PGE2 (prostaglandin E2) is a hormone-like molecule made by the body from fatty acids. It plays a major role in inflammation, pain, fever, and immune regulation, and elevated levels are commonly found in chronic inflammatory conditions and in many cancers, including mesothelioma.
Origin
Prostaglandins were first identified in the 1930s by Swedish physiologist Ulf von Euler, who named them after the prostate gland, where he mistakenly believed they originated. PGE2 was later characterized as one of several prostaglandin subtypes produced through the cyclooxygenase (COX) pathway from arachidonic acid.
Significance in Asbestos Context
Asbestos fibers lodged in the lungs or pleura trigger chronic inflammation, and PGE2 is one of the key inflammatory signals released by macrophages and mesothelial cells in response. Persistently elevated PGE2 contributes to the inflammatory environment that drives mesothelioma development, helps tumors evade immune attack, and promotes tumor growth and resistance to treatment. Patients may encounter PGE2 in discussions about COX-2 inhibitors (such as celecoxib), NSAID use, or experimental treatments aimed at reducing tumor-promoting inflammation. In medical records and research reports tied to a case, PGE2 levels are sometimes cited as biological evidence linking asbestos-induced inflammation to malignancy.
Example Sentence
The oncologist explained that asbestos-driven inflammation raises PGE2 in the pleural tissue, which can help the tumor suppress the immune response.
Related Terms
Chronic Inflammation, COX-2, Macrophage, Mesothelioma, Cytokines, Tumor Microenvironment
Notes
- Ask your oncologist whether anti-inflammatory strategies (such as COX-2 inhibitors) are being considered as part of your treatment plan or any clinical trial you may qualify for.
- If you regularly take NSAIDs or aspirin, tell your care team. These affect prostaglandin pathways and may interact with treatment decisions or surgical planning.
- Preserve any pathology reports, research correlations, or expert reports that discuss inflammatory markers like PGE2, as they may support the biological link between asbestos exposure and your disease.
In the research library
7 studies in our medical research library mention PGE2 in the title or abstract. Among the most cited:
- Augmentation of CAR T-cell Trafficking and Antitumor Efficacy by Blocking Protein Kinase A LocalizationK. Newick, S. O'Brien, J. Sun, et al, 2016 · Cancer Immunology Research · cited 169 times
- Production of arachidonic acid metabolites by macrophages exposed in vitro to asbestos, carbonyl iron particles, or calcium ionophoreS. Kouzan, A.R. Brody, P. Nettesheim, et al, 1985 · The American Review of Respiratory Disease · cited 80 times
- Human alveolar macrophage cytokine release in response to in vitro and in vivo asbestos exposureR.C. Perkins, R.K. Scheule, R. Hamilton, et al, 1993 · Experimental Lung Research · cited 67 times
- Toxicity and carcinogenicity mechanisms of fibrous antigoriteV. Cardile, L. Lombardo, E. Belluso, et al, 2007 · International Journal of Environmental Research and Public Health · cited 21 times
- Clinical relevance of cellular mediators of inflammation in workers exposed to asbestosD.A. Schwartz, J.R. Galvin, K.L. Frees, et al, 1993 · The American Review of Respiratory Disease · cited 20 times
The journals that publish most on it: The American Review of Respiratory Disease (2), Experimental Lung Research (1), International Journal of Environmental Research and Public Health (1).
Category: Biological & Molecular Mechanisms · All Lexicon terms A–Z
This page is provided for general informational purposes and does not constitute legal advice. Every asbestos case turns on its own facts, exposure history, diagnosis, deadlines, available evidence, and applicable law. Reviewing this page does not create an attorney-client relationship. For advice about your specific situation, call 833-4-ASBESTOS for a free case review.