Biological effects of essential oils - A review

Prospective Cohort Study

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Modern Applied Statistics With S

The cytokinesis-block micronucleus cytome assay is a comprehensive system for measuring DNA damage, cytostasis and cytotoxicity. DNA damage events are scored specifically in once-divided binucleated (BN) cells and include (a) micronuclei (MNi), a biomarker of chromosome breakage and/or whole chromosome loss, (b) nucleoplasmic bridges (NPBs), a biomarker of DNA misrepair and/or telomere end-fusions, and (c) nuclear buds (NBUDs), a biomarker of elimination of amplified DNA and/or DNA repair complexes. Cytostatic effects are measured via the proportion of mono-, bi- and multinucleated cells and cytotoxicity via necrotic and/or apoptotic cell ratios. Further information regarding mechanisms leading to MNi, NPBs and NBUDs formation is obtained using centromere and/or telomere probes. The assay is being applied successfully for biomonitoring of in vivo genotoxin exposure, in vitro genotoxicity testing and in diverse research fields such as nutrigenomics and pharmacogenomics as well as a predictor of normal tissue and tumor radiation sensitivity and cancer risk. The procedure can take up to 5 days to complete.

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Cytokinesis-block micronucleus cytome assay

Recently, more than 1000 large intergenic noncoding RNAs (lincRNAs) have been reported. These RNAs are evolutionarily conserved in mammalian genomes and thus presumably function in diverse biological processes. Here, we report the identification of lincRNAs that are regulated by p53. One of these lincRNAs (lincRNA-p21) serves as a repressor in p53-dependent transcriptional responses. Inhibition of lincRNA-p21 affects the expression of hundreds of gene targets enriched for genes normally repressed by p53. The observed transcriptional repression by lincRNA-p21 is mediated through the physical association with hnRNP-K. This interaction is required for proper genomic localization of hnRNP-K at repressed genes and regulation of p53 mediates apoptosis. We propose a model whereby transcription factors activate lincRNAs that serve as key repressors by physically associating with repressive complexes and modulate their localization to sets of previously active genes.

A Large Intergenic Noncoding RNA Induced by p53 Mediates Global Gene Repression in the p53 Response

There are demonstrable associations in experimental animals between DNA damage in somatic cells and the development of cancer, and between DNA damage in germ cells and the incidence of genetic disease in offspring. Thus, there is substantial evidence of the need to detect and to quantitate chemically-induced genetic damage in humans in order to assess the potential for cancer and genetic disease. Current methods for estimating human risk of cancer have been based on knowledge of human exposure and epidemiological data. An alternative approach would base such estimates of risk on knowledge of exposure and of damage to the DNA of human cells and tissues. The principal difficulty in performing such assessments lies in the uncertainty of translating information from tests for genetic damage in human cells and tissues into reliable estimates of risk for cancer or genetic disease. This poster concerns: (1) the development of mammalian cell methods that may be used ultimately to evaluate genotoxic effects in humans and (2) our initial attempts to implement a 'parallelogram' approach whereby such methods can be used, collectively, to relate quantitative information on genetic damage to quantitative estimates of risk for cancer or genetic disease.

Michael D. Waters

Papers

Evaluation of Genotoxic Effects in Human Populations

What Stressors Cause Cancer and When

Unscheduled DNA synthesis testing of pesticides

Use of prolonged treatment and the fluctuation test to detect mutations in human fibroblasts treated with methyl methanesulfonate.

A tribute to Donald G. MacPhee