Evidence map›Paper›PMID 20564104›Full record

ArticleCancer2010

Epigenetic and genetic silencing of CHFR in esophageal adenocarcinomas.

Mohammed Soutto, Dunfa Peng, Mohammad Razvi, Petra Ruemmele, Arndt Hartmann, Albert Roessner, Regine Schneider-Stock, Wael El-Rifai

Open access · bronzeAbstract read
In one paragraph

Article in Cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. The hypermethylation of theTranslational cancer research · 2019
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Epigenetics in the Pathogenesis of Esophageal Adenocarcinoma.Clinical and translational science · 2015
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. CHFR: a key checkpoint component implicated in a wide range of cancers.Cellular and molecular life sciences : CMLS · 2012
    Review
  18. Article
  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

8 authors at 3 institutions in 2 countries.

Mohammed SouttoDepartment of Surgery, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37323, USA.
Dunfa Peng
Mohammad Razvi
Petra Ruemmele
Arndt Hartmann
Albert Roessner
Regine Schneider-Stock
Wael El-Rifai
Vanderbilt University Medical Center · USOtto-von-Guericke University Magdeburg · DEUniversity of Regensburg · DE

Funding

The Role of Aurora Kinase in Upper Gastrointestinal AdenocarcinomasR01CA131225 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI EL-RIFAI, WAEL · 2009 to 2018
$3.3M
Molecular Pathobiology of Barrett's TumorigenesisR01CA106176 · NCI · VANDERBILT UNIVERSITY · PI EL-RIFAI, WAEL · 2003 to 2014
$3.3M
NCI NIH HHS CA106176NCI NIH HHS R01 CA106176NCI NIH HHS R01 CA131225NCI NIH HHS R01CA131225
6 · The paper itself

Abstract

backgroundThe checkpoint with forkhead-associated domain and RING-finger domain (CHFR) is a mitotic checkpoint protein with tumor-suppressor functions. In this study, the authors investigated the epigenetic and genetic mechanisms that regulate CHFR expression in esophageal adenocarcinomas (EACs).

methodsQuantitative reverse transcriptase polymerase chain reaction analysis demonstrated downregulation of CHFR transcript in 79% of EACs (44 of 56) compared with 41 normal samples (P < .001). Immunohistochemical analysis of CHFR protein expression showed absence or weak immunostaining for CHFR in 75% of EACs (56 of 75) compared with normal tissue samples. The authors next examined the promoter DNA hypermethylation of CHFR by using quantitative bisulfite pyrosequencing technology. They detected significant CHFR promoter DNA hypermethylation in 31% of tumor samples (18 of 58) compared with normal samples (P < .001). Treatment of OE33 cells with 5-Aza-deoxycytidine led to reduction in the promoter DNA methylation levels with restoration of the CHFR mRNA expression, which confirmed promoter DNA methylation as an epigenetic mechanism regulating CHFR expression. However, they identified several EACs where the CHFR mRNA expression was silenced in the absence of notable methylation. Therefore, the authors examined the relative DNA copy number level of CHFR compared with normal samples.

resultsThe results confirmed a decrease or absence of the relative CHFR DNA copy number levels in 59% of tumor samples. Nine tumors that showed loss of CHFR mRNA expression, in absence of promoter DNA hypermethylation, demonstrated a significant loss of relative CHFR DNA copy numbers.

conclusionsTaken together, their findings demonstrated that both epigenetic and genetic mechanisms were involved in silencing CHFR expression in EACs.

Indexed as

DNA MethylationGene DosageGenes, cdcGene SilencingGenes, Tumor SuppressorAdenocarcinomaCell Cycle ProteinsDown-RegulationEsophageal NeoplasmsHumansImmunohistochemistryNeoplasm ProteinsPoly-ADP-Ribose Binding ProteinsUbiquitin-Protein LigasesCell Cycle ProteinsCHFR protein, humanNeoplasm ProteinsPoly-ADP-Ribose Binding ProteinsUbiquitin-Protein Ligases

Identifiers

PMID20564104
PMCPMC2930066
OpenAlexW2024389696

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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.