Molecular aspects of chemical carcinogenesis: The roles of oncogenes and tumour suppressor genes

KRAS and TP53 mutations in bronchoscopy samples from former lung cancer patients

“…Furthermore, these mutations were found in samples from both current smokers and ex‐smokers, with TP53 mutations occurring more frequently in current smokers than in ex‐smokers, whereas the KRAS mutation frequencies were not significantly different between the two groups of patients. The predominance of G to T transversion and G to A transition in both genes in bronchial tissues are in line with previous studies showing that such mutations were frequent in lung tumors obtained from active and ex‐smokers and that they are strongly associated with exposure to cigarette smoke . The frequency of TP53 hotspot mutation, such as codon 248 mutation (16 of 77, or 21%), was in agreement with our previous report demonstrating that TP53 codon 248 mutation was mostly found in primary lung tumors from NSCLC in smokers .…”

KRAS and TP53 mutations in bronchoscopy samples from former lung cancer patients

“…Furthermore, these mutations were found in samples from both current smokers and ex‐smokers, with TP53 mutations occurring more frequently in current smokers than in ex‐smokers, whereas the KRAS mutation frequencies were not significantly different between the two groups of patients. The predominance of G to T transversion and G to A transition in both genes in bronchial tissues are in line with previous studies showing that such mutations were frequent in lung tumors obtained from active and ex‐smokers and that they are strongly associated with exposure to cigarette smoke . The frequency of TP53 hotspot mutation, such as codon 248 mutation (16 of 77, or 21%), was in agreement with our previous report demonstrating that TP53 codon 248 mutation was mostly found in primary lung tumors from NSCLC in smokers .…”

BRG1 and BRM loss selectively impacts RB and P53, respectively: BRG1 and BRM have differential functions in vivo

“…We first conducted IHC for total Rb1 expression to exclude the loss of Rb1, and we observed that Rb1- negative tumor cells accounted for less than 5% of all tumor cells in tumors from each of the four genotypes, which is consistent with previously published reports [43]. Next, dual IF staining was conducted with anti-Brm and anti-pRb1S780 antibodies to determine the phosphorylation state of Rb1 as a function of Brm expression.…”

No mutations found in exons of TP53, H-RAS and K-RAS genes in liver of male Wistar rats submitted to a medium-term chemical carcinogenesis assay

“…These results are in accordance with other studies in the literature (14,17,23,25,27), as discussed below.…”

“…Similar results were found by Kress et al (1992) in tumors induced by UV radiation: no alterations were found in papilomas, but significant mutations were detected in carcinomas (17). Taken together, these data suggest that alterations in TP53 gene are not necessarily limited to the initiation or promotion stages of carcinogenesis and probably occur late in the carcinogenic process (27).…”

KRAS and TP53 mutations in bronchoscopy samples from former lung cancer patients

“…Furthermore, these mutations were found in samples from both current smokers and ex‐smokers, with TP53 mutations occurring more frequently in current smokers than in ex‐smokers, whereas the KRAS mutation frequencies were not significantly different between the two groups of patients. The predominance of G to T transversion and G to A transition in both genes in bronchial tissues are in line with previous studies showing that such mutations were frequent in lung tumors obtained from active and ex‐smokers and that they are strongly associated with exposure to cigarette smoke . The frequency of TP53 hotspot mutation, such as codon 248 mutation (16 of 77, or 21%), was in agreement with our previous report demonstrating that TP53 codon 248 mutation was mostly found in primary lung tumors from NSCLC in smokers .…”

BRG1 and BRM loss selectively impacts RB and P53, respectively: BRG1 and BRM have differential functions in vivo

“…We first conducted IHC for total Rb1 expression to exclude the loss of Rb1, and we observed that Rb1- negative tumor cells accounted for less than 5% of all tumor cells in tumors from each of the four genotypes, which is consistent with previously published reports [43]. Next, dual IF staining was conducted with anti-Brm and anti-pRb1S780 antibodies to determine the phosphorylation state of Rb1 as a function of Brm expression.…”

No mutations found in exons of TP53, H-RAS and K-RAS genes in liver of male Wistar rats submitted to a medium-term chemical carcinogenesis assay

“…These results are in accordance with other studies in the literature (14,17,23,25,27), as discussed below.…”

“…Similar results were found by Kress et al (1992) in tumors induced by UV radiation: no alterations were found in papilomas, but significant mutations were detected in carcinomas (17). Taken together, these data suggest that alterations in TP53 gene are not necessarily limited to the initiation or promotion stages of carcinogenesis and probably occur late in the carcinogenic process (27).…”

KRAS and TP53 mutations in bronchoscopy samples from former lung cancer patients

“…Furthermore, these mutations were found in samples from both current smokers and ex‐smokers, with TP53 mutations occurring more frequently in current smokers than in ex‐smokers, whereas the KRAS mutation frequencies were not significantly different between the two groups of patients. The predominance of G to T transversion and G to A transition in both genes in bronchial tissues are in line with previous studies showing that such mutations were frequent in lung tumors obtained from active and ex‐smokers and that they are strongly associated with exposure to cigarette smoke . The frequency of TP53 hotspot mutation, such as codon 248 mutation (16 of 77, or 21%), was in agreement with our previous report demonstrating that TP53 codon 248 mutation was mostly found in primary lung tumors from NSCLC in smokers .…”

BRG1 and BRM loss selectively impacts RB and P53, respectively: BRG1 and BRM have differential functions in vivo

“…We first conducted IHC for total Rb1 expression to exclude the loss of Rb1, and we observed that Rb1- negative tumor cells accounted for less than 5% of all tumor cells in tumors from each of the four genotypes, which is consistent with previously published reports [43]. Next, dual IF staining was conducted with anti-Brm and anti-pRb1S780 antibodies to determine the phosphorylation state of Rb1 as a function of Brm expression.…”

No mutations found in exons of TP53, H-RAS and K-RAS genes in liver of male Wistar rats submitted to a medium-term chemical carcinogenesis assay

“…These results are in accordance with other studies in the literature (14,17,23,25,27), as discussed below.…”

“…Similar results were found by Kress et al (1992) in tumors induced by UV radiation: no alterations were found in papilomas, but significant mutations were detected in carcinomas (17). Taken together, these data suggest that alterations in TP53 gene are not necessarily limited to the initiation or promotion stages of carcinogenesis and probably occur late in the carcinogenic process (27).…”