Evidence map›Paper›PMID 19329776›Full record

ArticleBlood2009

TSC-22 contributes to hematopoietic precursor cell proliferation and repopulation and is epigenetically silenced in large granular lymphocyte leukemia.

Jianhua Yu, Maxim Ershler, Li Yu, Min Wei, Björn Hackanson, Akihiko Yokohama, Takeki Mitsui, Chunhui Liu, Hsiaoyin Mao, Shujun Liu and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

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  6. Yeast two-hybrid screening identified WDR77 as a novel interacting partner of TSC22D2.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

20 authors at 7 institutions in 4 countries.

Jianhua YuDepartment of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, Columbus, OH 43210, USA. jianhua.yu@osumc.edu
Maxim Ershler
Li Yu
Min Wei
Björn Hackanson
Akihiko Yokohama
Takeki Mitsui
Chunhui Liu
Hsiaoyin Mao
Shujun Liu
Zhongfa Liu
Rossana Trotta
Chang-gong Liu
Xiuping Liu
Kun Huang
Jan Visser
Guido Marcucci
Christoph Plass
Alexander V Belyavsky
Michael A Caligiuri
The Ohio State University · USThe Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · USAxcella Health (United States) · USChinese PLA General Hospital · CNEngelhardt Institute of Molecular Biology · RUFederal State Institution Hematology Research Center · RUUniversity Medical Center Freiburg · DE

Funding

TWO SIGNAL REQUIREMENT FOR NATURAL KILLER IMMUNITYP01CA095426 · NCI · OHIO STATE UNIVERSITY · PI CALIGIURI, MICHAEL A · 2002 to 2016
$29.6M
PathologyP01CA101956 · NCI · OHIO STATE UNIVERSITY · PI BYRD, JOHN C. · 2006 to 2010
$11.4M
IL-15--CHARACTERIZATION THROUGH EXPERIMENTAL IMMUNOLOGYR01CA068458 · NCI · ROSWELL PARK CANCER INSTITUTE · PI CALIGIURI, MICHAEL A, YU, JIANHUA · 1996 to 2019
$4.5M
DNA methylation as a diagnostic marker in AMLR01CA093548 · NCI · OHIO STATE UNIVERSITY · PI PLASS, CHRISTOPH · 2002 to 2006
$1.5M
IL-15 characterization through experimental immunologyR37CA068458 · NCI · OHIO STATE UNIVERSITY · PI CALIGIURI, MICHAEL A · 2010 to 2014
$1.4M
NCI NIH HHS CA101956NCI NIH HHS CA68458NCI NIH HHS CA93548NCI NIH HHS CA95426NCI NIH HHS P01 CA095426NCI NIH HHS P01 CA101956NCI NIH HHS R01 CA068458NCI NIH HHS R01 CA093548NCI NIH HHS R37 CA068458
6 · The paper itself

Abstract

Aberrant methylation of tumor suppressor genes can lead to their silencing in many cancers. TSC-22 is a gene silenced in several solid tumors, but its function and the mechanism(s) responsible for its silencing are largely unknown. Here we demonstrate that the TSC-22 promoter is methylated in primary mouse T or natural killer (NK) large granular lymphocyte (LGL) leukemia and this is associated with down-regulation or silencing of TSC-22 expression. The TSC-22 deregulation was reversed in vivo by a 5-aza-2'-deoxycytidine therapy of T or NK LGL leukemia, which significantly increased survival of the mice bearing this disease. Ectopic expression of TSC-22 in mouse leukemia or lymphoma cell lines resulted in delayed in vivo tumor formation. Targeted disruption of TSC-22 in wild-type mice enhanced proliferation and in vivo repopulation efficiency of hematopoietic precursor cells (HPCs). Collectively, our data suggest that TSC-22 normally contributes to the regulation of HPC function and is a putative tumor suppressor gene that is hypermethylated and silenced in T or NK LGL leukemia.

Indexed as

Cell ProliferationAnimalsCell MovementCells, CulturedDNA MethylationEpigenesis, GeneticGene Expression Regulation, LeukemicGene SilencingGenes, Tumor SuppressorHematopoietic Stem CellsHumansLeukemia, Large Granular LymphocyticMiceMice, Inbred C57BLMice, KnockoutPromoter Regions, GeneticRepressor ProteinsTgfb1i4 protein, mouse

Identifiers

PMID19329776
PMCPMC2689053
OpenAlexW2040660779

What OpenQuestion holds

Textmetadata
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.