Evidence map›Paper›PMID 28319062›Full record

ArticleOncogene2017

CTCF genetic alterations in endometrial carcinoma are pro-tumorigenic.

A D Marshall, C G Bailey, K Champ, M Vellozzi, P O'Young, C Metierre, Y Feng, A Thoeng, A M Richards, U Schmitz and 6 more

Open access · hybridAbstract 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 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

44 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  11. Review
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  13. Article
  14. Article
  15. Chromatin architectural factor CTCF is essential for progesterone-dependent uterine maturation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
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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 6 institutions in 2 countries.

A D MarshallGene and Stem Cell Therapy Program, Centenary Institute, Camperdown, New South Wales, Australia.
C G BaileyGene and Stem Cell Therapy Program, Centenary Institute, Camperdown, New South Wales, Australia.
K ChampGene and Stem Cell Therapy Program, Centenary Institute, Camperdown, New South Wales, Australia.
M VellozziGene and Stem Cell Therapy Program, Centenary Institute, Camperdown, New South Wales, Australia.
P O'YoungGene and Stem Cell Therapy Program, Centenary Institute, Camperdown, New South Wales, Australia.
C MetierreGene and Stem Cell Therapy Program, Centenary Institute, Camperdown, New South Wales, Australia.
Y FengGene and Stem Cell Therapy Program, Centenary Institute, Camperdown, New South Wales, Australia.
A ThoengGene and Stem Cell Therapy Program, Centenary Institute, Camperdown, New South Wales, Australia.
A M RichardsGynaecological Oncology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia.
U SchmitzGene and Stem Cell Therapy Program, Centenary Institute, Camperdown, New South Wales, Australia.
M BiroCell Motility and Mechanobiology, School of Medical Sciences, University of New South Wales, Sydney, New South Wales, Australia.
R JayasingheCancer Genomics, McDonnell Genome Institute, Washington University in St Louis, St Louis, MO, USA.
L DingCancer Genomics, McDonnell Genome Institute, Washington University in St Louis, St Louis, MO, USA.
L AndersonSydney Medical School, University of Sydney, Sydney, New South Wales, Australia.
E R MardisCancer Genomics, McDonnell Genome Institute, Washington University in St Louis, St Louis, MO, USA.
J E J RaskoGene and Stem Cell Therapy Program, Centenary Institute, Camperdown, New South Wales, Australia.
Centenary Institute · AUUniversity of Sydney · AUJames S. McDonnell Foundation · USRoyal Prince Alfred Hospital · AUUNSW Sydney · AUWashington University in St. Louis · US

Funding

TRAINING PROGRAM IN CELLULAR AND MOLECULAR BIOLOGYT32GM007067 · NIGMS · WASHINGTON UNIVERSITY · PI TRUE-KROB, HEATHER L · 1985 to 2020
$20.4M
Deep Discovery and Clinical Interpretation of Germline and Somatic Cancer DriversU24CA211006 · NCI · WASHINGTON UNIVERSITY · PI DING, LI, GOVINDAN, RAMASWAMY · 2016 to 2020
$1.8M
CANCER SUSCEPTIBILITY VARIANT DISCOVERY IN HIGH THROUGHPUT SEQUENCING DATAR01CA180006 · NCI · WASHINGTON UNIVERSITY · PI DING, LI · 2013 to 2016
$1.1M
NCI NIH HHS R01 CA180006NCI NIH HHS U24 CA211006NIGMS NIH HHS T32 GM007067
6 · The paper itself

Abstract

CTCF is a haploinsufficient tumour suppressor gene with diverse normal functions in genome structure and gene regulation. However the mechanism by which CTCF haploinsufficiency contributes to cancer development is not well understood. CTCF is frequently mutated in endometrial cancer. Here we show that most CTCF mutations effectively result in CTCF haploinsufficiency through nonsense-mediated decay of mutant transcripts, or loss-of-function missense mutation. Conversely, we identified a recurrent CTCF mutation K365T, which alters a DNA binding residue, and acts as a gain-of-function mutation enhancing cell survival. CTCF genetic deletion occurs predominantly in poor prognosis serous subtype tumours, and this genetic deletion is associated with poor overall survival. In addition, we have shown that CTCF haploinsufficiency also occurs in poor prognosis endometrial clear cell carcinomas and has some association with endometrial cancer relapse and metastasis. Using shRNA targeting CTCF to recapitulate CTCF haploinsufficiency, we have identified a novel role for CTCF in the regulation of cellular polarity of endometrial glandular epithelium. Overall, we have identified two novel pro-tumorigenic roles (promoting cell survival and altering cell polarity) for genetic alterations of CTCF in endometrial cancer.

Indexed as

CarcinogenesisCCCTC-Binding FactorCell Line, TumorEndometrial NeoplasmsFemaleGene ExpressionHumansMutation, MissenseNeoplasm Recurrence, LocalRepressor ProteinsCCCTC-Binding FactorCTCF protein, humanRepressor Proteins

Identifiers

PMID28319062
PMCPMC5519450
OpenAlexW2598314069

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.