Robert J. Preston

Works (3)

Updated: July 5th, 2023 16:03

2000 journal article

A comparison of the roles of p53 mutation and AraC inhibition in the enhancement of bleomycin-induced chromatid aberrations in mouse and human cells

MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS, 447(2), 227–237.

By: T. Allio n, E. Donner * & R. Preston*

author keywords: p53; DNA repair; bleomycin; 1-beta-D-arabinofuranosylcytosine; AraC
MeSH headings : Animals; Bleomycin / pharmacology; Cell Line; Cells, Cultured; Chromosome Aberrations / genetics; Cytarabine / pharmacology; DNA Repair / genetics; Dose-Response Relationship, Drug; G2 Phase; Humans; Mice; Mice, Knockout; Mitomycin / pharmacology; Mitotic Index / drug effects; Mutation; Nucleic Acid Synthesis Inhibitors / pharmacology; S Phase; Tumor Suppressor Protein p53 / genetics
TL;DR: The results suggest that an AraC-sensitive DNA repair component is altered or absent in p53-/- cells, and p53 deficiency does not affect DNA replication fidelity or the repair of MMC-induced DNA damage. (via Semantic Scholar)
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Source: Web Of Science
Added: August 6, 2018

2000 journal article

Increased sensitivity to chromatid aberration induction by bleomycin and neocarzinostatin results from alterations in a DNA damage response pathway

MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS, 453(1), 5–15.

By: T. Allio n & R. Preston*

author keywords: DNA damage response pathways; ATM; p53; Brca1; Brca2; DNA-PK
MeSH headings : Ataxia Telangiectasia Mutated Proteins; Bleomycin / pharmacology; Cell Cycle Proteins; Cell Line; Chromatids / drug effects; Chromosome Aberrations; DNA Damage; DNA-Binding Proteins; Genes, p53; Humans; Mitosis; Mutagens / pharmacology; Protein Serine-Threonine Kinases / genetics; Tumor Suppressor Proteins; Zinostatin / pharmacology
TL;DR: Differential sensitivities suggest that the ATM phenotype is the result of dual cellular defects, one involving p53 and the other a wortmannin-sensitive component, and the response to BLM- and NCS-induced lesions involves different mechanisms. (via Semantic Scholar)
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Source: Web Of Science
Added: August 6, 2018

1998 journal article

Attenuation of G(1) checkpoint function by the non-genotoxic carcinogen phenobarbital

CARCINOGENESIS, 19(7), 1173–1183.

By: A. Gonzales *, J. Christensen, R. Preston, T. Goldsworthy, T. Tlsty & T. Fox

MeSH headings : Animals; Bleomycin / pharmacology; Carcinogens / toxicity; Cell Cycle / drug effects; Cell Cycle / physiology; Cells, Cultured; DNA / drug effects; DNA / metabolism; DNA Damage; G1 Phase / drug effects; G1 Phase / physiology; Liver / cytology; Liver / drug effects; Liver / metabolism; Liver Neoplasms, Experimental / chemically induced; Liver Neoplasms, Experimental / genetics; Male; Mice; Mice, Inbred C57BL; Phenobarbital / toxicity; S Phase / drug effects; S Phase / physiology; Tumor Suppressor Protein p53 / biosynthesis; Tumor Suppressor Protein p53 / metabolism
TL;DR: Altered G1 checkpoint function represents an epigenetic mechanism by which phenobarbital may prevent the detection and repair of DNA damage and indirectly increase the frequency of genotoxic events above that occurring spontaneously. (via Semantic Scholar)
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3. Good Health and Well-being (Web of Science; OpenAlex)
Source: Web Of Science
Added: August 6, 2018

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