Evidence map›Paper›PMID 22005521›Full record

ArticleGynecologic oncology2012

Phosphatase and tensin homolog (PTEN) pseudogene expression in endometrial cancer: a conserved regulatory mechanism important in tumorigenesis?

Yevgeniya J Ioffe, Katherine B Chiappinelli, David G Mutch, Israel Zighelboim, Paul J Goodfellow

Open access · greenAbstract read
In one paragraph

Article in Gynecologic oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
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  5. Cancers · 2023
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  8. The Complex Landscape ofCold Spring Harbor perspectives in medicine · 2020
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  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Pseudogenes in Human Cancer.Frontiers in medicine · 2015
    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

5 authors at 1 institution in 1 country.

Yevgeniya J IoffeDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, Washington University School of Medicine and Siteman Cancer Center, St. Louis, MO, USA. ioffey@wudosis.wustl.edu
Katherine B Chiappinelli
David G Mutch
Israel Zighelboim
Paul J Goodfellow
Washington University in St. Louis · US

Funding

DEFECTIVE DNA MISMATCH REPAIR IN ENDOMETRIAL CANCERSR01CA071754 · NCI · WASHINGTON UNIVERSITY · PI GOODFELLOW, PAUL JOSEPH · 1997 to 2009
$2.6M
Tissue and Pathology CoreP50CA134254 · NCI · WASHINGTON UNIVERSITY · PI POLLOCK, PAMELA M, POWELL, MATTHEW A · 2009 to 2011
$1.7M
NCI NIH HHS P50 CA134254NCI NIH HHS R01 CA071754NCI NIH HHS R01 CA71754-13
6 · The paper itself

Abstract

objectivesThe PTEN pseudogene, PTENP1, was recently shown to play a role in cell proliferation in a prostate cancer model. In the present study, we sought to determine whether PTENP1 is expressed in endometrial cancer (EMCA) cell lines and primary tumors along with the microRNAs (miRNAs) that are predicted to regulate PTEN and PTENP1 transcript levels.

methodsRNA was prepared from six EMCA cell lines, three normal endometrial samples, and 61 primary tumors. TaqMan® RT-PCR was used to quantitate PTEN expression in all specimens and PTENP1 expression in cell lines, and normal endometrial (NE) samples. PTENP1 expression was evaluated using conventional RT-PCR in primary tumors. MicroRNA profiling was undertaken using NanoString(TM) technology in AN3CA and KLE cell lines. The relationship between PTEN transcript levels, PTENP1 expression, and PTEN mutation status was investigated.

resultsAll NE samples, cell lines, and primary tumors expressed PTEN. PTENP1 transcript was expressed in NE, cell lines, and 34/61 (56%) primary tumors. The median relative PTEN level was 2.9 arbitrary expression units in PTENP1-positive tumors and 2.3 in PTENP1-negative tumors (p=0.09). PTEN levels in wild-type and haploinsufficient tumors were variable compared to PTEN-null tumors (p=0.015). Four microRNAs predicted to bind PTEN/PTENP1 ranked in the top 20 most abundant microRNA subtypes in the AN3CA and KLE cell lines.

conclusionsPTENP1 is expressed in NE and EMCA cell lines, as are PTEN/PTENP1 targeting inhibitory miRNAs (cell lines). Further studies are needed to evaluate the impact of PTEN/PTENP1/miRNA interactions on tumorigenesis regulation in EMCA.

Indexed as

PseudogenesCell Line, TumorEndometrial NeoplasmsFemaleHumansMicroRNAsPTEN PhosphohydrolaseRNA, MessengerTumor Suppressor ProteinsMicroRNAsPTEN PhosphohydrolasePTEN protein, humanRNA, MessengerTumor Suppressor Proteins

Identifiers

PMID22005521
PMCPMC3954782
OpenAlexW2038197188

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.