Evidence map›Paper›PMID 21763452›Full record

ArticleMutation research

The role of XPC: implications in cancer and oxidative DNA damage.

Joost P M Melis, Mirjam Luijten, Leon H F Mullenders, Harry van Steeg

Open access · greenAbstract read
In one paragraph

Article in Mutation research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Quantitative assessment of the association between XPC Lys939Gln polymorphism and cutaneous melanoma risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
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  9. Gadd45 in Neuronal Development, Function, and Injury.Advances in experimental medicine and biology · 2022
    Review
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  19. Comparative study of cytotoxic effects induced by environmental genotoxins using XPC- and CSB-deficient human lymphoblastoid TK6 cells.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2019
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Joost P M MelisNational Institute of Public Health and the Environment, Laboratory for Health Protection Research, Bilthoven, The Netherlands.
Mirjam Luijten
Leon H F Mullenders
Harry van Steeg
Leiden University Medical Center · NLNational Institute for Public Health and the Environment · NL

Funding

THE IMPACT OF CELLULAR DEFENSE ON THE ROLE OF Ku80 IN GENOME MAINTENANCE AND LONGP01AG017242 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI VIJG, JAN · 1999 to 2023
$46.1M
NIA NIH HHS P01 AG017242NIA NIH HHS P01 AG17242
6 · The paper itself

Abstract

The accumulation of DNA damage is a slow but hazardous phenomenon that may lead to cell death, accelerated aging features and cancer. One of the most versatile and important defense mechanisms against the accumulation of DNA damage is nucleotide excision repair (NER), in which the Xeroderma pigmentosum group C (XPC) protein plays a prominent role. NER can be divided into global genome repair (GG-NER) and transcription coupled repair (TC-NER). XPC is a key factor in GG-NER where it functions in DNA damage recognition and after which the repair machinery is recruited to eliminate the DNA damage. Defective XPC functioning has been shown to result in a cancer prone phenotype, in human as well as in mice. Mutation accumulation in XPC deficient mice is accelerated and increased, resulting in an increased tumor incidence. More recently XPC has also been linked to functions outside of NER since XPC deficient mice show a divergent tumor spectrum compared to other NER deficient mouse models. Multiple in vivo and in vitro experiments indicate that XPC appears to be involved in the initiation of several DNA damage-induced cellular responses. XPC seems to function in the removal of oxidative DNA damage, redox homeostasis and cell cycle control. We hypothesize that this combination of increased oxidative DNA damage sensitivity, disturbed redox homeostasis together with inefficient cell cycle control mechanisms are causes of the observed increased cancer susceptibility in oxygen exposed tissues. Such a phenotype is absent in other NER-deficient mice, including Xpa.

Indexed as

DNA DamageAgingAnimalsCell Cycle CheckpointsDisease Models, AnimalDNA-Binding ProteinsDNA RepairHumansMiceNeoplasmsPolymorphism, Single NucleotideXeroderma PigmentosumDNA-Binding ProteinsXPC protein, human

Identifiers

PMID21763452
PMCPMC3203325
OpenAlexW1995991297

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.