Evidence map›Paper›PMID 37803061›Full record

ArticleLeukemia2023

Expression profiling of extramedullary acute myeloid leukemia suggests involvement of epithelial-mesenchymal transition pathways.

T Ottone, G Silvestrini, R Piazza, S Travaglini, C Gurnari, F Marchesi, A M Nardozza, E Fabiani, E Attardi, L Guarnera and 12 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Cancers · 2025
    Article
  5. Diagnostic Approaches in Myeloid Sarcoma.Current issues in molecular biology · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. 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

22 authors at 4 institutions in 2 countries.

T Ottone *Department of Biomedicine and Prevention, Tor Vergata University, Rome, Italy.ORCID http://orcid.org/0000-0003-1936-3592
G Silvestrini *Department of Biomedicine and Prevention, PhD in Immunology, Molecular Medicine and Applied Biotechnology, University of Rome Tor Vergata, Rome, Italy.ORCID http://orcid.org/0009-0001-0665-6241
R PiazzaDepartment of Medicine and Surgery, University of Milano-Bicocca, Milan, Italy.ORCID http://orcid.org/0000-0003-4198-9620
S TravagliniDepartment of Biomedicine and Prevention, Tor Vergata University, Rome, Italy.ORCID http://orcid.org/0000-0002-5411-1502
C GurnariDepartment of Biomedicine and Prevention, PhD in Immunology, Molecular Medicine and Applied Biotechnology, University of Rome Tor Vergata, Rome, Italy.ORCID http://orcid.org/0000-0001-6829-5544
F MarchesiHematology and Stem Cell Transplant Unit, IRCCS Regina Elena National Cancer Institute, Rome, Italy.ORCID http://orcid.org/0000-0001-6353-2272
A M NardozzaDepartment of Biomedicine and Prevention, Tor Vergata University, Rome, Italy.
E FabianiDepartment of Biomedicine and Prevention, Tor Vergata University, Rome, Italy.
E AttardiDepartment of Biomedicine and Prevention, PhD in Immunology, Molecular Medicine and Applied Biotechnology, University of Rome Tor Vergata, Rome, Italy.ORCID http://orcid.org/0009-0008-4801-5048
L GuarneraDepartment of Biomedicine and Prevention, Tor Vergata University, Rome, Italy.
M DivonaDepartment of Biomedicine and Prevention, Tor Vergata University, Rome, Italy.
P RicciDepartment of Biomedicine and Prevention, Tor Vergata University, Rome, Italy.
M A Irno ConsalvoDepartment of Biomedicine and Prevention, Tor Vergata University, Rome, Italy.
S IenziDepartment of Anatomical Pathology, F. Spaziani Hospital, Frosinone, Italy.
R ArceseDepartment of Anatomical Pathology, F. Spaziani Hospital, Frosinone, Italy.
A BiagiHematology and Transplant Unit, Santa Maria Goretti Hospital, AUSL, Latina, Italy.
L FioriHematology and Transplant Unit, Santa Maria Goretti Hospital, AUSL, Latina, Italy.
M NovelloPathology Department, IRCCS-Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144, Rome, Italy.
A MaurielloDepartment of Experimental Medicine, Faculty of Medicine, Tor Vergata University, Rome, Italy.
A VendittiDepartment of Biomedicine and Prevention, Tor Vergata University, Rome, Italy.
L AnemonaDepartment of Experimental Medicine, Faculty of Medicine, Tor Vergata University, Rome, Italy.
M T VosoDepartment of Biomedicine and Prevention, Tor Vergata University, Rome, Italy. voso@med.uniroma2.it.ORCID http://orcid.org/0000-0002-6164-4761
University of Rome Tor Vergata · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITOspedale Santa Maria Goretti · ITUniversity of Milano-Bicocca · IT

Funding

Associazione Italiana per la Ricerca sul Cancro (Italian Association for Cancer Research) 21267Ministero della Salute (Ministry of Health, Italy) NET-2018-12365935Ministero dell'Istruzione, dell'Università e della Ricerca (Ministry of Education, University and Research) 2017WXR7ZTMinistero dell'Istruzione, dell'Università e della Ricerca (Ministry of Education, University and Research) PE00000019
6 · The paper itself

Abstract

Extramedullary (EM) colonization is a rare complication of acute myeloid leukemia (AML), occurring in about 10% of patients, but the processes underlying tissue invasion are not entirely characterized. Through the application of RNAseq technology, we examined the transcriptome profile of 13 AMLs, 9 of whom presented an EM localization. Our analysis revealed significant deregulation within the extracellular matrix (ECM)-receptor interaction and focal-adhesion pathways, specifically in the EM sites. The transcription factor TWIST1, which is known to impact on cancer invasion by dysregulating epithelial-mesenchymal-transition (EMT) processes, was significantly upregulated in EM-AML. To test the functional impact of TWIST1 overexpression, we treated OCI-AML3s with TWIST1-siRNA or metformin, a drug known to inhibit tumor progression in cancer models. After 48 h, we showed downregulation of TWIST1, and of the EMT-related genes FN1 and SNAI2. This was associated with significant impairment of migration and invasion processes by Boyden chamber assays. Our study shed light on the molecular mechanisms associated with EM tissue invasion in AML, and on the ability of metformin to interfere with key players of this process. TWIST1 may configure as candidate marker of EM-AML progression, and inhibition of EMT-pathways may represent an innovative therapeutic intervention to prevent or treat this complication.

Indexed as

Leukemia, Myeloid, AcuteMetforminCell Line, TumorEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessRNA, Small InterferingMetforminRNA, Small Interfering

Identifiers

PMID37803061
OpenAlexW4387409921

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.