Evidence map›Paper›PMID 16810501›Full record

ArticleJournal of cancer research and clinical oncology2006

Epigenetic silencing of the putative tumor suppressor gene testisin in testicular germ cell tumors.

Carsten Kempkensteffen, Frank Christoph, Steffen Weikert, Hans Krause, Jens Köllermann, Martin Schostak, Kurt Miller, Mark Schrader

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Membrane-anchored serine proteases in health and disease.Progress in molecular biology and translational science · 2011
    Review
  9. Review
  10. DNA methylation of cancer genome.Birth defects research. Part C, Embryo today : reviews · 2009
    Review
  11. 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.

Carsten KempkensteffenDepartment of Urology, Charité, Campus Benjamin Franklin, Universitätsmedizin Berlin, Hindenburgdamm 30, 12200, Berlin, Germany. carsten.kempkensteffen@charite.de
Frank Christoph
Steffen Weikert
Hans Krause
Jens Köllermann
Martin Schostak
Kurt Miller
Mark Schrader
Franklin University · USCharité - Universitätsmedizin Berlin · DEKlinikum Fulda · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTestisin, a serine protease abundantly expressed only in normal testes, is thought to be a tumor suppressor gene silenced by aberrant methylation in testicular germ cell tumors (TGCT). This study aimed at identifying the CpG sites relevant for testisin gene silencing when methylated and evaluating the potential of aberrant methylation as a biomarker in TGCT.

methodsBisulfite sequencing and subsequent real-time RT-PCR were carried out in germ cell tumor cell lines and a cervical carcinoma cell line to reveal CpG sites implicated in testisin gene silencing. The normalized index of methylation (NIM) and the relative gene expression (RGE) were calculated in 33 TGCT and 19 normal testicular tissue samples by quantitative methylation-specific PCR (QMSP) and real-time RT-PCR.

resultsCpG sites in the 5'untranslated region proved to be relevant for testisin gene silencing when methylated. Targeting these CpG sites by QMSP, we demonstrated that the median NIM was 8.6 times higher in the TGCT group than in normal testicular samples. This was associated with a median 23.6 times lower RGE in the TGCT probes. Non-seminomas had a significantly higher NIM than seminomas, but RGE was downregulated to comparable levels in both subgroups. QMSP was highly sensitive and distinguished TGCT from normal samples with excellent specificity.

conclusionsOur results demonstrate for the first time that aberrant methylation of specific CpG sites near the transcription initiation site is an important factor in testisin gene silencing in TGCT.

Indexed as

Gene Expression Regulation, NeoplasticGene Silencing5' Untranslated RegionsCell Line, TumorCpG IslandsDNA MethylationEpigenesis, GeneticGene Expression ProfilingGPI-Linked ProteinsHumansMaleMembrane ProteinsNeoplasms, Germ Cell and EmbryonalReverse Transcriptase Polymerase Chain ReactionRNASerine Endopeptidases5' Untranslated RegionsGPI-Linked ProteinsMembrane ProteinsPRSS21 protein, humanRNASerine Endopeptidases

Identifiers

PMID16810501
PMCPMC12161029
OpenAlexW1990938030

What OpenQuestion holds

Textmetadata
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.