Asbestos is a naturally-occurring fibrous mineral that has been associated with lung cancer, asbestosis, pleural plaques, and malignant mesothelioma. Most mesothelioma patients are people who worked in the asbestos industry or in other industries – such as construction and ship-building – where asbestos was once commonly used.
But a new study conducted by some of the world’s top cancer researchers found that mesothelioma patients with a particular inherited genetic mutation often contract the disease without ever having worked in an asbestos-related industry.
“To date, we found that none of the mesothelioma patients carrying germline BAP1 mutations were professionally exposed to asbestos,” writes Andrea Napolitano, a graduate research assistant at the University of Hawaii Cancer Center whose name appears first on the paper.
The BAP1 (BRCA1 Associated Protein-1) is a tumor-suppressing gene that has been associated with an increased risk for several cancers including melanomas, renal cell carcinoma, and mesothelioma. To understand why it may take only a little asbestos to trigger mesothelioma in people with this mutation, researchers exposed BAP1 mutated mice to asbestos. They found that the inflammatory response, which causes healthy mesothelial cells to become cancerous, was more pronounced in these mice.
According to the report, “Consistent with these data, BAP1+/- mice had a significantly higher incidence of mesothelioma after exposure to very low doses of asbestos, doses that rarely induced mesothelioma in wild-type [non-mutated] mice.”
The researchers conclude that, for people with the BAP1 mutation, even very minimal exposure to a carcinogen like asbestos could dramatically raise the risk of mesothelioma by triggering a pronounced inflammatory response.
Napolitano, A, et al, “Minimal asbestos exposure in germline BAP1 heterozygous mice is associated with deregulated inflammatory response and increased risk of mesothelioma”, June 29, 2015, Oncogene, Epub ahead of print, http://www.nature.com/onc/journal/vaop/ncurrent/full/onc2015243a.html