Evidence map›Paper›PMID 27486062›Full record

ArticleLeukemia research2016

TLE4 regulation of wnt-mediated inflammation underlies its role as a tumor suppressor in myeloid leukemia.

Thomas H Shin, Christopher Brynczka, Farshid Dayyani, Miguel N Rivera, David A Sweetser

Open access · greenAbstract read
In one paragraph

Article in Leukemia research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

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  14. Tle corepressors are differentially partitioned to instruct CD8The Journal of experimental medicine · 2018
    Article
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  16. 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 2 institutions in 1 country.

Thomas H ShinDepartment of Pediatrics, Divisions of Pediatric Hematology/Oncology and Medical Genetics, Massachusetts General Hospital, Boston, MA 02114, United States; Department of Molecular and Translational Medicine, Boston University School of Medicine, Boston, MA 02118, United States.
Christopher BrynczkaDepartment of Pediatrics, Divisions of Pediatric Hematology/Oncology and Medical Genetics, Massachusetts General Hospital, Boston, MA 02114, United States.
Farshid DayyaniDepartment of Pediatrics, Divisions of Pediatric Hematology/Oncology and Medical Genetics, Massachusetts General Hospital, Boston, MA 02114, United States.
Miguel N RiveraDepartment of Pathology, Molecular Pathology Unit, Massachusetts General Hospital, Charlestown, MA 02129, United States.
David A SweetserDepartment of Pediatrics, Divisions of Pediatric Hematology/Oncology and Medical Genetics, Massachusetts General Hospital, Boston, MA 02114, United States. Electronic address: dsweetser@partners.org.
Massachusetts General Hospital · USBoston University · US

Funding

Molecular Analysis of Del(9q) Acute Myeloid LeukemiaR01CA115772 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI SWEETSER, DAVID A · 2006 to 2010
$2.0M
NCI NIH HHS R01 CA115772
6 · The paper itself

Abstract

The presence of AML1-ETO (RUNX1-CBF2T1), a fusion oncoprotein resulting from a t(8;21) chromosomal translocation, has been implicated as a necessary but insufficient event in the development of a subset of acute myeloid leukemias (AML). While AML1-ETO prolongs survival and inhibits differentiation of hematopoietic stem cells (HSC), other contributory events are needed for cell proliferation and leukemogenesis. We have postulated that specific tumor suppressor genes keep the leukemic potential of AML1-ETO in check. In studying del(9q), one of the most common concomitant chromosomal abnormalities with t(8;21), we identified the loss of an apparent tumor suppressor, TLE4, that appears to cooperate with AML1-ETO to confer a leukemic phenotype. This study sought to identify the molecular basis of this cooperation. We show that the loss of TLE4 confers proliferative advantage to leukemic cells, simultaneous with an upregulation of a pro- inflammatory signature mediated through aberrant increases in Wnt signaling activity. We further demonstrate that inhibition of cyclooxygenase (COX) activity partly reverses the pro-leukemic phenotype due to TLE4 knockdown, pointing towards a novel therapeutic approach for myeloid leukemia.

Indexed as

InflammationChromosome DeletionChromosomes, Human, Pair 9Cyclooxygenase InhibitorsGene DeletionGene Expression Regulation, LeukemicGenes, Tumor SuppressorHumansLeukemia, MyeloidNuclear ProteinsRepressor ProteinsTumor Cells, CulturedTumor Suppressor ProteinsWnt ProteinsCyclooxygenase InhibitorsNuclear ProteinsRepressor ProteinsTLE4 protein, humanTumor Suppressor ProteinsWnt ProteinsAcute myeloid leukemiaAML1-ETOInflammationTLE4Tumor suppressorWnt signaling

Identifiers

PMID27486062
PMCPMC5266616
OpenAlexW2492699395

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.