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John J. Roberts

Researcher at Institute of Cancer Research

Publications -  42
Citations -  2842

John J. Roberts is an academic researcher from Institute of Cancer Research. The author has contributed to research in topics: DNA & Cisplatin. The author has an hindex of 28, co-authored 42 publications receiving 2806 citations.

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Journal ArticleDOI

The Walker 256 carcinoma: a cell type inherently sensitive only to those difunctional agents that can form DNA interstrand crosslinks.

TL;DR: In their sensitivity only to difunctional compounds and lack of an apparent DNA excision repair defect the phenotype of Walker cells strongly resembles those cells from human patients suffering from Fanconi's anaemia and also of yeast snm1 mutant cells.
Journal ArticleDOI

The Excision of N-Methyl-N-nitrosourea-Induced Lesions from the DNA of Chinese Hamster Cells as Measured by the Loss of Sites Sensitive to an Enzyme Extract that Excises 3-Methylpurines but not O6-Methylguanine

TL;DR: The extract was used to detect lesions in the DNA of Chinese hamster cells treated in culture with N-methyl-N-nitrosourea and it was concluded that 3-methyladenine is excised from these cells with a half-life of about 2.3 h.
Journal ArticleDOI

Caffeine, aminoimidazolecarboxamide and dicoumarol, inhibitors of NAD(P)H dehydrogenase (quinone) (DT diaphorase), prevent both the cytotoxicity and DNA interstrand crosslinking produced by 5-(aziridin-1-yl)-2,4-dinitrobenzamide (CB 1954) in Walker cells.

TL;DR: Caffeine was shown to be a novel inhibitor of NAD(P)H dehydrogenase (quinone) and also elicited the above protective effects and all of the above inhibitors were also shown to potentiate the toxic effects of menadione against the Walker cell.
Book ChapterDOI

The Role of Platinum-DNA Interactions in the Cellular Toxicity and Anti-Tumour Effects of Platinum Co-Ordination Compounds

TL;DR: Important questions are whether cells differ in their responses to platinum compounds and whether such differences are a function of the extent of drug uptake and binding of platinum to macromolecules and, if so, how much these differences are due to differences in their abilities to remove platinum adducts from their DNA by various excision repair processes.
Journal ArticleDOI

Caffeine inhibits excision of 7-bromomethylbenz (a) anthracene-DNA adducts from exponentially growing but not from stationary phase Chinese hamster cells

TL;DR: Findings lend support to a previous proposition that the caffeine-induced inhibition of elongation of nascent DNA on a template containing chemical lesions results in an interference with the excision repair mechanism that removes these lesions.