Evidence map›Paper›PMID 32214204›Full record

ArticleLeukemia2020

SIRT7: an influence factor in healthy aging and the development of age-dependent myeloid stem-cell disorders.

Alexander Kaiser, Martin Schmidt, Otmar Huber, Jochen J Frietsch, Sebastian Scholl, Florian H Heidel, Andreas Hochhaus, Jörg P Müller, Thomas Ernst

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Leukemia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Alexander KaiserKlinik für Innere Medizin II, Abteilung Hämatologie und Internistische Onkologie, Universitätsklinikum Jena, Jena, Germany.
Martin SchmidtInstitut für Biochemie II, Universitätsklinikum Jena, Friedrich-Schiller-Universität, Jena, Germany.
Otmar HuberInstitut für Biochemie II, Universitätsklinikum Jena, Friedrich-Schiller-Universität, Jena, Germany.ORCID http://orcid.org/0000-0003-4359-1747
Jochen J FrietschKlinik für Innere Medizin II, Abteilung Hämatologie und Internistische Onkologie, Universitätsklinikum Jena, Jena, Germany.ORCID http://orcid.org/0000-0002-1476-8059
Sebastian SchollKlinik für Innere Medizin II, Abteilung Hämatologie und Internistische Onkologie, Universitätsklinikum Jena, Jena, Germany.
Florian H HeidelKlinik für Innere Medizin II, Abteilung Hämatologie und Internistische Onkologie, Universitätsklinikum Jena, Jena, Germany.
Andreas HochhausKlinik für Innere Medizin II, Abteilung Hämatologie und Internistische Onkologie, Universitätsklinikum Jena, Jena, Germany.
Jörg P Müller *Institut für Molekulare Zellbiologie, CMB, Universitätsklinikum Jena, Friedrich-Schiller-Universität, Jena, Germany.
Thomas Ernst *Klinik für Innere Medizin II, Abteilung Hämatologie und Internistische Onkologie, Universitätsklinikum Jena, Jena, Germany. thomas.ernst@med.uni-jena.de.
Jena University Hospital · DELeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Molecular alterations within the hematopoietic system influence cellular longevity and development of age-related myeloid stem-cell disorders like acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). A reduced SIRT7-expression in aged murine hematopoietic stem cells (HSC) resulted in reduced longevity and increased proliferation. In this study we investigated age-related changes of SIRT7-expression in healthy humans and relevant pathomechanisms in AML and CML. SIRT7-expression in leukocytes of healthy people decreased in an age-dependent manner. Low SIRT7 mRNA levels were also detected in AML and CML patients. With positive treatment response, SIRT7-expression increased, but showed reduction when patients progressed or relapsed. Pharmacologic inhibition of driver mutations in AML (FLT3-ITD) or CML (BCR-ABL) also restored SIRT7 levels in cell lines and patient samples. Furthermore, SIRT7-expression increased with time during PMA-mediated monocyte differentiation of THP-1 cells. SIRT7-overexpression in THP-1 cells resulted in increased expression of differentiation markers. BCR-ABL, FLT3-ITD, and differentiation-associated SIRT7-expression in general were positively regulated by C/EBPα, -β, and -ε binding to two different C/EBP-binding sites within the SIRT7 promoter. SIRT7 is important in human hematopoietic cell aging and longevity. It might act as tumor suppressor and could potentially serve as general biomarker for monitoring treatment response in myeloid stem-cell disorders.

Indexed as

Healthy AgingAdultAgedAged, 80 and overAge FactorsCCAAT-Enhancer-Binding Protein-alphaCell Differentiationfms-Like Tyrosine Kinase 3Fusion Proteins, bcr-ablHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveLeukemia, Myeloid, AcuteMiddle AgedMutationSirtuinsTHP-1 CellsCCAAT-Enhancer-Binding Protein-alphaFLT3 protein, humanfms-Like Tyrosine Kinase 3Fusion Proteins, bcr-ablSIRT7 protein, humanSirtuins

Identifiers

PMID32214204
PMCPMC8318878
OpenAlexW3013911906

What OpenQuestion holds

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LicenceCC BY
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.