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- W2023204499 abstract "Mice deficient in the Ung uracil-DNA glycosylase have an increased level of uracil in their genome, consistent with a major role of Ung counteracting U:A base pairs arising by misincorporation of dUMP during DNA replication. A complementary uracil-excising activity apparently acts on premutagenic U : G lesions resulting from deamination of cytosine throughout the genome. However, Ung specifically processes U : G lesions targeted to immunoglobulin variable (V) genes during somatic hypermutation and class-switch recombination. Gene-targeted Ung -/- null mice remained tumour-free and showed no overt pathological phenotype up to ∼12 months of age. We have monitored a large cohort of ageing Ung -/- mice and, beyond 18 months of age, they had a higher morbidity than Ung +/+ controls. Post-mortem analyses revealed pathological changes in lymphoid organs, abnormal lymphoproliferation, and a greatly increased incidence of B-cell lymphomas in older Ung-deficient mice. These are the first data reporting the development of spontaneous malignancies in mice due to deficiency in a DNA glycosylase. Furthermore, they support a specific role for Ung in the immune system, with lymphomagenesis being related to perturbed processing of antibody genes in germinal centre B cells." @default.
- W2023204499 created "2016-06-24" @default.
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- W2023204499 date "2003-08-21" @default.
- W2023204499 modified "2023-10-18" @default.
- W2023204499 title "B cells pay a price" @default.
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- W2023204499 doi "https://doi.org/10.1038/sj.onc.1206874" @default.
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