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Molecular Approaches Towards the Isolation of Pediatric Cancer Predisposition Genes
Published in John T. Kemshead, Pediatric Tumors: Immunological and Molecular Markers, 2020
Cells from Rb patients may be more prone than normal cells to radiation induced mutation. Several groups have tried to investigate this possibility. Sister chromatid exchange (SCE) has been used as an index of fragility in cells from Rb patients. Whereas Wechselbaum et al.60 claimed increased SCE frequencies in fibroblasts, others61 could not repeat this observation. Recently, Sanford and colleagues have shown chromosome fragility in all Rb patients compared with normal controls.62 In their experiments, lymphocytes were subjected to radiation but only in the more sensitive G2 period of the cell cycle. This stage specificity may account for the variability seen by others. Interestingly, the same sensitivity was shown in cells from Wilms’ tumor patients.62
General Biological Aspects of Oncogenesis
Published in Pimentel Enrique, Oncogenes, 2020
An increase in the frequency of sister chromatid exchange (SCE) is considered as an excellent parameter for demonstrating the mutagenic action of a wide number of physical, biological, and chemical agents. In cancer patients, cancer-prone families, or in patients with high risk for cancer no significant differences in SCE frequencies have been found.319 Many other examples of discrepancy between mutagenicity and carcinogenicity could be mentioned but there will always remain criticisms related to methodological aspects. Indeed, it is a very difficult task to exclude mutagenicity or carcinogenicity since the appropriate experimental conditions could have not been fulfilled.
B Cells and Humoral Immunity
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
Two additional mechanisms may also result in class-switching, although they are not thought to occur with significant frequency, if at all. One hypothesis is identical to the differential splicing of a transcript containing μ and δ. If we imagine that RNA polymerase may continue along the DNA transcribing all of the C region genes, then VDJH joined to any isotype can be generated by differential splicing. Another model for class-switching invokes unequal sister chromatid exchange. During mitosis, sister chromatids may exchange some portions of themselves. If the positions of the joints between chromatids are identical, one has homologous recombination, or equal crossing over. The amount of genetic information in each chromatid remains unchanged. If the breaks occur in different positions in the chromatids, one has non-homologous recombination, or unequal crossing over. This results in deletion of genetic information from one chromatid, and its duplication in the other.
Citral presents cytotoxic and genotoxic effects in human cultured cells
Published in Drug and Chemical Toxicology, 2020
Ana C. S. Souza, Laís K. Silva, Thais B. Queiroz, Eduardo S. Marques, Clélia A. Hiruma-Lima, Isabel O. M. Gaivão, Edson L. Maistro
Our literature review showed that there were some initial efforts to establish the teratogenic, genotoxic and carcinogenic potentials of citral. Nogueira et al. (1995) showed that citral at doses above 60 mg/kg induces maternal toxicity and embryofeto-toxicity. Duerksen-Hughes et al. (1999) reported that citral is genotoxic, using an increase in cellular p53 protein as evidence for DNA damage. The National Toxicology Program (NTP 2003) reported that, after 2-years of animal supplementation studies, there was no evidence of citral carcinogenic activities in F344/N rats (males and females) and in B6C3F1 mice (males). However, there was equivocal evidence of carcinogenic activity in B6C3F1 females based on malignant lymphoma increased incidences. Regarding genotoxicity, the same study concluded that citral presented negative results in in vitro and in vivo tests, with the exception of the in vitro mammalian cell test for sister chromatid exchange induction. More recently, Porto et al. (2014) stated that citral exhibits genotoxic activity in murine peritoneal macrophages, but also chemopreventive effects against doxorubicin induced DNA damages. Furthermore, there are no studies evaluating citral cytotoxicity and genotoxicity in human cells with hepatic metabolism.
Correlation between cytogenetic biomarkers obtained from DC and CBMN assays caused by low dose radon exposure in smokers
Published in International Journal of Radiation Biology, 2019
Micronucleus is small, extra nuclear bodies that are formed from acentric fragments. Radiation induced micronuclei originates from acentric fragments whereas spontaneous micronuclei contains whole chromosomes (Pala et al. 2008; Durante and Formenti 2018). Available body of evidence between micronuclei and dicentric correlation gives varied results. In the present study, positive correlation was observed between micronuclei and acentric fragments in non-smokers. There was positive correlation between the dicentric level in lymphocytes and micronuclei level in exfoliated buccal mucosa cells (Lucero et al 2000, Patel et al 2009; Pinto et al. 2000). However, few studies found no positive correlation between micronuclei and acentric fragments (Kryscio et al. 2001; Müller et al. 2004). Albering et al. (1992) observed no correlation between any cytogenetic endpoint (sister chromatid exchange, micronuclei, chromosome aberrations).
Genotoxic and mutagenic studies of teratogens in developing rat and mouse
Published in Drug and Chemical Toxicology, 2019
Eyyüp Rencüzoğulları, Muhsin Aydın
Many articles have been published that show in vitro or in vivo tests give extremely reliable results when performed in accordance with international guidelines. Sister chromatid exchange is the exchange of DNA replication products between the homologous loci of sister chromatids that repair DNA double chain breaks by homologous recombination (Sonoda et al. 1999, Helleday 2003). In humans and animals that are exposed to substances known to be mutagenic and carcinogenic, the frequency of SCE is increased and a linear relationship was found between the increase in single-gene mutations and the frequency of SCE (Perry and Evans 1975, Carrano et al. 1978, Albertini et al. 2000). Cheng et al. (1981) reported a similar relationship between the increase of SCE and the formation of in vivo tumors. Unlike CA, SCE is insufficient to determine genotoxic risk alone. However, in experimental studies, SCE is still used as an indicator test that is a suitable method for demonstrating genotoxic effects in humans (Norppa et al. 2006).