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      Genetic and cellular mechanisms in chromium and nickel carcinogenesis considering epidemiologic findings.

      Molecular and Cellular Biochemistry
      Animals, Carcinogens, Environmental, metabolism, toxicity, Cell Transformation, Neoplastic, chemically induced, genetics, Chromium, chemistry, Drosophila, Electron Spin Resonance Spectroscopy, Environmental Exposure, Gene Expression Regulation, Neoplastic, drug effects, Humans, Mutation, Neoplasms, epidemiology, Nickel, Occupational Diseases, Occupational Exposure, Occupational Health, Public Health, Recombination, Genetic

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          Abstract

          Genetic and environmental interactions determine cancer risks but some cancer incidence is primarily a result of inherited genetic deficits alone. Most cancers have an occupational, viral, nutritional, behavioral or iatrogenic etiology. Cancer can sometimes be controlled through broad public health interventions including industrial hygiene and engineering controls. Chromium and nickel are two human carcinogens associated with industrial exposures where public health measures apparently work. Carcinogenic mechanisms of these metals are examined by electron-spin-resonance-spectroscopy and somatic-mutation-and-recombination in Drosophila melanogaster in this report. Both metals primarily affect initiation processes in cancer development suggesting important theoretical approaches to prevention and followup.

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