2021
DOI: 10.1007/s00204-021-03146-5
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Cobalt-induced oxidative stress contributes to alveolar/bronchiolar carcinogenesis in B6C3F1/N mice

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Cited by 6 publications
(3 citation statements)
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“…Alveolar/bronchiolar carcinomas in rodents, whether occurring spontaneously or due to chemical exposure, bear resemblance to a specific subtype of lung adenocarcinomas observed in humans. Oxidative stress is a key factor in pulmonary carcinogenesis induced by cobalt metal dust (CMD) in rodents, and these discoveries may have implications for understanding human lung cancers as well [54]. The impact of CoCl2 was also examined on numerous histone modifications at a global level.…”
Section: Cobaltmentioning
confidence: 99%
“…Alveolar/bronchiolar carcinomas in rodents, whether occurring spontaneously or due to chemical exposure, bear resemblance to a specific subtype of lung adenocarcinomas observed in humans. Oxidative stress is a key factor in pulmonary carcinogenesis induced by cobalt metal dust (CMD) in rodents, and these discoveries may have implications for understanding human lung cancers as well [54]. The impact of CoCl2 was also examined on numerous histone modifications at a global level.…”
Section: Cobaltmentioning
confidence: 99%
“…For example, G to T transversions in codon 12 of Kras gene are commonly noted in lung cancers resulting from tobacco smoke exposure and also in rodent lung tumors resulting from chronic exposure to cobalt, which is mechanistically attributed to metal-induced oxidative stress. 9,10…”
Section: Introductionmentioning
confidence: 99%
“…For example, G to T transversions in codon 12 of Kras gene are commonly noted in lung cancers resulting from tobacco smoke exposure and also in rodent lung tumors resulting from chronic exposure to cobalt, which is mechanistically attributed to metal-induced oxidative stress. 9,10 In human non-small-cell lung cancer (NSCLC), the incidence of Kras mutations is approximately 26%, with the majority of the point mutations seen in codon 12 followed by fewer mutations in codons 13 and 61. 5,11 Point mutations in codons 12, 13, and 61 of Kras are activating mutations that result in constitutive activation of the KRAS protein, making it refractory to the inhibitory GTPase-activating proteins, which results in stimulus-independent, persistent activation of downstream effectors, in particular, the RAF-MEK-ERK cascade.…”
Section: Introductionmentioning
confidence: 99%