Evidence map›Paper›PMID 20616346›Full record

ArticleThe American journal of pathology2010

The DNA damage-binding protein XPC is a frequent target for inactivation in squamous cell carcinomas.

Sebastien de Feraudy, Katie Ridd, Lauren M Richards, Pui-Yan Kwok, Ingrid Revet, Dennis Oh, Luzviminda Feeney, James E Cleaver

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 34 citations in OpenAlex.

  1. UVA-light-induced mutagenesis in the exome of human nucleotide excision repair-deficient cells.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025
    Article
  2. Review
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  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Sex-specific molecular genetic response to UVB exposure in Xiphophorus maculatus skin.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2015
    Article
  11. Article
  12. Skin cancer in organ transplant recipients: more than the immune system.Journal of the American Academy of Dermatology · 2014
    Review
  13. Article
  14. Article
  15. Protection from UV-induced skin carcinogenesis by genetic inhibition of the ataxia telangiectasia and Rad3-related (ATR) kinase.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  16. 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

8 authors at 3 institutions in 2 countries.

Sebastien de FeraudyDepartment of Dermatology, University of California, San Francisco, CA 94143-0808, USA.
Katie Ridd
Lauren M Richards
Pui-Yan Kwok
Ingrid Revet
Dennis Oh
Luzviminda Feeney
James E Cleaver
University of California, San Francisco · USCardiovascular Institute Hospital · JPSan Francisco VA Medical Center · US

Funding

Tissue CoreP01AR050440 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI EPSTEIN, ERVIN HAROLD · 2003 to 2007
$6.9M
XP VARIANT--A HUMAN MUTATOR GENE FOR UV DAMAGER01ES008061 · NIEHS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI CLEAVER, JAMES E · 1998 to 2005
$1.8M
Mechanism of Triplex DNA Damage and Repair in Skin CellsR01CA105958 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI OH, DENNIS H · 2003 to 2007
$1.1M
NCI NIH HHS R01 CA105958NCI NIH HHS R01/CA105958NIAMS NIH HHS P01 AR050440NIAMS NIH HHS P01 AR050440-01NIEHS NIH HHS 1 R01 ES 8061NIEHS NIH HHS R01 ES008061
6 · The paper itself

Abstract

XPC, the main damage-recognition protein responsible for nucleotide excision repair of UVB damage to DNA, is lost or mutated in xeroderma pigmentosum group C (XP-C), a rare inherited disease characterized by high incidence and early onset of non-melanoma and melanoma skin cancers. The high incidence of skin cancers in XP-C patients suggests that loss of expression of XPC protein might also provide a selective advantage for initiation and progression of similar cancers in non XP-C patients in the general population. To test whether XPC is selectively lost in squamous cell carcinomas from non XP-C patients, we examined XPC expression by immunohistochemistry on a tissue microarray with 244 tissue cores, including in situ and invasive squamous-cell carcinomas (SCCs), keratoacanthoma (KA), and normal skin samples from both immunocompetent and immunosuppressed patients. We found that XPC expression was lost in 49% of invasive squamous cell carcinomas from immunocompetent patients and 59% from immunosuppressed patients. Loss of expression was correlated with deletions of chromosomal 3p and mutations in the XPC gene. The XPC gene is consequently inactivated or lost in almost half of squamous cell carcinomas from non XP-C patients. Loss or mutation of XPC may be an early event during skin carcinogenesis that provides a selective advantage for initiation and progression of squamous cell carcinomas in non XP-C patients.

Indexed as

DNA DamageGene SilencingAnimalsCarcinoma, Squamous CellCell LineDNA-Binding ProteinsHumansMicroarray AnalysisTumor Suppressor Protein p53Xeroderma PigmentosumDNA-Binding ProteinsTumor Suppressor Protein p53XPC protein, human

Identifiers

PMID20616346
PMCPMC2913339
OpenAlexW2063781594

What OpenQuestion holds

Textmetadata
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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.