Evidence map›Paper›PMID 17015482›Full record

ArticleMolecular and cellular biology2006

UV-B radiation induces epithelial tumors in mice lacking DNA polymerase eta and mesenchymal tumors in mice deficient for DNA polymerase iota.

Tsuyoshi Ohkumo, Yuji Kondo, Masayuki Yokoi, Tetsuya Tsukamoto, Ayumi Yamada, Taiki Sugimoto, Rie Kanao, Yujiro Higashi, Hisato Kondoh, Masae Tatematsu and 2 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

57 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. E3 ubiquitin ligase RNF2 protects polymerase ι from destabilization.Biochimica et biophysica acta. Molecular cell research · 2024
    Article
  6. Article
  7. Article
  8. DNA polymerase ι compensates for Fanconi anemia pathway deficiency by countering DNA replication stress.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Translesion DNA polymerases in eukaryotes: what makes them tick?Critical reviews in biochemistry and molecular biology · 2017
    Review
  15. Article
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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

12 authors at 5 institutions in 3 countries.

Tsuyoshi OhkumoCellular Biology Laboratory, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871, Japan.
Yuji Kondo
Masayuki Yokoi
Tetsuya Tsukamoto
Ayumi Yamada
Taiki Sugimoto
Rie Kanao
Yujiro Higashi
Hisato Kondoh
Masae Tatematsu
Chikahide Masutani
Fumio Hanaoka
Osaka University · JPFrontier Science Foundation · CHAichi Cancer Center · JPJapan Science and Technology Agency · JPUbe Frontier University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA polymerase eta (Pol eta) is the product of the Polh gene, which is responsible for the group variant of xeroderma pigmentosum, a rare inherited recessive disease which is characterized by susceptibility to sunlight-induced skin cancer. We recently reported in a study of Polh mutant mice that Pol eta is involved in the somatic hypermutation of immunoglobulin genes, but the cancer predisposition of Polh-/- mice has not been examined until very recently. Another translesion synthesis polymerase, Pol iota, a Pol eta paralog encoded by the Poli gene, is naturally deficient in the 129 mouse strain, and the function of Pol iota is enigmatic. Here, we generated Polh Poli double-deficient mice and compared the tumor susceptibility of them with Polh- or Poli-deficient animals under the same genetic background. While Pol iota deficiency does not influence the UV sensitivity of mouse fibroblasts irrespective of Polh genotype, Polh Poli double-deficient mice show slightly earlier onset of skin tumor formation. Intriguingly, histological diagnosis after chronic treatment with UV light reveals that Pol iota deficiency leads to the formation of mesenchymal tumors, such as sarcomas, that are not observed in Polh(-/-) mice. These results suggest the involvement of the Pol eta and Pol iota proteins in UV-induced skin carcinogenesis.

Indexed as

AllelesAnimalsCells, CulturedCell Transformation, NeoplasticDNA-Directed DNA PolymeraseDNA Polymerase iotaEpithelial CellsFibroblastsMesodermMiceMice, KnockoutMutationSkin NeoplasmsY-Family DNA PolymerasesDNA-Directed DNA PolymeraseDNA Polymerase iotaRad30 proteinY-Family DNA Polymerases

Identifiers

PMID17015482
PMCPMC1636855
OpenAlexW2142233919

What OpenQuestion holds

Textmetadata
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.