.M. Coussens, Y.C. Chen, E.M. El-Omar, G. Trinchieri, S.M. Dubinett, J.T. Mao, E. Szabo, A. Krieg, G.J. Weiner, B.A. Fox, G. Coukos, E. Wang, R.T. Abraham, M. Carbone, M.T. Lotze
• Journal: Journal of Immunotherapy
• Published: 2010;33(4):335-51
• Type of article: Review
• Cited by: 240 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Cancers often arise as the end stage of inflammation in adults, but not in children. As such there is a complex interplay between host immune cells during neoplastic development, with both an ability to promote cancer and limit or eliminate it, most often complicit with the host. In humans, defining inflammation and the presence of inflammatory cells within or surrounding the tumor is a critical aspect of modern pathology. Groups defining staging for neoplasms are strongly encouraged to assess and incorporate measures of the presence of apoptosis, autophagy, and necrosis and also the nature and quality of the immune infiltrate. Both environmental and genetic factors enhance the risk of cigarette smoking, Helicobacter pylori, hepatitis B/C, human papilloma virus, solar irradiation, asbestos, pancreatitis, or other causes of chronic inflammation. Identifying suitable genetic polymorphisms in cytokines, cytokine receptors, and Toll-like receptors among other immune response genes is also seen as high value as genomic sequencing becomes less expensive. Animal models that incorporate and assess not only the genetic anlagen but also the inflammatory cells and the presence of microbial pathogens and damage-associated molecular pattern molecules are necessary. Identifying micro-RNAs involved in regulating the response to damage or injury are seen as highly promising. Although no therapeutic strategies to prevent or treat cancers based on insights into inflammatory pathways are currently approved for the common epithelial malignancies, there remains substantial interest in agents targeting COX2 or PPARgamma, ethyl pyruvate and steroids, and several novel agents on the horizon.

In plain English

This article was a review, not a new study. It summarized a one-day workshop on cancer and inflammation held by the International Society for Biologic Therapy of Cancer in San Diego on October 30, 2008. Its six sections covered defining inflammation in tumors, genetic variants that affect inflammation and cancer risk (using prostate and gastric cancer as examples), mouse models, damage-associated molecules such as HMGB1, clinical trials aimed at preventing cancer, and new treatments. Asbestos came up only briefly. The authors noted that the chronic inflammatory response caused by asbestos has been linked to mesothelioma, citing earlier research, and listed the pleura among organs where chronic inflammation raises cancer risk. Among the prevention trials the review described, anti-inflammatory drugs reduced colorectal polyps, but COX-2 inhibitors were linked to more cardiovascular events. The authors concluded that targeting factors such as HMGB1, RAGE and IL-1 beta may lower the rate of cancers that arise in chronic inflammation. They added that a clinical trial targeting such molecules in established cancer would be premature.

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: Review article summarizing a 2008 scientific workshop; no new data were collected
• Who was studied: No study population; the article reported the content of a one-day iSBTc workshop held October 30, 2008 in San Diego, drawn from session chairs and participants
• Exposure: Chronic inflammation and cancer in general; asbestos was mentioned only once, as a cause of a chronic inflammatory response linked to mesothelioma (no fiber type specified)
• Main results:
  • Citing earlier research, the review stated that the chronic inflammatory response caused by asbestos has been linked to mesothelioma, and listed the pleura among organs where chronic inflammatory diseases increase cancer risk
  • From published trials it reviewed, several NSAIDs reduced colorectal polyps in familial adenomatous polyposis (FAP) and prevented recurrence of sporadic colorectal adenomas
  • The review reported that extended use of COX-2 inhibitors in colorectal cancer prevention trials was associated with more cardiovascular events, leading to rofecoxib's withdrawal
  • Ethyl pyruvate, an anti-inflammatory agent discussed as a possible antitumor drug, had not been tested in people with cancer
• The authors' conclusion: The authors concluded that targeting factors such as HMGB1, RAGE and IL-1 beta may decrease the incidence of cancers arising in chronic inflammation, but that a clinical trial targeting such molecules to treat cancer progression would be premature

Topics

Medical terms in this study, explained in our Lexicon: Inflammation, Pathology, Staging, Neoplasm, Apoptosis, Necrosis, Chronic Inflammation, Cytokine.

Related studies

• Targeting Inflammation in Cancer Prevention and Therapy — J. Todoric, L. Antonucci, et al. (2016)
• Late Inflammation Induced by Asbestiform Fibers in Mice Is Ameliorated by a Small Molecule Synthetic Lignan — R. Badger, K. Park, et al. (2021)
• A preclinical model to investigate the role of surgically-induced inflammation in tumor responses to intraoperative photodynamic therapy — R.W. Davis, E. Papasavvas, et al. (2018)
• The maximum tolerated dose and biologic effects of 3-aminopyridine-2-carboxaldehyde thiosemicarbazone (3-AP) in combination with irinotecan for patients with refractory solid tumors — B.S. Choi, D.B. Alberti, et al. (2010)
• New approaches for mesothelioma: biologics, vaccines, gene therapy, and other novel agents — A.K. Nowak, R.A. Lake, et al. (2002)
• Inflammation and cancer — M. Murata (2018)

Browse more research in Journal of Immunotherapy, or return to medical research.