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

Impaired processing of DNA photoproducts and ultraviolet hypermutability with loss of p16INK4a or p19ARF.

Journal of the National Cancer Institute - 1 Dec 2004

Sarkar-Agrawal Papri, Vergilis Irene, Sharpless Norman E, DePinho Ronald A, Rünger Thomas M

Abstract excerpt

Reduced DNA repair has been linked to an increased risk of cutaneous malignant melanoma, but insights into the molecular mechanisms of that link are scarce. The INK4a/ARF (CDKN2a) locus, which codes for the p16(INK4a) and p19ARF proteins, is often mutated in sporadic and familial malignant melanoma, but it has not been directly associated with reduced DNA repair. We transfected unirradiated mouse fibroblast cells...

Read the complete abstract on PubMed

Topics

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

Share to Cyclin-Dependent Kinase Inhibitor p16
Share to DNA Damage

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fibroblasts

Share to Genes, p16

Share to Melanoma

Share to Skin Neoplasms

Share to Tumor Suppressor Protein p14ARF

Share to Ultraviolet Rays

Source

Identifiers

PMID: 15572761
DOI: 10.1093/jnci/djh307

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Impaired processing of DNA photoproducts and ultraviolet hypermutability with loss of p16INK4a or p19ARF.PMID 15572761Read ↗

How disruption of cell cycle regulating genes might predispose to sun-induced skin cancer.Semantic proximity Read ↗

Components of the Rb pathway are critical targets of UV mutagenesis in a murine melanoma model.Semantic proximity Read ↗

Deciphering UV‐induced DNA Damage Responses to Prevent and Treat Skin CancerSemantic proximity Read ↗

DNA damage and repair in melanoma and non-melanoma skin cancer.Semantic proximity Read ↗

The role of altered nucleotide excision repair and UVB-induced DNA damage in melanomagenesis.Semantic proximity Read ↗

Genome-wide profiles of UV lesion susceptibility, repair, and mutagenic potential in melanoma.Semantic proximity Read ↗

Defective postreplication repair of UV photoproducts in melanoma: a mutator phenotype.Semantic proximity Read ↗

Use of human tissue to assess the oncogenic activity of melanoma-associated mutations.Semantic proximity Read ↗

Similar nucleotide excision repair capacity in melanocytes and melanoma cells.Semantic proximity Read ↗

Loss of p16Ink4a confers susceptibility to metastatic melanoma in mice.Semantic proximity Read ↗

UVB mutagenesis differs in <i>NRAS</i> - and <i>BRAF</i> -mutant mouse models of melanomaSemantic proximity Read ↗

INK4a-ARF mutations in skin carcinomas from UV irradiated hairless mice.Semantic proximity Read ↗

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