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DNA damage responses protect xeroderma pigmentosum variant from UVC-induced clastogenesis.

Carcinogenesis - 1 Jun 2002

Cordeiro-Stone Marila, Frank Alexandra, Bryant Miriam, Oguejiofor Ikechukwu, Hatch Stephanie B, McDaniel Lisa D, Kaufmann William K

Abstract excerpt

Lack of DNA polymerase eta and the attendant defect in bypass replication of pyrimidine dimers induced in DNA by ultraviolet light (UV) underlie the enhanced mutagenesis and carcinogenesis observed in xeroderma pigmentosum variant (XP-V). We investigated whether diploid XP-V fibroblasts growing in culture are also more susceptible to UV-induced clastogenesis than normal human fibroblasts (NHF). This study...

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PMID: 12082017
DOI: 10.1093/carcin/23.6.959

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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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DNA damage responses protect xeroderma pigmentosum variant from UVC-induced clastogenesis.PMID 12082017Read ↗

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Uncovering the Role of DNA Repair Impairment in UVA-Induced Mutagenesis in Human Xeroderma Pigmentosum Variant Cells.Semantic proximity Read ↗

Clastogenesis by nucleotide lesions requires the completion of two cell cyclesSemantic proximity Read ↗

Abnormal, error-prone bypass of photoproducts by xeroderma pigmentosum variant cell extracts results in extreme strand bias for the kinds of mutations induced by UV light.Semantic proximity Read ↗

Evidence from mutation spectra that the UV hypermutability of xeroderma pigmentosum variant cells reflects abnormal, error-prone replication on a template containing photoproducts.Semantic proximity Read ↗

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