Evidence map›Paper›PMID 21937738›Full record

ArticleEndocrine-related cancer2011

Genome-wide alterations in gene methylation by the BRAF V600E mutation in papillary thyroid cancer cells.

Peng Hou, Dingxie Liu, Mingzhao Xing

Open access · bronzeAbstract read
In one paragraph

Article in Endocrine-related cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Association of DNA Promoter Methylation andCurrent oncology (Toronto, Ont.) · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. DNA methylation alterations as therapeutic prospects in thyroid cancer.Journal of endocrinological investigation · 2019
    Review
  10. Article
  11. Methylation of tumour suppressor genes associated with thyroid cancer.Cancer biomarkers : section A of Disease markers · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Peng HouLaboratory for Cellular and Molecular Thyroid Research, Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
Dingxie Liu
Mingzhao Xing
Johns Hopkins University · US

Funding

Genetic & Epigenetic Events in Papillary Thyroid CancerR01CA113507 · NCI · JOHNS HOPKINS UNIVERSITY · PI XING, MICHAEL MINGZHAO · 2006 to 2015
$2.2M
NCI NIH HHS R0-1 CA113507NCI NIH HHS R01 CA113507
6 · The paper itself

Abstract

The BRAF V600E mutation plays an important role in the tumorigenesis of papillary thyroid cancer (PTC). To explore an epigenetic mechanism involved in this process, we performed a genome-wide DNA methylation analysis using a methylated CpG island amplification (MCA)/CpG island microarray system to examine gene methylation alterations after shRNA knockdown of BRAF V600E in thyroid cancer cells. Our results revealed numerous methylation targets of BRAF V600E mutation with a large cohort of hyper- or hypo-methylated genes in thyroid cancer cells, which are known to have important metabolic and cellular functions. As hypomethylation of numerous genes by BRAF V600E was particularly a striking finding, we took a further step to examine the selected 59 genes that became hypermethylated in both cell lines upon BRAF V600E knockdown and found them to be mostly correspondingly under-expressed (i.e. they were normally maintained hypomethylated and over-expressed by BRAF V600E in thyroid cancer cells). We confirmed the methylation status of selected genes revealed on MCA/CpG microarray analysis by performing methylation-specific PCR. To provide proof of concept that some of the genes uncovered here may play a direct oncogenic role, we selected six of them to perform shRNA knockdown and examined its effect on cellular functions. Our results demonstrated that the HMGB2 gene played a role in PTC cell proliferation and the FDG1 gene in cell invasion. Thus, this study uncovered a prominent epigenetic mechanism through which BRAF V600E can promote PTC tumorigenesis by altering the methylation and hence the expression of numerous important genes.

Indexed as

Gene Expression Regulation, NeoplasticAmino Acid SubstitutionCarcinomaCarcinoma, PapillaryCluster AnalysisCpG IslandsDNA MethylationGene Expression ProfilingGene Knockdown TechniquesGenome, HumanGlutamic AcidHumansMicroarray AnalysisMutation, MissenseProto-Oncogene Proteins B-rafThyroid Cancer, PapillaryBRAF protein, humanGlutamic AcidProto-Oncogene Proteins B-rafValine

Identifiers

PMID21937738
PMCPMC3346957
OpenAlexW2162596935

What OpenQuestion holds

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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.