Evidence map›Paper›PMID 33539590›Full record

ArticleStem cells (Dayton, Ohio)2021

Autonomous TGFβ signaling induces phenotypic variation in human acute myeloid leukemia.

Yasuhiro Shingai, Takafumi Yokota, Daisuke Okuzaki, Takao Sudo, Tomohiko Ishibashi, Yukiko Doi, Tomoaki Ueda, Takayuki Ozawa, Ritsuko Nakai, Akira Tanimura and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Epithelial-Mesenchymal Transition in Acute Leukemias.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Article
  6. Review
  7. 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

14 authors at 3 institutions in 1 country.

Yasuhiro ShingaiDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.ORCID 0000-0003-1017-4664
Takafumi YokotaDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Daisuke OkuzakiGenome Information Research Center, Research Institute for Microbial Disease, Osaka University, Suita, Japan.
Takao SudoDepartment of Immunology and Cell Biology, Osaka University Graduate School of Medicine, Suita, Japan.
Tomohiko IshibashiDepartment of Vascular Physiology, National Cerebral and Cardiovascular Center Research Institute, Suita, Japan.
Yukiko DoiDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Tomoaki UedaDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Takayuki OzawaDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Ritsuko NakaiDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Akira TanimuraDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Michiko IchiiDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Hirohiko ShibayamaDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Yuzuru KanakuraDepartment of Hematology, Sumitomo Hospital, Osaka, Japan.
Naoki HosenDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
The University of Osaka · JPNational Cerebral and Cardiovascular Center · JPSumitomo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heterogeneity of leukemia stem cells (LSCs) is involved in their collective chemoresistance. To eradicate LSCs, it is necessary to understand the mechanisms underlying their heterogeneity. Here, we aimed to identify signals responsible for heterogeneity and variation of LSCs in human acute myeloid leukemia (AML). Monitoring expression levels of endothelial cell-selective adhesion molecule (ESAM), a hematopoietic stem cell-related marker, was useful to detect the plasticity of AML cells. While healthy human hematopoietic stem/progenitor cells robustly expressed ESAM, AML cells exhibited heterogeneous ESAM expression. Interestingly, ESAM

Indexed as

Cell Line, TumorCell ProliferationHematopoietic Stem CellsHumansLeukemia, Myeloid, AcuteNeoplastic Stem CellsSignal TransductionTransforming Growth Factor betaTransforming Growth Factor betaacute myeloid leukemiaautonomous signalingchemoresistanceendothelial cell-selective adhesion moleculeheterogeneityleukemia stem cellsphenotypic variationTGFβ

Identifiers

PMID33539590
PMCPMC8248163
OpenAlexW3128399442

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.