Evidence map›Paper›PMID 30681412›Full record

ArticleeLife2019

Different genetic mechanisms mediate spontaneous versus UVR-induced malignant melanoma.

Blake Ferguson, Herlina Y Handoko, Pamela Mukhopadhyay, Arash Chitsazan, Lois Balmer, Grant Morahan, Graeme J Walker

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. 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
1.5field-weighted citation impact, top 18% 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, 28 citations in OpenAlex.

  1. Assessment of the Influence of UVR in Cutaneous Melanoma.Photodermatology, photoimmunology & photomedicine · 2025
    Review
  2. Article
  3. High UV damage and low repair, but not cytosine deamination, stimulate mutation hotspots at ETS binding sites in melanoma.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  4. Article
  5. Article
  6. Genetic Mapping of Behavioral Traits Using the Collaborative Cross Resource.International journal of molecular sciences · 2022
    Article
  7. Review
  8. Journal of biosciences · 2022
    Review
  9. Review
  10. Article
  11. Systems genetics analysis of oral squamous cell carcinoma susceptibility using the mouse model: current position and new perspective.Mammalian genome : official journal of the International Mammalian Genome Society · 2021
    Review
  12. Article
  13. Review
  14. Article
  15. Genomic sites hypersensitive to ultraviolet radiation.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  16. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

Blake FergusonDrug Discovery Group, QIMR Berghofer Medical Research Institute, Herston, Australia.ORCID 0000-0002-5643-6976
Herlina Y HandokoDrug Discovery Group, QIMR Berghofer Medical Research Institute, Herston, Australia.
Pamela MukhopadhyayDrug Discovery Group, QIMR Berghofer Medical Research Institute, Herston, Australia.
Arash ChitsazanDrug Discovery Group, QIMR Berghofer Medical Research Institute, Herston, Australia.
Lois BalmerCentre for Diabetes Research, Harry Perkins Institute of Medical Research, Perth, Australia.
Grant MorahanCentre for Diabetes Research, Harry Perkins Institute of Medical Research, Perth, Australia.
Graeme J WalkerDrug Discovery Group, QIMR Berghofer Medical Research Institute, Herston, Australia.ORCID 0000-0002-9392-8769
QIMR Berghofer Medical Research Institute · AUEdith Cowan University · AUHarry Perkins Institute of Medical Research · AUThe University of Queensland · AU

Funding

Melanoma Research Alliance Investigator Grant Award Number: 346859 2015-2018
6 · The paper itself

Abstract

Genetic variation conferring resistance and susceptibility to carcinogen-induced tumorigenesis is frequently studied in mice. We have now turned this idea to melanoma using the collaborative cross (CC), a resource of mouse strains designed to discover genes for complex diseases. We studied melanoma-prone transgenic progeny across seventy CC genetic backgrounds. We mapped a strong quantitative trait locus for rapid onset spontaneous melanoma onset to

Indexed as

Ultraviolet RaysAnimalsAnimals, NewbornAnimals, Outbred StrainsCell ProliferationChromosome MappingChromosomes, MammalianCutaneous Malignant MelanomaDisease Models, AnimalGene Expression Regulation, NeoplasticGene Regulatory NetworksGenetic LociHumansMelanocytesMelanomaMice, TransgenicBraf protein, mouseMonomeric GTP-Binding ProteinsNras protein, mouseProto-Oncogene Proteins B-rafcancer biologygenesmelanomamicemouseQTLultraviolet radiaton

Identifiers

PMID30681412
PMCPMC6428585
OpenAlexW2896656693

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.