Evidence map›Paper›PMID 29290626›Full record

ArticleStem cell reports2018

TET2 Loss Dysregulates the Behavior of Bone Marrow Mesenchymal Stromal Cells and Accelerates Tet2

Rong Li, Yuan Zhou, Zeng Cao, Lin Liu, Jinhuan Wang, Zizhen Chen, Wen Xing, Shi Chen, Jie Bai, Weiping Yuan and 4 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 48 citations in OpenAlex.

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  17. TETology: Epigenetic Mastermind in Action.Applied biochemistry and biotechnology · 2021
    Review
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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

14 authors at 6 institutions in 2 countries.

Rong LiState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300020, China.
Yuan ZhouState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300020, China.
Zeng CaoDepartment of Hematology and Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China.
Lin LiuDepartment of Hematology and Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China.
Jinhuan WangDepartment of Oncology, The Second Affiliated Hospital of Tianjin Medical University, Tianjin 300211, China.
Zizhen ChenState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300020, China.
Wen XingState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300020, China.
Shi ChenSylvester Comprehensive Cancer Center, Department of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Jie BaiState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300020, China.
Weiping YuanState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300020, China.
Tao ChengState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300020, China.
Mingjiang XuSylvester Comprehensive Cancer Center, Department of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Feng-Chun YangSylvester Comprehensive Cancer Center, Department of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine, Miami, FL 33136, USA. Electronic address: fxy37@med.miami.edu.
Zhigang ZhaoDepartment of Hematology and Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China. Electronic address: zzhao01@tmu.edu.cn.
Institute of Hematology & Blood Diseases Hospital · CNTianjin Medical University Cancer Institute and Hospital · CNSylvester Comprehensive Cancer Center · USChinese Academy of Medical Sciences & Peking Union Medical College · CNSecond Hospital of Tianjin Medical University · CNUniversity of Miami · US

Funding

Role of Asxl1 in normal hematopoiesis and pathogenesis of myeloid malignanciesR01CA172408 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI XU, MINGJIANG, YANG, FENG-CHUN · 2014 to 2024
$3.4M
Role of TET2 in normal hematopoiesis and pathogenesis of myeloid malignanciesR01HL112294 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI XU, MINGJIANG · 2012 to 2016
$1.9M
NCI NIH HHS R01 CA172408NHLBI NIH HHS R01 HL112294
6 · The paper itself

Abstract

TET2 is a methylcytosine dioxygenase that regulates cytosine hydroxymethylation. Although there are extensive data implicating a pivotal role of TET2 in hematopoietic stem/progenitor cells (HSPCs), the importance of TET2 in bone marrow mesenchymal stromal cells (BMSCs) remains unknown. In this study, we show that loss of TET2 in BMSCs increases cell proliferation and self-renewal and enhances osteoblast differentiation potential of BMSCs, which may in turn alter their behavior in supporting HSPC proliferation and differentiation. In addition, Tet2 loss alters BMSCs in promoting Tet2-deficiency-mediated myeloid malignancy progression. Tet2 loss in BMSCs also dysregulates hydroxylation of 5-methylcytosine (5mC) and the expression of genes that are key for BMSC proliferation and osteoblast differentiation, leading to alteration of biological characteristics in vivo. These results highlight the critical role of TET2 in the maintenance of BMSC functions and osteoblast differentiation and provide evidence that dysregulation of epigenetic modifiers in BMSCs contributes to the progression of myeloid malignancies.

Indexed as

AnimalsBone Marrow CellsDioxygenasesDNA-Binding ProteinsHematologic NeoplasmsHematopoietic Stem CellsMesenchymal Stem CellsMiceMice, KnockoutMyeloid CellsProto-Oncogene ProteinsDioxygenasesDNA-Binding ProteinsProto-Oncogene ProteinsTet2 protein, mousebone marrow mesenchymal stromal cellsbone marrow nichemyeloid malignanciesTET2

Identifiers

PMID29290626
PMCPMC5768963
OpenAlexW2779417942

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.