Evidence map›Paper›PMID 23650282›Full record

ArticleCancer research2013

Loss of ARF sensitizes transgenic BRAFV600E mice to UV-induced melanoma via suppression of XPC.

Chi Luo, Jinghao Sheng, Miaofen G Hu, Frank G Haluska, Rutao Cui, Zhengping Xu, Philip N Tsichlis, Guo-Fu Hu, Philip W Hinds

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Loss of Lkb1 cooperates with BrafMolecular oncology · 2025
    Article
  4. Article
  5. Review
  6. UVB mutagenesis differs inLife science alliance · 2021
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Mechanisms and prevention of UV-induced melanoma.Photodermatology, photoimmunology & photomedicine · 2018
    Review
  12. Article
  13. Mouse models of UV-induced melanoma: genetics, pathology, and clinical relevance.Laboratory investigation; a journal of technical methods and pathology · 2017
    Review
  14. Article
  15. Article
  16. Article
  17. UV and melanoma: the TP53 link.Cell research · 2014
    Article
  18. Article
  19. Review
  20. Molecular regulation of UV-induced DNA repair.Photochemistry and photobiology
    Review
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

9 authors at 5 institutions in 1 country.

Chi LuoGraduate Program in Genetics, Sackler School of Graduate Biomedical Sciences, Tufts University, Boston, Massachusetts, USA.
Jinghao Sheng
Miaofen G Hu
Frank G Haluska
Rutao Cui
Zhengping Xu
Philip N Tsichlis
Guo-Fu Hu
Philip W Hinds
Boston University · USTufts University · USAriadne Diagnostics (United States) · USMolecular Oncology (United States) · USTufts Medical Center · US

Funding

Role of pRb in Osteogenesis, Cell Cycle Exit and CancerR01AG020208 · NIA · TUFTS MEDICAL CENTER · PI HINDS, PHILIP W. · 2002 to 2011
$3.6M
Genetics of RAS, PTEN, BRAF and CDKN2A in MelanomaR01CA095798 · NCI · TUFTS MEDICAL CENTER · PI HINDS, PHILIP W. · 2005 to 2009
$1.4M
Proliferative effects of cdk4 and cdk6 dysregulationR01CA096527 · NCI · TUFTS MEDICAL CENTER · PI HINDS, PHILIP W. · 2003 to 2006
$1.1M
NCI NIH HHS CA095798NCI NIH HHS R01 CA095798NCI NIH HHS R01 CA096527NIA NIH HHS AG020208NIA NIH HHS R01 AG020208
6 · The paper itself

Abstract

Both genetic mutations and UV irradiation (UVR) can predispose individuals to melanoma. Although BRAF(V600E) is the most prevalent oncogene in melanoma, the BRAF(V600E) mutant is not sufficient to induce tumors in vivo. Mutation at the CDKN2A locus is another melanoma-predisposing event that can disrupt the function of both p16(INK4a) and ARF. Numerous studies have focused on the role of p16(INK4a) in melanoma, but the involvement of ARF, a well-known p53 activator, is still controversial. Using a transgenic BRAF(V600E) mouse model previously generated in our laboratory, we report that loss of ARF is able to enhance spontaneous melanoma formation and cause profound sensitivity to neonatal UVB exposure. Mechanistically, BRAF(V600E) and ARF deletion synergize to inhibit nucleotide excision repair by epigenetically repressing XPC and inhibiting the E2F4/DP1 complex. We suggest that the deletion of ARF promotes melanomagenesis not by abrogating p53 activation but by acting in concert with BRAF(V600E) to increase the load of DNA damage caused by UVR.

Indexed as

AnimalsCell Line, TumorCells, CulturedCyclin-Dependent Kinase Inhibitor p16DNA-Binding ProteinsDNA MethylationDNA RepairE2F4 Transcription FactorHumansMelanomaMelanoma, ExperimentalMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNeoplasms, Radiation-InducedBraf protein, mouseCdkn2a protein, mouseCyclin-Dependent Kinase Inhibitor p16DNA-Binding ProteinsE2f4 protein, mouseE2F4 Transcription FactorProto-Oncogene Proteins B-rafTfdp1 protein, mouseTranscription Factor DP1Tumor Suppressor Protein p53Xpc protein, mouse

Identifiers

PMID23650282
PMCPMC3715591
OpenAlexW2001743422

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.