Evidence map›Paper›PMID 24602166›Full record

ArticleBMC cancer2014

Increased paired box transcription factor 8 has a survival function in glioma.

Noelyn Hung, Yu-Jen Chen, Ahmad Taha, Magnus Olivecrona, Ronald Boet, Anna Wiles, Tracy Warr, Alisha Shaw, Ramona Eiholzer, Bruce C Baguley and 5 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. PAX8 in the Junction between Development and Tumorigenesis.International journal of molecular sciences · 2022
    Review
  5. Review
  6. PAX8, an Emerging Player in Ovarian Cancer.Advances in experimental medicine and biology · 2021
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Telomere profiles and tumor-associated macrophages with different immune signatures affect prognosis in glioblastoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016
    Article
  12. 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

15 authors at 6 institutions in 4 countries.

Noelyn Hung
Yu-Jen Chen
Ahmad Taha
Magnus Olivecrona
Ronald Boet
Anna Wiles
Tracy Warr
Alisha Shaw
Ramona Eiholzer
Bruce C Baguley
Michael R Eccles
Antony W Braithwaite
Martin Macfarlane
Janice A Royds
Tania SlatterDepartment of Pathology, University of Otago, Dunedin, New Zealand. tania.slatter@otago.ac.nz.
University of Otago · NZChristchurch Hospital · NZDunedin Public Hospital · NZNational Hospital for Neurology and Neurosurgery · GBUmeå University · SEUniversity of Auckland · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe molecular basis to overcome therapeutic resistance to treat glioblastoma remains unclear. The anti-apoptotic b cell lymphoma 2 (BCL2) gene is associated with treatment resistance, and is transactivated by the paired box transcription factor 8 (PAX8). In earlier studies, we demonstrated that increased PAX8 expression in glioma cell lines was associated with the expression of telomerase. In this current study, we more extensively explored a role for PAX8 in gliomagenesis.

methodsPAX8 expression was measured in 156 gliomas including telomerase-negative tumours, those with the alternative lengthening of telomeres (ALT) mechanism or with a non-defined telomere maintenance mechanism (NDTMM), using immunohistochemistry and quantitative PCR. We also tested the affect of PAX8 knockdown using siRNA in cell lines on cell survival and BCL2 expression.

resultsSeventy-two percent of glioblastomas were PAX8-positive (80% telomerase, 73% NDTMM, and 44% ALT). The majority of the low-grade gliomas and normal brain cells were PAX8-negative. The suppression of PAX8 was associated with a reduction in both cell growth and BCL2, suggesting that a reduction in PAX8 expression would sensitise tumours to cell death.

conclusionsPAX8 is increased in the majority of glioblastomas and promoted cell survival. Because PAX8 is absent in normal brain tissue, it may be a promising therapeutic target pathway for treating aggressive gliomas.

Indexed as

Cell ProliferationCell SurvivalGene ExpressionGene SilencingGliomaHumansImmunohistochemistryPaired Box Transcription FactorsPAX5 Transcription FactorPAX8 Transcription FactorProto-Oncogene Proteins c-bcl-2RNA, Small InterferingPaired Box Transcription FactorsPAX5 protein, humanPAX5 Transcription FactorPAX8 protein, humanPAX8 Transcription FactorProto-Oncogene Proteins c-bcl-2RNA, Small Interfering

Identifiers

PMID24602166
PMCPMC4015841
OpenAlexW2140077263

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.