Titlebook: Genetic Consequences of Nucleotide Pool Imbalance; Frederick J. Serres Book 1985 Plenum Press, New York 1985 DNA.Nucleotide.enzyme.gene.ge

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Misincorporation of Deoxyuridine in Human Cells: Consequences of Antifolate Exposurealkaline sucrose gradient analysis. Significantly, new replication of DNA was inhibited only ∿50% by 50 μM BW301U when [.H]dU incorporation was ≥97% inhibited. Additional preliminary findings suggest that newly replicated DNA containing misincorporated dUMP is rapidly degraded. by extensive excision-repair processes.

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Book 1985d the majority of papers in this volume de­ scribe the effects of nucleotide pool imbalance on DNA replication and repair, and the induction of gene mutations in various organisms. This book grew out of a Conference on "Genetic Consequences of Nu­ cleotide Pool Imbalance" which was held at the Natio

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https://doi.org/10.1007/978-981-97-3674-4bility of genes, and of the ‘fluidity’ of the genome. It is responsible, ultimately, for the origin of species, but more immediately, for a substantial number of serious human diseases, including cancer.

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Criminal Procedural Trial in Chinaining to the mechanisms of the above synergistic effects, and we discuss some possible practical applications of our findings to the control of the development of drug resistance in cells treated with chemicals used in cancer chemotherapy.

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Molecular Mechanisms in Genetic Stability and Change: The Role of Deoxyribonucleotide Pool Balancebility of genes, and of the ‘fluidity’ of the genome. It is responsible, ultimately, for the origin of species, but more immediately, for a substantial number of serious human diseases, including cancer.

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Biological Consequences of Guanine Starvationan CCRF-CEM, wild type and HGPRT-ase negative) [3], which suggests a more general applicability of the finding that DNA synthesis inhibition by guanine starvation is independent of the total dGTP cellular pool size.

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The Genetic Consequences of the Thy- Mutation to CHO Cellss of Chinese hamster ovary (CHO) cells, called Thy., and we speculate how the pool alterations produced by this metabolic defect might contribute to increased mutational rates and altered sensitivity to DNA damaging agents.

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Deoxyribonucleoside-Induced Selective Modulation of Cytotoxicity and Mutagenesisining to the mechanisms of the above synergistic effects, and we discuss some possible practical applications of our findings to the control of the development of drug resistance in cells treated with chemicals used in cancer chemotherapy.