Evidence map›Paper›PMID 35357426›Full record

ArticleHuman molecular genetics2022

Defining novel causal SNPs and linked phenotypes at melanoma-associated loci.

Carolina Castaneda-Garcia, Vivek Iyer, Jérémie Nsengimana, Adam Trower, Alastair Droop, Kevin M Brown, Jiyeon Choi, Tongwu Zhang, Mark Harland, Julia A Newton-Bishop and 4 more

Abstract read
In one paragraph

Article in Human molecular genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

14 authors.

Carolina Castaneda-GarciaLaboratorio Internacional de Investigación sobre el Genoma Humano, Universidad Nacional Autónoma de México, Santiago de Querétaro, México 76230, USA.
Vivek IyerCancer, Ageing and Somatic Mutation, Wellcome Sanger Institute, Hinxton, Cambridgeshire CB101SA, UK.
Jérémie NsengimanaBiostatistics Research Group, Population Health Sciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne NE2 4BN, UK.
Adam TrowerLeeds Institute of Medical Research, School of Medicine, University of Leeds, Leeds LS9 7TF, UK.
Alastair DroopCancer, Ageing and Somatic Mutation, Wellcome Sanger Institute, Hinxton, Cambridgeshire CB101SA, UK.
Kevin M BrownDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Jiyeon ChoiDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Tongwu ZhangDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Mark HarlandLeeds Institute of Medical Research, School of Medicine, University of Leeds, Leeds LS9 7TF, UK.
Julia A Newton-BishopLeeds Institute of Medical Research, School of Medicine, University of Leeds, Leeds LS9 7TF, UK.
D Timothy BishopLeeds Institute of Medical Research, School of Medicine, University of Leeds, Leeds LS9 7TF, UK.
David J AdamsCancer, Ageing and Somatic Mutation, Wellcome Sanger Institute, Hinxton, Cambridgeshire CB101SA, UK.
Mark M IlesLeeds Institute of Medical Research, School of Medicine, University of Leeds, Leeds LS9 7TF, UK.
Carla Daniela Robles-EspinozaLaboratorio Internacional de Investigación sobre el Genoma Humano, Universidad Nacional Autónoma de México, Santiago de Querétaro, México 76230, USA.ORCID 0000-0003-3277-7466

Funding

Cancer Research UK 11963Cancer Research UK 19167Medical Research Council MR/S01473X/1Medical Research Council MR/V000292/1Wellcome Trust
6 · The paper itself

Abstract

A number of genomic regions have been associated with melanoma risk through genome-wide association studies; however, the causal variants underlying the majority of these associations remain unknown. Here, we sequenced either the full locus or the functional regions including exons of 19 melanoma-associated loci in 1959 British melanoma cases and 737 controls. Variant filtering followed by Fisher's exact test analyses identified 66 variants associated with melanoma risk. Sequential conditional logistic regression identified the distinct haplotypes on which variants reside, and massively parallel reporter assays provided biological insights into how these variants influence gene function. We performed further analyses to link variants to melanoma risk phenotypes and assessed their association with melanoma-specific survival. Our analyses replicate previously known associations in the melanocortin 1 receptor (MC1R) and tyrosinase (TYR) loci, while identifying novel potentially causal variants at the MTAP/CDKN2A and CASP8 loci. These results improve our understanding of the architecture of melanoma risk and outcome.

Indexed as

MelanomaSkin NeoplasmsGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansPhenotypePolymorphism, Single NucleotideReceptor, Melanocortin, Type 1Receptor, Melanocortin, Type 1

Identifiers

PMID35357426
PMCPMC9433725

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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.