Evidence map›Paper›PMID 26103569›Full record

ArticleBritish journal of cancer2015

MC1R gene variants and non-melanoma skin cancer: a pooled-analysis from the M-SKIP project.

E Tagliabue, M C Fargnoli, S Gandini, P Maisonneuve, F Liu, M Kayser, T Nijsten, J Han, R Kumar, N A Gruis and 14 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

40 citing papers in PubMed, 60 citations in OpenAlex.

  1. Trial
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  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Assessment of the Influence of UVR in Cutaneous Melanoma.Photodermatology, photoimmunology & photomedicine · 2025
    Review
  10. Gray Hair: From Preventive to Treatment.Clinical, cosmetic and investigational dermatology · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
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  17. 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

24 authors at 14 institutions in 11 countries.

E TagliabueDivision of Epidemiology and Biostatistics, European Institute of Oncology, Via Ripamonti 435, Milan 20141, Italy.
M C FargnoliDepartment of Dermatology, University of L'Aquila, 47100 L'Aquila, Italy.
S GandiniDivision of Epidemiology and Biostatistics, European Institute of Oncology, Via Ripamonti 435, Milan 20141, Italy.
P MaisonneuveDivision of Epidemiology and Biostatistics, European Institute of Oncology, Via Ripamonti 435, Milan 20141, Italy.
F LiuDepartment of Forensic Molecular Biology, Erasmus MC University Medical Center, 3000 DR Rotterdam, The Netherlands.
M KayserDepartment of Forensic Molecular Biology, Erasmus MC University Medical Center, 3000 DR Rotterdam, The Netherlands.
T NijstenDepartment of Dermatology, Erasmus MC University Medical Center, 3000 DR Rotterdam, The Netherlands.
J Han1] Department of Dermatology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA [2] Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA [3] Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA.
R KumarDivision of Molecular Genetic Epidemiology, German Cancer Research Center, D-69120 Heidelberg, Germany.
N A GruisDepartment of Dermatology, Leiden University Medical Center, 2300 RC Leiden, The Netherlands.
L FerrucciDepartment of Chronic Disease Epidemiology, Yale School of Public Health, Yale Cancer Center, New Haven, CT 06520-8034, USA.
W BranickiInstitute of Forensic Research, 31-033 Krakow, Poland.
T DwyerMurdoch Childrens Research Institute, Royal Children's Hospital, Victoria 3052, Australia.
L BlizzardMenzies Research Institute Tasmania, University of Tasmania, Hobart, 7001 Australia.
P HelsingDepartment of Pathology, Oslo University Hospital, N-0027 Oslo, Norway.
P AutierInternational Prevention Research Institute, Lyon 69006, France.
J C García-BorrónDepartment of Biochemistry, Molecular Biology and Immunology, University of Murcia, 30100 Murcia, Spain.
P A KanetskyDepartment of Cancer Epidemiology, Moffitt Cancer Center, Tampa, FL 33612, USA.
M T LandiDivision of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD 20892-7236, USA.
J LittleSchool of Epidemiology, Public Health and Preventive Medicine, University of Ottawa, Ottawa, Canada ON K1N 6N5.
J Newton-BishopSection of Epidemiology and Biostatistics, Institute of Cancer and Pathology, University of Leeds, Leeds LS9 7TF, UK.
F SeraUCL Institute of Child Health, London WC1N 1EH, UK.
S RaimondiDivision of Epidemiology and Biostatistics, European Institute of Oncology, Via Ripamonti 435, Milan 20141, Italy.
M-SKIP Study Group
Ripamonti · ITErasmus MC · NLBrigham and Women's Hospital · USMoffitt Cancer Center · USOslo University Hospital · NOUniversity of L'Aquila · ITUniversity of Leeds · GBGerman Cancer Research Center · DEInternational Prevention Research Institute · FRLeiden University Medical Center · NLRoyal Children's Hospital · AUUniversity of Ottawa · CAUniversity of Tasmania · AUYale Cancer Center · US

Funding

Cancer Research UK 19167
6 · The paper itself

Abstract

backgroundThe melanocortin-1-receptor (MC1R) gene regulates human pigmentation and is highly polymorphic in populations of European origins. The aims of this study were to evaluate the association between MC1R variants and the risk of non-melanoma skin cancer (NMSC), and to investigate whether risk estimates differed by phenotypic characteristics.

methodsData on 3527 NMSC cases and 9391 controls were gathered through the M-SKIP Project, an international pooled-analysis on MC1R, skin cancer and phenotypic characteristics. We calculated summary odds ratios (SOR) with random-effect models, and performed stratified analyses.

resultsSubjects carrying at least one MC1R variant had an increased risk of NMSC overall, basal cell carcinoma (BCC) and squamous cell carcinoma (SCC): SOR (95%CI) were 1.48 (1.24-1.76), 1.39 (1.15-1.69) and 1.61 (1.35-1.91), respectively. All of the investigated variants showed positive associations with NMSC, with consistent significant results obtained for V60L, D84E, V92M, R151C, R160W, R163Q and D294H: SOR (95%CI) ranged from 1.42 (1.19-1.70) for V60L to 2.66 (1.06-6.65) for D84E variant. In stratified analysis, there was no consistent pattern of association between MC1R and NMSC by skin type, but we consistently observed higher SORs for subjects without red hair.

conclusionsOur pooled-analysis highlighted a role of MC1R variants in NMSC development and suggested an effect modification by red hair colour phenotype.

Indexed as

Genetic Predisposition to DiseaseBasal Cell CarcinomaCarcinoma, Squamous CellHair ColorHumansOdds RatioPhenotypeReceptor, Melanocortin, Type 1RiskSkin NeoplasmsReceptor, Melanocortin, Type 1

Identifiers

PMID26103569
PMCPMC4506395
OpenAlexW2133476042

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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.