Topic
Sister chromatid exchange
About: Sister chromatid exchange is a research topic. Over the lifetime, 3187 publications have been published within this topic receiving 90029 citations. The topic is also known as: replication-born DSB repair by SCE & GO:1990414.
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TL;DR: The combined use of these two experimental tools has defined the biological consequences of 3-methyladenine, a DNA lesion produced by endogenous cellular metabolites, environmental carcinogens, and chemotherapeutic alkylating agents.
131 citations
TL;DR: This report identifies those modifications to previously described methods that are used on a regular basis and clarifies confusing or inconsistent practices.
Abstract: A recommended protocol has been developed for chromosomal aberration and sister-chromatid exchange assays in CHO, V79 and human lymphocyte cultures. The protocol was based on the responses to a detailed questionnaire completed by North-American and European governmental, university, and contract laboratories using these tests. This report identifies those modifications to previously described methods that are used on a regular basis and clarifies confusing or inconsistent practices. These protocols can be modified for use in other types of cells.
131 citations
TL;DR: The SCEs of patients under chemotherapy were about five times higher than those of healthy subjects, and the oncology nurses had a higher SCE frequency than other hospital nurses, but this difference was not statistically significant.
Abstract: In oncology units, personnel handling chemotherapeutic drugs may occasionally be exposed to small amounts of genotoxic agents. This exposure was obviously the cause of the increased frequencies of sister chromatid exchange (SCE) observed in nurses in daily contact with cytostatics (N = 20, mean SCEs/cell +/- SE 9.4 +/- 0.3) as compared to a group of office workers (N = 10, mean SCEs/cell 8.1 +/- 0.3). The oncology nurses also had a higher SCE frequency than other hospital nurses (N = 10, mean SCEs/cell 8.7 +/- 0.2), but this difference was not statistically significant. The SCEs of patients under chemotherapy were about five times higher (mean SCEs/cell 36.8 +/- 0.6) than those of healthy subjects.
131 citations
TL;DR: Reviewing the investigations published in scientific journals during 1990–2003 attempts to identify probable reason(s) for the conflicting results and makes recommendations for future research to address some of the controversial observations.
Abstract: Vijayalaxmi and Obe, G. Controversial Cytogenetic Observations in Mammalian Somatic Cells Exposed to Radiofrequency Radiation. Radiat. Res. 162, 481–496 (2004). During the years 1990–2003 a large number of investigations were conducted using rodents, cultured rodent and human cells, and freshly collected human blood lymphocytes to determine the genotoxic potential of exposure to radiofrequency (RF) radiation. The results of most of these studies (58%) did not indicate increased damage to the genetic material (assessed from DNA strand breaks, incidence of chromosomal aberrations, micronuclei and sister chromatid exchanges) in cells exposed to RF radiation compared to sham-exposed and/or unexposed cells. Some investigations (23%) reported an increase in such damage in cells exposed to RF radiation. The observations from other studies (19%) were inconclusive. This paper reviews the investigations published in scientific journals during 1990–2003 and attempts to identify probable reason(s) for the co...
131 citations
TL;DR: It is proposed that Rad50, an SMC‐like protein, promotes the use of the sister chromatid as the template for homologous recombinational repair, and functions in the same pathway for the repair of MMS‐induced damage as Rad21, the homologue of the Saccharomyces cerevisiae Scc1 cohesin protein.
Abstract: To study the role of Rad50 in the DNA damage response, we cloned and deleted the Schizosaccharo myces pombe RAD50 homologue The deletion is sensitive to a range of DNA-damaging agents and shows dynamic epistatic interactions with other recombination?repair genes We show that Rad50 is necessary for recombinational repair of the DNA lesion at the mating-type locus and that rad50 shows slow DNA replication We also find that Rad50 is not required for slowing down S phase in response to hydroxy urea or methyl methanesulfonate (MMS) treatment Interestingly, in rad50 cells, the recombination frequency between two homologous chromosomes is increased at the expense of sister chromatid recombination We propose that Rad50, an SMC-like protein, promotes the use of the sister chromatid as the template for homologous recombinational repair In support of this, we found that Rad50 functions in the same pathway for the repair of MMS-induced damage as Rad21, the homologue of the Saccharomyces cerevisiae Scc1 cohesin protein We speculate that Rad50 interacts with the cohesin complex during S phase to assist repair and possibly re-initiation of replication after replication fork collapse
130 citations