Stephen E. Bloom

Bio: Stephen E. Bloom is an academic researcher from Ithaca College. The author has contributed to research in topics: Sister chromatid exchange & Sister Chromatid Exchange Assay. The author has an hindex of 1, co-authored 1 publications receiving 571 citations.

Sister-chromatid exchanges: a report of the GENE-TOX program.

Abstract: This paper reviews the ability of a number of chemicals to induce sister-chromatid exchanges (SCEs). The SCE data for animal cells in vivo and in vitro, and human cells in vitro are presented in 6 tables according to their relative effectiveness. A seventh table summarizes what is known about the effects of specific chemicals on SCEs for humans exposed in vivo. The data support the concept that SCEs provide a useful indication of exposure, although the mechanism and biological significance of SCE formation still remain to be elucidated.

IPCS guidelines for the monitoring of genotoxic effects of carcinogens in humans

Abstract: The purpose of these guidelines is to provide concise guidance on the planning, performing and interpretation of studies to monitor groups or individuals exposed to genotoxic agents. Most human carcinogens are genotoxic but not all genotoxic agents have been shown to be carcinogenic in humans. Although the main interest in these studies is due to the association of genotoxicity with carcinogenicity, there is also an inherent interest in monitoring human genotoxicity independently of cancer as an endpoint. The most often studied genotoxicity endpoints have been selected for inclusion in this document and they are structural and numerical chromosomal aberrations assessed using cytogenetic methods (classical chromosomal aberration analysis (CA), fluorescence in situ hybridisation (FISH), micronuclei (MN)); DNA damage (adducts, strand breaks, crosslinking, alkali-labile sites) assessed using bio-chemical/electrophoretic assays or sister chromatid exchanges (SCE); protein adducts; and hypoxanthine-guanine phosphoribosyltransferase (HPRT) mutations. The document does not consider germ cells or gene mutation assays other than HPRT or markers of oxidative stress, which have been applied on a more limited scale.

Chromosome aberrations, micronuclei, aneuploidy, sister chromatid exchanges, and cancer risk assessment.

Abstract: This paper describes the four cytogenetic endpoints most frequently used in hazard identification assays as the first step in the risk assessment process. These are structural chromosome aberrations, micronuclei, aneuploidy, and sister chromatid exchanges. The biological mechanisms involved in the formation of the alterations observed in each assay are briefly discussed. Variations in and recent improvements to each assay are described, with an emphasis on the use of molecular techniques to improve the sensitivity of the assay, and to allow for detection of specific alterations that are, or could be, associated with cancer induction. This, in turn, will make the data obtained in the cytogenetic assays more useful in cancer and genetic risk assessment. Thus, the aim of this paper is to encourage cytogeneticists to design their experiments in such a way that the data obtained will be of maximum possible benefit for characterizing and quantifying adverse human health effects, particularly cancer.

Cyclophosphamide: Review of its mutagenicity for an assessment of potential germ cell risks

Abstract: Cyclophosphamide (CP) is used to treat a wide range of neoplastic diseases as well as some non-malignant ones such as rheumatoid arthritis It is also used as an immunosuppressive agent prior to organ transplantation CP is, however, a known carcinogen in humans and produces secondary tumors There is little absorption either orally or intravenously and 10% of the drug is excreted unchanged CP is activated by hepatic mixed function oxidases and metabolites are delivered to neoplastic cells via the bloodstream Phosphoramide mustard is thought to be the major anti-neoplastic metabolite of CP while acrolein, which is highly toxic and is produced in equimolar amounts, is thought to be responsible for most of the toxic side effects DNA adducts have been formed after CP treatment in a variety of in vitro systems as well as in rats and mice using 3H-labeled CP 32P-postlabeling techniques have also been used in mice However, monitoring of adducts in humans has not yet been carried out CP has also been shown to induce unscheduled DNA synthesis in a human cell line CP has produced mutations in base-pair substituting strains of Salmonella tryphimurium in the presence of metabolic activation, but it has been shown to be negative in the E coli chromotest It has also been shown to be positive in Saccharomyces cerevisiae in D7 strain for many endpoints but negative in D62M for aneuploidy/malsegregation It has produced positive responses in Drosophila melanogaster for various endpoints and in Anopheles stephensi In somatic cells, CP has been shown to produce gene mutations, chromosome aberrations, micronuclei and sister chromatid exchanges in a variety of cultured cells in the presence of metabolic activation as well as sister chromatid exchanges without metabolic activation It has also produced chromosome damage and micronuclei in rats, mice and Chinese hamsters, and gene mutations in the mouse spot test and in the transgenic lacZ construct of Muta Mouse Increases in chromosome damage and gene mutations have been found in the peripheral blood lymphocytes of nurses, pharmacists and female workers occupationally exposured to CP during its production or distribution Chromosome aberrations, sister chromatid exchanges and gene mutations have been observed in somatic cells of patients treated therapeutically with CP In general, there is a maximum dose and an optimum time for the detection of genetic effects because the toxicity associated with high doses of CP will affect cell division In germ cells, CP has been shown to induce genetic damage in mice, rats and hamsters although the vast majority of such studies have used male mice(ABSTRACT TRUNCATED AT 400 WORDS)

Stimulated Human Phagocytes Produce Cytogenetic Changes in Cultured Mammalian Cells

Abstract: CHRONIC inflammation can be associated with cancer.1 Phagocytes in inflammatory lesions enzymatically reduce oxygen to reactive metabolites, which include Superoxide anions, hydrogen peroxide, and ...