Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Why Cockayne syndrome patients do not get cancer despite their DNA repair deficiency.

Proceedings of the National Academy of Sciences of the United States of America - 6 Sept 2016

Reid-Bayliss Kate S, Arron Sarah T, Loeb Lawrence A, Bezrookove Vladimir, Cleaver James E

Abstract excerpt

Cockayne syndrome (CS) and xeroderma pigmentosum (XP) are human photosensitive diseases with mutations in the nucleotide excision repair (NER) pathway, which repairs DNA damage from UV exposure. CS is mutated in the transcription-coupled repair (TCR) branch of the NER pathway and exhibits developmental and neurological pathologies. The XP-C group of XP patients have mutations in the global genome repair (GGR)...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cockayne Syndrome
Share to DNA Breaks, Double-Stranded

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Healthy Volunteers

Share to Keratinocytes

Share to Primary Cell Culture

Share to Skin Neoplasms

Share to Ultraviolet Rays

Share to Xeroderma Pigmentosum

Source

Open in PubMed Open full text

Identifiers

PMID: 27543334
DOI: 10.1073/pnas.1610020113
PMCID: PMC5018765

Provenance

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.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Why Cockayne syndrome patients do not get cancer despite their DNA repair deficiency.PMID 27543334Read ↗

Absence of skin cancer in the DNA repair-deficient disease Cockayne Syndrome (CS): A survey studySemantic proximity Read ↗

UVB radiation-induced cancer predisposition in Cockayne syndrome group A (Csa) mutant mice.Semantic proximity Read ↗

Novel XPG (ERCC5) mutations affect DNA repair and cell survival after ultraviolet but not oxidative stress.Semantic proximity Read ↗

A common mutational pattern in Cockayne syndrome patients from xeroderma pigmentosum group G: implications for a second XPG function.Semantic proximity Read ↗

Disorders of nucleotide excision repair.Semantic proximity Read ↗

Mutations in UVSSA cause UV-sensitive syndrome and impair RNA polymerase IIo processing in transcription-coupled nucleotide-excision repair.Semantic proximity Read ↗

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

Mutagenicity Profile Induced by UVB Light in Human Xeroderma Pigmentosum Group C Cells.Semantic proximity Read ↗

A UV-sensitive syndrome patient with a specific CSA mutation reveals separable roles for CSA in response to UV and oxidative DNA damage.Semantic proximity Read ↗

Xeroderma pigmentosum and related disorders: defects in DNA repair and transcription.Semantic proximity Read ↗

Primary fibroblasts of Cockayne syndrome patients are defective in cellular repair of 8‐hydroxyguanine and 8‐hydroxyadenine resulting from oxidative stressSemantic proximity Read ↗

Somatic cell mutation frequency at the HPRT, T-cell antigen receptor and glycophorin A loci in Cockayne syndrome.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.