Evidence map›Paper›PMID 35450883›Full record

ArticleGenes & development2022

In vivo temporal resolution of acute promyelocytic leukemia progression reveals a role of

Glòria Mas, Fabio Santoro, Enrique Blanco, Gianni Paolo Gamarra Figueroa, François Le Dily, Gianmaria Frigè, Enrique Vidal, Francesca Mugianesi, Cecilia Ballaré, Arantxa Gutierrez and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
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 2 countries.

Glòria MasCentre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology (BIST), Barcelona 08003, Spain.
Fabio SantoroDepartment of Experimental Oncology, European Institute of Oncology (IEO), Milan 20139, Italy.
Enrique BlancoCentre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology (BIST), Barcelona 08003, Spain.
Gianni Paolo Gamarra FigueroaCentre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology (BIST), Barcelona 08003, Spain.
François Le DilyCentre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology (BIST), Barcelona 08003, Spain.
Gianmaria FrigèDepartment of Experimental Oncology, European Institute of Oncology (IEO), Milan 20139, Italy.
Enrique VidalCentre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology (BIST), Barcelona 08003, Spain.
Francesca MugianesiCentre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology (BIST), Barcelona 08003, Spain.
Cecilia BallaréCentre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology (BIST), Barcelona 08003, Spain.
Arantxa GutierrezCentre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology (BIST), Barcelona 08003, