Evidence map›Paper›PMID 31356589›Full record

ArticlePLoS computational biology2019

The impact of DNA methylation on the cancer proteome.

Majed Mohamed Magzoub, Marcos Prunello, Kevin Brennan, Olivier Gevaert

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Crosstalk Between Inflammatory Signaling and Methylation in Cancer.Frontiers in cell and developmental biology · 2021
    Review
  7. Article
  8. Review
  9. Article
  10. 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

4 authors at 3 institutions in 2 countries.

Majed Mohamed MagzoubBiomedical Informatics Training Program, Department of Biomedical Data Science, Stanford University, Palo Alto, California, United States of America.ORCID 0000-0001-9455-8221
Marcos PrunelloDepartment of Statistics, College of Pharmaceutical and Biochemical Sciences, National University of Rosario, Rosario, Argentina.ORCID 0000-0002-9611-527X
Kevin BrennanStanford Center for Biomedical Informatics Research, Department of Medicine, Stanford University, Palo Alto, California, United States of America.ORCID 0000-0001-9018-9852
Olivier GevaertStanford Center for Biomedical Informatics Research, Department of Medicine, Stanford University, Palo Alto, California, United States of America.ORCID 0000-0002-9965-5466
Stanford University · USNational University of Rosario · ARPalo Alto University · US

Funding

POSTDOCTORAL TRAINING IN MEDICAL INFORMATION SCIENCEST15LM007033 · NLM · STANFORD UNIVERSITY · PI SYLVIA KATINA PLEVRITIS · 1985 to 2026
$25.5M
Organoid-based Discovery of Oncogenic Drivers and Treatment Resistance MechanismsU01CA217851 · NCI · STANFORD UNIVERSITY · PI CURTIS, CHRISTINA N, JI, HANLEE P · 2017 to 2021
$4.7M
Identification of Cooperative Genetic Alterations in the Pathogenesis of Oral CancerU01DE025188 · NIDCR · STANFORD UNIVERSITY · PI GEVAERT, OLIVIER, KUO, CALVIN J · 2015 to 2018
$3.8M
Radiogenomics Framework for Non-Invasive Personalized MedicineR01EB020527 · NIBIB · STANFORD UNIVERSITY · PI GEVAERT, OLIVIER · 2015 to 2018
$2.3M
NCI NIH HHS U01 CA217851NIBIB NIH HHS R01 EB020527NIDCR NIH HHS U01 DE025188NLM NIH HHS T15 LM007033
6 · The paper itself

Abstract

Aberrant DNA methylation disrupts normal gene expression in cancer and broadly contributes to oncogenesis. We previously developed MethylMix, a model-based algorithmic approach to identify epigenetically regulated driver genes. MethylMix identifies genes where methylation likely executes a functional role by using transcriptomic data to select only methylation events that can be linked to changes in gene expression. However, given that proteins more closely link genotype to phenotype recent high-throughput proteomic data provides an opportunity to more accurately identify functionally relevant abnormal methylation events. Here we present a MethylMix analysis that refines nominations for epigenetic driver genes by leveraging quantitative high-throughput proteomic data to select only genes where DNA methylation is predictive of protein abundance. Applying our algorithm across three cancer cohorts we find that using protein abundance data narrows candidate nominations, where the effect of DNA methylation is often buffered at the protein level. Next, we find that MethylMix genes predictive of protein abundance are enriched for biological processes involved in cancer including functions involved in epithelial and mesenchymal transition. Moreover, our results are also enriched for tumor markers which are predictive of clinical features like tumor stage and we find clustering using MethylMix genes predictive of protein abundance captures cancer subtypes.

Indexed as

DNA MethylationAlgorithmsBiomarkers, TumorComputational BiologyDisease ProgressionEpigenesis, GeneticEpithelial-Mesenchymal TransitionGene Expression ProfilingGene Expression Regulation, NeoplasticHumansModels, GeneticMultigene FamilyNeoplasmsProteomeBiomarkers, TumorProteome

Identifiers

PMID31356589
PMCPMC6695193
OpenAlexW2964640842

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.