Objective: According to the World Health Organization, radon is the second leading cause of lung cancer after smoking. Cell free circulating mitochondrial DNA (cf mtDNA) have been used not only as a biomarker of carcinogenesis but also as a biomarker of exposure to radiation, but nothing is known about changes in the level of cf mtDNA following radon exposure. Therefore, the purpose of this study was to estimate the cf mtDNA copy number as a biomarker of the response to radon exposure in lung cancer pathogenesis. Methods: 207 subjects were examined including 41 radon-exposed lung cancer patients, 40 lung cancer patients without radon exposure and 126 healthy controls exposed/not exposed to high level of radon. Total cell free circulating DNA from blood samples was extracted and used to detect cell free circulating mitochondrial DNA copy number by quantitative real-time polymerase chain reaction (qRT-PCR). Results: Our data indicate that the level of cf mtDNA in the radon-induced lung cancer patients was significantly higher than that of the other study participants. There was a significant difference in the level of cf mtDNA in the blood plasma of healthy volunteers exposed and not exposed to high doses of radon. Moreover, in healthy volunteers living in areas with high radon levels, the mtDNA copy number was higher than that in patients with lung cancer who were not exposed to high doses of radon. Conclusion: Our study provides evidence for a possible role of cf mtDNA as a promising biomarker of lung cancer induced by exposure to high dose of radon.

The level of free-circulating mtDNA in patients with radon-induced lung cancer

Kussainova A.;Izzotti A.;
2021-01-01

Abstract

Objective: According to the World Health Organization, radon is the second leading cause of lung cancer after smoking. Cell free circulating mitochondrial DNA (cf mtDNA) have been used not only as a biomarker of carcinogenesis but also as a biomarker of exposure to radiation, but nothing is known about changes in the level of cf mtDNA following radon exposure. Therefore, the purpose of this study was to estimate the cf mtDNA copy number as a biomarker of the response to radon exposure in lung cancer pathogenesis. Methods: 207 subjects were examined including 41 radon-exposed lung cancer patients, 40 lung cancer patients without radon exposure and 126 healthy controls exposed/not exposed to high level of radon. Total cell free circulating DNA from blood samples was extracted and used to detect cell free circulating mitochondrial DNA copy number by quantitative real-time polymerase chain reaction (qRT-PCR). Results: Our data indicate that the level of cf mtDNA in the radon-induced lung cancer patients was significantly higher than that of the other study participants. There was a significant difference in the level of cf mtDNA in the blood plasma of healthy volunteers exposed and not exposed to high doses of radon. Moreover, in healthy volunteers living in areas with high radon levels, the mtDNA copy number was higher than that in patients with lung cancer who were not exposed to high doses of radon. Conclusion: Our study provides evidence for a possible role of cf mtDNA as a promising biomarker of lung cancer induced by exposure to high dose of radon.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11567/1060396
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