Evidence map›Paper›PMID 28836580›Full record

ArticleActa pharmacologica Sinica2017

BCR-ABL1-positive microvesicles malignantly transform human bone marrow mesenchymal stem cells in vitro.

Fen-Fen Fu, Xiao-Jian Zhu, Hong-Xiang Wang, Li-Ming Zhang, Guo-Lin Yuan, Zhi-Chao Chen, Qiu-Bai Li

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta pharmacologica Sinica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

15 citing papers in PubMed, 17 citations in OpenAlex.

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  10. Cancer and stem cells.Experimental biology and medicine (Maywood, N.J.) · 2021
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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

7 authors at 5 institutions in 1 country.

Fen-Fen FuInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Xiao-Jian ZhuInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Hong-Xiang WangDepartment of Hematology, Wuhan Central Hospital, Wuhan 430000, China.
Li-Ming ZhangDepartment of Hematology, Jinzhou Central Hospital, Jinzhou 434020, China.
Guo-Lin YuanDepartment of Hematology, Xiangyang Central Hospital, the Affiliated Hospital of Hubei University of Arts and Science, Xiangyang 441021, China.
Zhi-Chao ChenInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Qiu-Bai LiInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Union Hospital · CNCentral Hospital of Wuhan · CNHuazhong University of Science and Technology · CNJinzhou Central Hospital · CNXiangyang Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The intercellular communication between leukemia cells and bone marrow mesenchymal stem cells (BM-MSCs) plays more important role in chronic myeloid leukemia (CML) than we previously understood. Recently, we found that microvesicles released from human leukemia cell line K562 (K562-MVs) containing BCR-ABL1 mRNA malignantly transformed normal hematopoietic transplants. Here, we investigated whether K562-MVs contribute to the transformation of human bone marrow mesenchymal stem cells (BM-MSCs). We showed that K562-MVs could be integrated into co-cultured normal BM-MSCs and dose-dependently enhanced the proliferation of BM-MSCs. Meanwhile, K562-MVs (400 ng/mL) significantly increased the expression of BCR-ABL1 in these BM-MSCs, accompanied by the enhanced secretion of TGF-β1. These BM-MSCs in turn could trigger the TGF-β1-dependent proliferation of K562 cells. Moreover, we confirmed the presence of BCR-ABL1 in circulating MVs from 11 CML patients. Compared to the normal BM-MSCs, the BM-MSCs from CML patients more effectively increased the BCR-ABL1 expression and TGF-β1 secretion in K562 cells as well as the proliferation of K562 cells. Our findings enrich the mechanisms involved in the interaction between leukemia cells and BM-MSCs and provide novel ways to monitor minimal residual disease and worthwhile approaches to treat CML.

Indexed as

Cell CommunicationAdolescentAdultBone Marrow CellsCell-Derived MicroparticlesCell-Free Nucleic AcidsCell ProliferationCell Transformation, NeoplasticCoculture TechniquesFemaleFusion Proteins, bcr-ablHumansK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMesenchymal Stem CellsBCR-ABL1 fusion protein, humanCell-Free Nucleic AcidsFusion Proteins, bcr-ablRNA, MessengerTGFB1 protein, humanTransforming Growth Factor beta1

Identifiers

PMID28836580
PMCPMC5672071
OpenAlexW2747910946

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.