p53 mutations and codon 213 polymorphism of p53 in lung cancers of former uranium miners

Popp, Walter; Vahrenholz, C.; Schuster, H.; Wiesner, B; Bauer, Peter; Täuscher, Frank; Plogmann, Helmut; Morgenroth, K; Konietzko, N.; Norpoth, K.

doi:10.1007/s004320050279

Cited by 10 publications

(7 citation statements)

References 18 publications

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“…Popp et al [68] studied the lung cancers of 16 uranium miners (12 squamous cell carcinomas, 3 adenocarcinomas and 1 small-cell carcinoma) in Germany and 13 non-mining patients who had lung cancer (4 squamous cell carcinomas, 8 adenocarcinomas and 1 large cell carcinoma) and were all from the same geographical region. In line with many of the previous studies, they found no codon 249 G to T transversion in any of investigated patients, with the exception of the only non-smoking uranium miner present in the study.…”

Section: Genetic Effectsmentioning

confidence: 99%

The Cellular and Molecular Carcinogenic Effects of Radon Exposure: A Review

Robertson

Allen

Laney

et al. 2013

IJMS

124

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Radon-222 is a naturally occurring radioactive gas that is responsible for approximately half of the human annual background radiation exposure globally. Chronic exposure to radon and its decay products is estimated to be the second leading cause of lung cancer behind smoking, and links to other forms of neoplasms have been postulated. Ionizing radiation emitted during the radioactive decay of radon and its progeny can induce a variety of cytogenetic effects that can be biologically damaging and result in an increased risk of carcinogenesis. Suggested effects produced as a result of alpha particle exposure from radon include mutations, chromosome aberrations, generation of reactive oxygen species, modification of the cell cycle, up or down regulation of cytokines and the increased production of proteins associated with cell-cycle regulation and carcinogenesis. A number of potential biomarkers of exposure, including translocations at codon 249 of TP53 in addition to HPRT mutations, have been suggested although, in conclusion, the evidence for such hotspots is insufficient. There is also substantial evidence of bystander effects, which may provide complications when calculating risk estimates as a result of exposure, particularly at low doses where cellular responses often appear to deviate from the linear, no-threshold hypothesis. At low doses, effects may also be dependent on cellular conditions as opposed to dose. The cellular and molecular carcinogenic effects of radon exposure have been observed to be both numerous and complex and the elevated chronic exposure of man may therefore pose a significant public health risk that may extend beyond the association with lung carcinogenesis.

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Section: Genetic Effectsmentioning

confidence: 99%

The Cellular and Molecular Carcinogenic Effects of Radon Exposure: A Review

Robertson

Allen

Laney

et al. 2013

IJMS

124

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“…Deletions of 17p and TP53 mutations are frequent in human NSCLC, and have also been described in radon‐related tumors (Vahakangas et al, 1992; Taylor et al, 1994; Hollstein et al, 1997; Popp et al, 1999; Yngveson et al, 1999). No alteration within RNO 10, where the rat TP53 homolog is located, however, was observed in our series.…”

Section: Discussionmentioning

confidence: 99%

“…Most studies have focused on TP53 and RAS gene mutations, mainly due to the frequent alterations of these genes in human lung carcinomas. One study described a specific codon 249 TP53 mutation in 31% of lung tumors from a cohort of uranium miners (Taylor et al, 1994), whereas others found a lower frequency without any specific hot‐spot mutations (Vahakangas et al, 1992; Hollstein et al, 1997; Popp et al, 1999; Yngveson et al, 1999). Similarly, the frequency of RAS mutations in radon‐related lung cancer has been rather low (Vahakangas et al, 1992; Johnson and Kelley, 1993) except for one study in which 9 of 23 lung adenocarcinomas contained mutation in the KRAS gene (McDonald et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

CGH analysis of radon‐induced rat lung tumors indicates similarities with human lung cancers

Dano

Guilly

Muleris

et al. 2000

Genes Chromosom. Cancer

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“…The study of Popp et al indicated an overrepresentation of codon 213/3 polymorphism in p53 in radiation-caused cancers [69]. Some studies reported a radon-related TP53 hotspot in codon 249, exon 7.…”

Section: Genetics and Epigenetic Effects Of Radonmentioning

confidence: 99%

Residential Radon Exposure and Lung Cancer Risk in Kazakhstan

Bersimbaev¹,

Bulgakova²

2017

Radon

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Many published data have demonstrated the potential of radon exposure to induce biological damage. All these studies suggest that exposure to radon and its progeny can represent a significant public health risk. Radon exposure is considered as the second cause of lung cancer and it is the first in never smokers. Many countries have depicted residential radon exposure maps in order to characterize those areas with the highest indoor radon concentrations. There are areas in Kazakhstan with a number of factors leading to natural radioactivity. The genotoxic effects of radon on population of Kazakhstan are poorly understood. These studies conducted in compliance with all requirements of genotoxic studies will provide an extensive and reliable data for a detailed radon zoning of Kazakhstan. Our review attempts to integrate data about the association between residential radon levels and morbidity of population in Kazakhstan. In addition, we tried to cover all points of the cytogenetic and molecular changes induced by radon exposure.

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p53 mutations and codon 213 polymorphism of p53 in lung cancers of former uranium miners

Cited by 10 publications

References 18 publications

The Cellular and Molecular Carcinogenic Effects of Radon Exposure: A Review

The Cellular and Molecular Carcinogenic Effects of Radon Exposure: A Review

CGH analysis of radon‐induced rat lung tumors indicates similarities with human lung cancers

Residential Radon Exposure and Lung Cancer Risk in Kazakhstan

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