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Article

Disruption of the Cockayne syndrome B gene impairs spontaneous tumorigenesis in cancer-predisposed Ink4a/ARF knockout mice.

Molecular and cellular biology - 1 Mar 2001

Lu Y, Lian H, Sharma P, Schreiber-Agus N, Russell R G, Chin L, van der Horst G T, Bregman D B

Abstract excerpt

Cells isolated from individuals with Cockayne syndrome (CS) have a defect in transcription-coupled DNA repair, which rapidly corrects certain DNA lesions located on the transcribed strand of active genes. Despite this DNA repair defect, individuals with CS group A (CSA) or group B (CSB) do not exhibit an increased spontaneous or UV-induced cancer rate. In order to investigate the effect of CSB deficiency on...

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Identifiers

PMID: 11238917
DOI: 10.1128/MCB.21.5.1810-1818.2001
PMCID: PMC86742

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Disruption of the Cockayne syndrome B gene impairs spontaneous tumorigenesis in cancer-predisposed Ink4a/ARF knockout mice.PMID 11238917Read ↗

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