Disease relevance of Sister Chromatid Exchange

• In BS cells, chromosomal abnormalities such as sister chromatid exchanges occur at highly elevated rates [1].
• REV3(-/-) cells showed significant increase in sister chromatid exchange events and chromosomal breaks even in the absence of exogenous genotoxic stress [2].
• The increase in sister chromatid exchanges induced in Fanconi's anemia lymphocytes by the monofunctional alkylating agent ethylmethane sulfonate (0.25 mg/ml) was slightly less than that in normal cells [3].
• Reduced level of DNA cross-links and sister chromatid exchanges in 1,3-bis(2-chloroethyl)-1-nitrosourea-resistant rat brain tumor cells [4].
• Induction of sister chromatid exchange by diethylstilbestrol in metabolically competent hepatoma cell lines but not in fibroblasts [5].

Psychiatry related information on Sister Chromatid Exchange

• Mitomycin C and ethyl methanesulphonate-induced sister-chromatid exchanges in lymphocytes from individuals with Alzheimer's pre-senile dementia [6].
• Effects of alcohol-drinking on mouse chromosomes. I. Sister-chromatid exchanges in the lymphocytes of mice administered ethanol [7].
• In order to study individual differences in response to the genotoxicity of diepoxybutane, we devised a human lymphocyte culture system that involves short-term culture of T lymphocytes and measurement of sister chromatid exchange (SCE) and chromosomal aberration frequency as genotoxic end-points [8].

High impact information on Sister Chromatid Exchange

• We propose that this recA-independent instability of tandemly repeated sequences is due to unequal intramolecular recombination events in replicating DNA molecules, a mechanism analogous to sister chromatid exchange in eucaryotes [9].
• The disruption of Nbs1 reduces gene conversion and sister chromatid exchanges, similar to other HR-deficient mutants [10].
• Critical test of a sister chromatid exchange model for the immunoglobulin heavy-chain class switch [11].
• These findings formally exclude both unequal sister chromatid exchange and recombination between homologues as mechanisms for creating a gene encoding the gamma 2b chain [11].
• To determine the relationship of metabolic potential to an easily quantified, short-term in vivo end point of genetic damage, we compared the ability of AHH inducible and uninducible mice to metabolize a procarcinogen, benzo(a)pyrene (BP), with the in vivo induction by BP of sister chromatid exchanges (SCEs) [12].

Chemical compound and disease context of Sister Chromatid Exchange

• By a recently developed technique using 33258 Hoechst and 5-bromodeoxyuridine, it was observed that the baseline frequency of sister chromatid exchanges in phytohemagglutinin-stimulated lymphocytes from four males with Fanconi's anemia differed little from that of normal lymphocytes [3].
• The induction of sister chromatid exchange (SCE) by N-methyl-N-nitrosourea (MNU) was studied in spleen and thymus lymphocytes from AKR mice, which are highly susceptible to MNU-produced thymomas, CBA mice, which are much less sensitive to induction of thymomas by MNU, and C57BL/6N x DBA/2J F1 mice [13].
• Induction of sister chromatid exchanges and chromosomal aberrations by busulfan in Philadelphia chromosome-positive chronic myeloid leukemia and normal bone marrow [14].
• The hematoporphyrin derivative incubation and photosensitization conditions used in this study did induce sister chromatid exchanges at frequencies comparable to those induced by X-rays but at lower frequencies than for UV treatments [15].
• When the effects of caffeine are compared in a normal Indian muntjac cell line and a simian virus 40 (SV40)-transformed, ultraviolet light (u.v.)-sensitive line in which u.v. induces many sister chromatid exchanges, different cell cycle sensitivities are seen [16].

Biological context of Sister Chromatid Exchange

• The sensitivity of 9L cells in mixed-cell spheroids treated with 1,3-bis(2-chloroethyl)-1-nitrosourea, estimated by changes in the number of sister chromatid exchanges per metaphase induced by treatment, decreased as the percentage of R3 cells increased [17].
• Normalization by cell fusion of sister chromatid exchange in Bloom syndrome lymphocytes [18].
• Somatic reconstitution of WRN function, but not a WRN helicase-deficient mutant, abolished telomere sister chromatid exchange (T-SCE), indicating that WRN normally represses T-SCEs [19].
• The effects of the flame retardant tris(2,3-dibromopropyl) phosphate (Tris-BP) on growth, sister chromatid exchanges (SCE), and chromosome aberrations of Chinese hamster V79 cells cultured either in vitro or in diffusion chambers (DC) implanted into mice were studied [20].
• Elevated sister chromatid exchange phenotype of Bloom syndrome cells is complemented by human chromosome 15 [21].

