Evidence map›Paper›PMID 35181301›Full record

ArticleThe Journal of investigative dermatology2022

Integrated Analysis of Coexpression and Exome Sequencing to Prioritize Susceptibility Genes for Familial Cutaneous Melanoma.

Sally Yepes, Margaret A Tucker, Hela Koka, Yanzi Xiao, Tongwu Zhang, Kristine Jones, Aurelie Vogt, Laurie Burdette, Wen Luo, Bin Zhu and 8 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 46% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Disruption of CTCF binding by germline non-coding variants inmedRxiv : the preprint server for health sciences · 2026
    Article
  2. Review
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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

18 authors at 2 institutions in 1 country.

Sally YepesDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. Electronic address: sally.yepestorres@nih.gov.
Margaret A TuckerDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Hela KokaDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Yanzi XiaoDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Tongwu ZhangDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Kristine JonesDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; Cancer Genomics Research Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc, Frederick, Maryland, USA.
Aurelie VogtDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; Cancer Genomics Research Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc, Frederick, Maryland, USA.
Laurie BurdetteDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; Cancer Genomics Research Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc, Frederick, Maryland, USA.
Wen LuoDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; Cancer Genomics Research Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc, Frederick, Maryland, USA.
Bin ZhuDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; Cancer Genomics Research Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc, Frederick, Maryland, USA.
Amy HutchinsonDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; Cancer Genomics Research Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc, Frederick, Maryland, USA.
Meredith YeagerDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; Cancer Genomics Research Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc, Frederick, Maryland, USA.
Belynda HicksDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; Cancer Genomics Research Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc, Frederick, Maryland, USA.
Kevin M BrownDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Neal D FreedmanDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Stephen J ChanockDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Alisa M GoldsteinDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Xiaohong R YangDivision of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
National Institutes of Health · USLeidos (United States) · US

Funding

Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

The application of whole-exome sequencing has led to the identification of high- and moderate-risk variants that contribute to cutaneous melanoma susceptibility. However, confirming disease-causing variants remains challenging. We applied a gene coexpression network analysis to prioritize the candidate genes identified from whole-exome sequencing of 34 melanoma-prone families, with at least three affected members sequenced per family (N = 119 cases). A coexpression network was constructed from genotype-tissue expression project, skin melanoma from the cancer genome atlas, and primary melanocyte cultures. We performed module-specific enrichment and focused on modules associated with pigmentation processes because they are the best-studied and most well-known risk factors for melanoma susceptibility. We found that pigmentation-associated modules across the four expression datasets examined were enriched for well-known melanoma susceptibility genes plus genes associated with pigmentation. We also used network properties to prioritize genes within pigmentation modules as candidate susceptibility genes. Integrating information from coexpression network analysis and variant prioritization, we identified 36 genes (such as DCT, TPCN2, TRPM1, ATP10A, and EPHA5) as potential melanoma risk genes in the families. Our approach also allowed us to link families with private gene mutations on the basis of gene coexpression patterns and thereby may provide an innovative perspective in gene identification in high-risk families.

Indexed as

MelanomaSkin NeoplasmsCutaneous Malignant MelanomaExomeExome SequencingGenetic Predisposition to DiseaseHumans

Identifiers

PMID35181301
PMCPMC9378750
OpenAlexW4212802425

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.