Evidence map›Paper›PMID 20671427›Full record

ArticleEpigenetics2010

Epigenetic differences in cytogenetically normal versus abnormal acute myeloid leukemia.

Elizabeth A Griffiths, Steven D Gore, Craig M Hooker, Helai P Mohammad, Michael A McDevitt, B Douglas Smith, Judith E Karp, James G Herman, Hetty E Carraway

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  5. Review
  6. Article
  7. A Phase 1 Study of the PARP Inhibitor Veliparib in Combination with Temozolomide in Acute Myeloid Leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Article
  8. Article
  9. CEBPA methylation and mutation in myelodysplastic syndrome.Medical oncology (Northwood, London, England) · 2015
    Article
  10. Methylation status of theOncology letters · 2015
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Methylation of the p73 gene in patients with myelodysplastic syndromes: correlations with apoptosis and prognosis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Article
  16. Article
  17. Article
  18. 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

9 authors at 2 institutions in 1 country.

Elizabeth A GriffithsThe Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD, USA.
Steven D Gore
Craig M Hooker
Helai P Mohammad
Michael A McDevitt
B Douglas Smith
Judith E Karp
James G Herman
Hetty E Carraway
Sidney Kimmel Comprehensive Cancer Center · USUniversity of Baltimore · US

Funding

Targeting Epigenomics in Myeloid NeoplasmsK24CA111717 · NCI · YALE UNIVERSITY · PI GORE, STEVEN D · 2005 to 2015
$1.7M
NCI NIH HHS CA06793NCI NIH HHS K24 CA111717
6 · The paper itself

Abstract

backgroundMethylation of tumor suppression genes (TSGs) is common in myeloid malignancies. However, application of this as a molecular marker for risk stratification in patients with AML is limited. DESIGN AND

methodsTo elucidate the impact of patterns of TSG methylation on outcome in cytogenetically normal patients, 106 samples from patients with having normal cytogenetic AML were evaluated for methylation of 12 genes by MSP. For sake of comparison, samples from patients with AML and abnormal cytogenetics (n = 63) were also evaluated.

resultsMethylation frequencies in the whole group (n = 169) were similar to previous reports for CDH1 (31%), ER (31%), FHIT (9%), p15 (INK4b) (44%), p73 (25%), and SOCS1 (75%). Methylation of CTNNA1 was observed in 10%, CEBP-α in16%, CEBP-δ in 2%, MLH1 in 24%, MGMT in 11% and DAPK in 2% of AML samples. We find that DNA methylation was more prevalent in patients with normal compared to karyotypically abnormal AML for most genes; CEBPα (20% vs 9%), CTNNA1 (14% vs 4%), and ER (41% vs 19%) (p < 0.05 for all comparisons). In contrast, p73 was more frequently methylated in patients with karyotypic abnormalities (17% vs 38%; p < 0.05), perhaps due to specific silencing of the pro-apoptotic promoter shifting p73 gene expression to the anti-apoptotic transcript. In AML patients with normal cytogenetics, TSG methylation was not associated with event free or overall survival in a multivariate analysis.

conclusionsIn patients with AML, TSG methylation is more frequent in patients with normal karyotype than those with karyotypic abnormalities but does not confer independent prognostic information for patients with normal cytogenetics.

Indexed as

Epigenesis, GeneticAgedalpha CateninBase SequenceCase-Control StudiesCCAAT-Enhancer-Binding ProteinsDNA-Binding ProteinsDNA MethylationDNA, Neoplasmfms-Like Tyrosine Kinase 3Genes, Tumor SuppressorHL-60 CellsHumansKaryotypingLeukemia, Myeloid, AcuteMiddle Agedalpha CateninCCAAT-Enhancer-Binding ProteinsCEBPA protein, humanCTNNA1 protein, humanDNA-Binding ProteinsDNA, NeoplasmFLT3 protein, humanfms-Like Tyrosine Kinase 3Nuclear ProteinsReceptors, EstrogenTP73 protein, humanTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID20671427
PMCPMC3052845
OpenAlexW2078107594

What OpenQuestion holds

Textmetadata
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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.