Polymorphisms of Selected DNA Repair Genes and Lung Cancer in Chromium Exposure

Halašová, Erika; Matáková, Tatiana; Škereňová, Mária; Krutakova, M.; Slovakova, P.; Dzian, Anton; Javorkova, Silvia; Péč, Martin; Kypusova, K.; Hamžík, J

doi:10.1007/5584_2016_218

Cited by 5 publications

(2 citation statements)

References 22 publications

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“…For instance, the A/A genotype was associated with the increased risk of glioblastoma (odds ratio (OR) = 3.14, 95% confidence interval (CI) = 1.09–9.06, p = 0.034) [ 44 ]. This SNP also increases the risk of lung adenocarcinoma in European, Korean and Taiwanese populations [ 45 , 46 , 47 , 48 ]. One European study described the association between the A/A genotype of this SNP and lung cancer in interaction with chromium exposure [ 48 ].…”

Section: Results On Mmr Gene Variantsmentioning

confidence: 99%

“…This SNP also increases the risk of lung adenocarcinoma in European, Korean and Taiwanese populations [ 45 , 46 , 47 , 48 ]. One European study described the association between the A/A genotype of this SNP and lung cancer in interaction with chromium exposure [ 48 ]. The accumulated evidence on the pathogenicity of this SNP in the lung cancer is highlighted in a meta-analysis comprising 1018 publications and 754 genes [ 49 ].…”

Section: Results On Mmr Gene Variantsmentioning

confidence: 99%

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DNA Mismatch Repair Gene Variants in Sporadic Solid Cancers

Čaja

Vodičková

Král

et al. 2020

IJMS

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The phenotypic effects of single nucleotide polymorphisms (SNPs) in the development of sporadic solid cancers are still scarce. The aim of this review was to summarise and analyse published data on the associations between SNPs in mismatch repair genes and various cancers. The mismatch repair system plays a unique role in the control of the genetic integrity and it is often inactivated (germline and somatic mutations and hypermethylation) in cancer patients. Here, we focused on germline variants in mismatch repair genes and found the outcomes rather controversial: some SNPs are sometimes ascribed as protective, while other studies reported their pathological effects. Regarding the complexity of cancer as one disease, we attempted to ascertain if particular polymorphisms exert the effect in the same direction in the development and treatment of different malignancies, although it is still not straightforward to conclude whether polymorphisms always play a clear positive role or a negative one. Most recent and robust genome-wide studies suggest that risk of cancer is modulated by variants in mismatch repair genes, for example in colorectal cancer. Our study shows that rs1800734 in MLH1 or rs2303428 in MSH2 may influence the development of different malignancies. The lack of functional studies on many DNA mismatch repair SNPs as well as their interactions are not explored yet. Notably, the concerted action of more variants in one individual may be protective or harmful. Further, complex interactions of DNA mismatch repair variations with both the environment and microenvironment in the cancer pathogenesis will deserve further attention.

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Section: Results On Mmr Gene Variantsmentioning

confidence: 99%

Section: Results On Mmr Gene Variantsmentioning

confidence: 99%

DNA Mismatch Repair Gene Variants in Sporadic Solid Cancers

Čaja

Vodičková

Král

et al. 2020

IJMS

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Mechanisms and individuality in chromium toxicity in humans

Pavesi

Moreira

2020

J of Applied Toxicology

169

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With regards to health, chromium (Cr) is an ambiguous chemical element. Although it is considered to be an important micronutrient, it also is connected with several pathologies, including carcinogenicity. The mechanism of action of Cr and its compounds in humans is not yet fully understood. Currently, three possible mechanisms have been proposed for carcinogenesis: Cr(VI)‐induced multistage carcinogenesis, genomic instability, and epigenetic modification. Therefore, in addition to the toxicity of this metal and its ions, human susceptibility to Cr‐induced pathologies depends on external factors and individual characteristics, such as enzymatic polymorphisms, carriers, endogenous reducing system, adduct formation and stability, and efficiency of DNA repair mechanisms, among other factors. In fact, the variability of individual molecular constitutive factors, such as individual polymorphisms, creates an individualized environment for Cr toxicity. This mini‐review contemplates the essential variables in this process.

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Lung injury and expression of p53 and p16 in Wistar rats induced by respirable chrysotile fiber dust from four primary areas of China

Zeng

Cui

et al. 2017

Environ Sci Pollut Res

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Chrysotile products were widely used in daily life, and a large amount of respirable dust was produced in the process of production and application. At present, there was seldom research on the safety of chrysotile fiber dust, and whether its long-term inhalation can lead to lung cancer was unknown. In order to determine whether respirable chrysotile fiber dust of China caused lung cancer, four major chrysotile-producing mine areas in China were selected for this study. Chrysotile fibers were prepared into respirable dust. Particle size was measured by laser particle analysis, morphology was observed by scanning electron microscope, chrysotile fiber phase was analyzed by X-ray diffraction, trace chemical elements were identified by X-ray fluorescence, and the structure and the active groups of the dust were determined after grinding by Fourier transform infrared spectroscopy. Male Wistar rats were exposed to non-exposed intratracheal instillation with different concentrations of chrysotile fiber dust. The rats were weighed after 1, 3, and 6 months, then the lung tissues were separated, the lung morphology was observed, and the pulmonary index was calculated. Pathological changes in lung tissues were observed by optical microscope after the HE staining of tissues, and the gene expression of p53 and p16 was determined by reverse transcription polymerase chain reaction. First, the results showed that the particle sizes of the four fibers were less than 10 μm. Four primary areas of chrysotile had similar fibrous structure, arranged in fascicles, or mixed with thin chunks of material. Second, the elementary composition of the four fibers was mainly chrysotile, and the structure and the active groups of the grinding dust were not damaged. Third, the weights of the treated rats were obviously lower, and the lung weights and the pulmonary index increased significantly (P < 0.05). Fourth, the treated Wistar rat lung tissues revealed different degrees of congestion, edema, inflammatory cell infiltration, and mild fibrosis. Fifth, the p53 and p16 genes decreased in the Mangnai group after 1 month of exposure, and the other groups increased. The expression of p53 and p16 in each group decreased significantly after 6 months (P < 0.05). In conclusion, the respirable chrysotile fiber dust from the four primary areas of China had the risk of causing lung injury, and these changes may be related to the physical and chemical characteristics of chrysotile from different production areas.

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Polymorphisms of Selected DNA Repair Genes and Lung Cancer in Chromium Exposure

Cited by 5 publications

References 22 publications

DNA Mismatch Repair Gene Variants in Sporadic Solid Cancers

DNA Mismatch Repair Gene Variants in Sporadic Solid Cancers

Mechanisms and individuality in chromium toxicity in humans

Lung injury and expression of p53 and p16 in Wistar rats induced by respirable chrysotile fiber dust from four primary areas of China

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