Evidence map›Paper›PMID 28504713›Full record

ArticleOncogene2017

Elevated PTTG and PBF predicts poor patient outcome and modulates DNA damage response genes in thyroid cancer.

M L Read, J C Fong, B Modasia, A Fletcher, W Imruetaicharoenchoke, R J Thompson, H Nieto, J J Reynolds, A Bacon, U Mallick and 6 more

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-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

17 citing papers in PubMed, 32 citations in OpenAlex.

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  9. Combined Vorinostat and Chloroquine Inhibit Sodium-Iodide Symporter Endocytosis and Enhance Radionuclide Uptake In Vivo.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
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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

16 authors at 4 institutions in 1 country.

M L ReadInstitute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK.
J C FongInstitute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK.
B ModasiaInstitute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK.
A FletcherInstitute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK.
W ImruetaicharoenchokeInstitute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK.
R J ThompsonInstitute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK.
H NietoInstitute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK.
J J ReynoldsInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
A BaconInstitute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK.
U MallickNorthern Centre for Cancer Care, Freeman Hospital, Newcastle upon Tyne, UK.
A HackshawCancer Research UK &UCL Cancer Trials Centre, University College London, London, UK.
J C WatkinsonDepartment of Otolaryngology Head and Neck Surgery, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.
K BoelaertInstitute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK.
A S TurnellInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
V E SmithInstitute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK.
C J McCabeInstitute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK.
University of Birmingham · GBCancer Research UK · GBFreeman Hospital · GBUniversity Hospitals Birmingham NHS Foundation Trust · GB

Funding

Medical Research Council G0601811Medical Research Council MR/J001414/1Medical Research Council MR/P000509/1Wellcome Trust
6 · The paper itself

Abstract

The proto-oncogene PTTG and its binding partner PBF have been widely studied in multiple cancer types, particularly thyroid and colorectal, but their combined role in tumourigenesis is uncharacterised. Here, we show for the first time that together PTTG and PBF significantly modulate DNA damage response (DDR) genes, including p53 target genes, required to maintain genomic integrity in thyroid cells. Critically, DDR genes were extensively repressed in primary thyrocytes from a bitransgenic murine model (Bi-Tg) of thyroid-specific PBF and PTTG overexpression. Irradiation exposure to amplify p53 levels further induced significant repression of DDR genes in Bi-Tg thyrocytes (P=2.4 × 10

Indexed as

DNA DamageAnimalsDisease Models, AnimalFemaleHumansIntracellular Signaling Peptides and ProteinsMaleMembrane ProteinsMiceMice, TransgenicPrognosisProto-Oncogene MasSecurinSurvival RateThyroid NeoplasmsTransfectionIntracellular Signaling Peptides and ProteinsMAS1 protein, humanMembrane Proteinspituitary tumor-transforming protein 1, humanProto-Oncogene MasPTTG1IP protein, humanSecurin

Identifiers

PMID28504713
PMCPMC5563453
OpenAlexW2616171702

What OpenQuestion holds

Textmetadata
LicenceTDM
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.