Associations of DNA-repair gene polymorphisms with a genetic susceptibility to ionizing radiation in residents of areas with high radon (<sup>222</sup>Rn) concentration

Sinitsky, M. Yu.; Ларионов, А. В.; Asanov, Maxim А.; Дружинин, В. Г.

doi:10.3109/09553002.2015.1012306

Cited by 14 publications

(9 citation statements)

References 50 publications

(43 reference statements)

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“… 15 Recent articles have demonstrated an increased frequency of cytogenetic damage in people with DNA-repair gene variations related with chronic exposure to radon and have indicated that ADPRT and NBS1 can be utilized as molecular genetic markers of increased radiosensitivity to long-term exposure to high concentrations of radon. 16 , 17 Another study suggested that radon exposure in never smokers seems to be a risk factor for lung cancer and that LCINS subjects diagnosed at a younger age might have been exposed to higher indoor radon concentrations, indicating an accumulative effect for radon levels on lung cancer features. 18 …”

Section: Introductionmentioning

confidence: 99%

Novel Genetic Associations Between Lung Cancer and Indoor Radon Exposure

et al. 2017

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BackgroundLung cancer is the leading cause of cancer-related death worldwide, for which smoking is considered as the primary risk factor. The present study was conducted to determine whether genetic alterations induced by radon exposure are associated with the susceptible risk of lung cancer in never smokers.MethodsTo accurately identify mutations within individual tumors, next generation sequencing was conduct for 19 pairs of lung cancer tissue. The associations of germline and somatic variations with radon exposure were visualized using OncoPrint and heatmap graphs. Bioinformatic analysis was performed using various tools.ResultsAlterations in several genes were implicated in lung cancer resulting from exposure to radon indoors, namely those in epidermal growth factor receptor (EGFR), tumor protein p53 (TP53), NK2 homeobox 1 (NKX2.1), phosphatase and tensin homolog (PTEN), chromodomain helicase DNA binding protein 7 (CHD7), discoidin domain receptor tyrosine kinase 2 (DDR2), lysine methyltransferase 2C (MLL3), chromodomain helicase DNA binding protein 5 (CHD5), FAT atypical cadherin 1 (FAT1), and dual specificity phosphatase 27 (putative) (DUSP27).ConclusionsWhile these genes might regulate the carcinogenic pathways of radioactivity, further analysis is needed to determine whether the genes are indeed completely responsible for causing lung cancer in never smokers exposed to residential radon.

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Section: Introductionmentioning

confidence: 99%

Novel Genetic Associations Between Lung Cancer and Indoor Radon Exposure

et al. 2017

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“…Finally, a number of studies have examined the effect of genetic polymorphisms of DNA damage repair genes in the outcome of individuals exposed to radon. For instance, individuals with a polymorphism leading to the Asp1104His substitution of DNA repair gene ERCC5 (XpG) displayed a higher frequency of micronuclei in their lymphocytes, representative of elevated cytogenetic damage and decreased radiosensitivity [116]. Alternatively, the absence of GSTM1 and GSTT1, members of the glutathione-s-transferase enzyme family-critical to detoxification and excretionis associated with an increased risk of lung cancer development [117,118].…”

Section: Prominent Cancer Genes Affected By Radonmentioning

confidence: 99%

Oncogenetics of Lung Cancer Induced by Environmental Carcinogens

Martínez¹,

Sage²,

Marshall³

et al. 2019

Oncogenes and Carcinogenesis

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The molecular landscape of non-tobacco-induced primary lung tumors displays specific oncogenetic features. The etiology of these tumors has been largely associated with exposure to well-established environmental lung carcinogens such as radon, arsenic, and asbestos. Environmental carcinogens can induce specific genetic and epigenetic alterations in lung tissue, leading to aberrant function of lung cancer oncogenes and tumor suppressor genes. These molecular events result in the disruption of key cellular mechanisms, such as protection against oxidative stress and DNA damage-repair, which promotes tumor development and progression. This chapter provides a comprehensive discussion of the specific carcinogenic mechanisms associated with exposure to radon, arsenic, and asbestos. It also summarizes the main protein-coding and non-coding genes affected by exposure to these environmental agents, and the underlying molecular mechanisms promoting their deregulation in lung cancer. Finally, the chapter examines the anticipated challenges in personalized intervention strategies in non-tobacco-induced lung cancer.

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“…Sinitsky MY et al suggested the elevated frequency of cytogenetic damage in people with DNA-repair gene polymorphisms due to chronic exposure to radon and XpG, ADPRT, and NBS1 gene can be used as molecular genetic markers of increased individual radiosensitivity in long-term residents with high concentrations of radon [ 39 ]. Another report suggested GSTM1 and GSTT1 genes deletion increase the risk of lung cancer and these genes might regulate the carcinogenic pathway by radon radiation [ 40 , 41 ].…”

Section: Radon Exposure and Genetic Factorsmentioning

confidence: 99%

Gene mutation discovery research of non-smoking lung cancer patients due to indoor radon exposure

Choi¹,

Park²,

Noh³

et al. 2016

Ann of Occup and Environ Med

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Although the incidence and mortality for most cancers such as lung and colon are decreasing in several countries, they are increasing in several developed countries because of an unhealthy western lifestyles including smoking, physical inactivity and consumption of calorie-dense food. The incidences for lung and colon cancers in a few of these countries have already exceeded those in the United States and other western countries. Among them, lung cancer is the main cause of cancer death in worldwide. The cumulative survival rate at five years differs between 13 and 21 % in several countries. Although the most important risk factors are smoking for lung cancer, however, the increased incidence of lung cancer in never smokers(LCINS) is necessary to improve knowledge concerning other risk factors. Environmental factors and genetic susceptibility are also thought to contribute to lung cancer risk. Patients with lung adenocarcinoma who have never smoking frequently contain mutation within tyrosine kinase domain of the epidermal growth factor receptor(EGFR) gene. Also, K-ras mutations are more common in individuals with a history of smoking use and are related with resistance to EFGR-tyrosine kinase inhibitors. Recently, radon(Rn), natural and noble gas, has been recognized as second common reason of lung cancer. In this review, we aim to know whether residential radon is associated with an increased risk for developing lung cancer and regulated by several genetic polymorphisms.

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Associations of DNA-repair gene polymorphisms with a genetic susceptibility to ionizing radiation in residents of areas with high radon (²²²Rn) concentration

Cited by 14 publications

References 50 publications

Novel Genetic Associations Between Lung Cancer and Indoor Radon Exposure

Novel Genetic Associations Between Lung Cancer and Indoor Radon Exposure

Oncogenetics of Lung Cancer Induced by Environmental Carcinogens

Gene mutation discovery research of non-smoking lung cancer patients due to indoor radon exposure

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Associations of DNA-repair gene polymorphisms with a genetic susceptibility to ionizing radiation in residents of areas with high radon (222Rn) concentration

Cited by 14 publications

References 50 publications

Novel Genetic Associations Between Lung Cancer and Indoor Radon Exposure

Novel Genetic Associations Between Lung Cancer and Indoor Radon Exposure

Oncogenetics of Lung Cancer Induced by Environmental Carcinogens

Gene mutation discovery research of non-smoking lung cancer patients due to indoor radon exposure

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Product

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Associations of DNA-repair gene polymorphisms with a genetic susceptibility to ionizing radiation in residents of areas with high radon (²²²Rn) concentration