Chromosome aberrations in peripheral blood lymphocytes of lung cancer patients exposed to radon and air pollution

Abstract

Lung cancer is one of the most common forms of cancer. The aim of this study was to validate chromosome aberrations in peripheral blood lymphocytes of lung cancer patients living in a region with high air pollution and increased background radon levels as a biomarker of cancer risk. A total of 417 lung cancer patients and 468 control participants were analysed using a chromosome aberration assay in peripheral blood lymphocytes. The results showed that chromatid-type aberrations (2.26±1.58 vs. 1.60±1.58) and chromosome-type aberrations (CSAs) (0.96±1.36 vs. 0.42±0.70) in lung cancer patients were increased significantly in comparison with the controls. The most significant two-fold increase was detected for CSAs (nonsmoking patients: 0.84±1.54 vs. 0.41±0.73%, smoking patients: 0.99±1.31 vs. 0.44±0.67%). The frequency of dicentric and ring chromosomes, double minutes and rogue cells was significantly higher (P=0.002, 0.00002, 0.01, 0.0007) in the lung cancer patients. As both analysed groups lived in the same environment, our results show that increased radon levels were not the only source for the detected genome damage. Using binomial logistic regression, the estimated odds ratios and 95% confidence intervals adjusted for the main confounders (smoking, occupational exposure, age) were 1.31 (1.20-1.40) for chromatid-type aberrations, 1.28 (1.17-1.33), and 1.68 (1.49-1.88) for CSAs. It may be suggested that lung cancer patients show a significant increase in genome damage that may be caused by an interplay between exposure and individual low capacity of DNA repair, leading to genome instability.

Circular RNA profiles in mouse lung tissue induced by radon

“…There have been strong evidences showing a significantly increased risk of lung cancer followed by long-term low radon exposure among Wismut miners [ 1 ]. Genome damage, such as genome instability, was found in peripheral blood lymphocytes of lung cancer patients living in a region with high air pollution and increased background radon levels [ 5 , 20 ]. Moreover, IL-6 promoter variant was associated with lung cancer in uranium miners [ 21 ].…”

Cytogenetic effects of excessive radon exposure depending on the individual dosage of active ribosomal genes

“…При проведении измерений ориен-тировались на нормативно-методическую документацию Минздрава России (2003) Генотоксические эффекты в лимфоцитах крови об-следованных изучали с помощью метода учета хромосом-ных аберраций (ХА) в 48-часовых культурах лимфоцитов периферической крови [14]. Подготовка препаратов метафазных хромосом и принципы учета ХА подробно описаны в работах, опубликованных нами ранее [15,16]. Анализ ХА проводился на зашифрованных препаратах двумя независимыми исследователями с использовани-ем метода рутинной окраски хромосом.…”

Follow-up studies on genome damage in children after Chernobyl nuclear power plant accident

“…Although etiology of cancer is very complex, an increased frequency of chromosome aberrations (CA) and micronuclei (MN) is found to be associated with increased cancer risk in general population and population occupationally exposed to ionizing radiation (Bonassi et al 2007(Bonassi et al , 2008Fucic et al 2016). Increased genome damage in peripheral lymphocytes of patients suffering from some cancer types is reported suggesting that genome instability may also have origin in the etiology of cancer (Minina et al 2016;Lombardi et al 2015;Kennedy and D'Andrea 2006). Genome instability may have origin from microsatellite instability and chromosomal instability (Kaiser et al 2014).…”

“…Recent publications on rogue cells in different populations strongly suggest that they are biomarker of internal exposure to high LET radiation, primarily by alpha particles, incorporated inside the body (Popova et al 2004;Aseeva et al 2010;Druzhinin et al 2016). Rogue cells were reported in cancer patients for different cancer types, both in children and adults, showing that such cells may be specific biomarkers of cancerogenesis (Minina et al 2016;Leonard et al 1995).…”