Anatomical context of Sister Chromatid Exchange

• Exposure to ethylene oxide at work increases sister chromatid exchanges in human peripheral lymphocytes [22].
• In vitro, Ku70-/- mouse fibroblasts displayed an increased rate of sister chromatid exchange and a high frequency of spontaneous neoplastic transformation [23].
• When nonisotopic bromodeoxyuridine (BUDR), 10(-6)-10(-4) M, was used with the B-cells and NTL, SCD were clearly evident and sister chromatid exchange (SCE) was relatively infrequent; when the concentration was 10(-7) M, SCD staining was poor but the frequency of SCE was high [24].
• The mouse myeloma cell line MPC 11 carries two C gamma 2a immunoglobulin heavy-chain genes on the expressed chromosome, a duplication shown to have occurred through unequal sister chromatid exchange (USCE) [25].
• The present study was performed to determine whether or not ascorbic acid affects sister chromatid exchanges (SCEs) induced by cyclophosphamide (CPA) and mitomycin C (MMC) in bone marrow and spleen cells in mice [26].

Associations of Sister Chromatid Exchange with chemical compounds

• We now report that DES is positive in sister chromatid exchange (SCE) induction, a short-term test for which a high correlation with the carcinogenicity of the compounds tested has been observed [27].
• Both that saccharin and a highly purified extract of it increased the yield of sister chromatid exchanges in both types of cells [28].
• However, higher concentrations (10 microM) of selenite had no effect on oxidant-induced sister chromatid exchange formation, and 0.1 mM selenite increased the number of exchanges [29].
• Estrogen effects on sister chromatid exchanges in mouse uterine cervical and kidney cells [30].
• On the other hand, cultivation of target cells with supplemental tocopherol protected them from the toxic effects of the enzymatic oxidant-producing system, indicating a role for membrane-associated free radicals in the mechanism of sister chromatid exchange induction [29].

Gene context of Sister Chromatid Exchange

• Sensitivity to DNA-damaging agents and sister-chromatid exchange were not affected in RAD54B-deficient cells [31].
• Molecular cloning of the human XRCC1 gene, which corrects defective DNA strand break repair and sister chromatid exchange [32].
• LIG3 mutant cells have relatively normal XRCC1 levels but elevated sister chromatid exchange [33].
• Cellular features of BS include an accumulation of abnormal replication intermediates and increased sister chromatid exchange [34].
• Consistent with a role for RAD51L2 in homologous recombination, irs3 cells show a reduction in sister chromatid exchange, an increase in isochromatid breaks, and a decrease in damage-dependent RAD51 focus formation compared with wild type cells [35].

Analytical, diagnostic and therapeutic context of Sister Chromatid Exchange

• Neither sister-chromatid exchange nor gene-targeting frequencies show a dependence on these NHEJ proteins [36].
• Recombination and ligation of transfected DNA in CHO mutant EM9, which has high levels of sister chromatid exchange [37].
• We suggested previously that VP-16-induced cytotoxicity is mediated by a series of events leading from cleavable complex formation to aberrant DNA recombination, as measured by sister chromatid exchange (SCE) and Southern blot analysis of the hypoxanthine phosphoribosyl transferase (hprt) gene mutations [38].
• Oral administration of 175 mg/kg ranitidine HCl + 80 mg/kg NaNO2 in fasted and histamine-injected mice induced a modest but statistically significant increase in the frequency of sister chromatid exchanges in bone marrow cells [39].
• We investigated the role of GSTM1 and GSTT1 polymorphisms in modifying the genotoxicity of a tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) using the sister chromatid exchange (SCE), and the tandem-probe fluorescence in situ hybridization chromosome aberration (CA) assays [40].

References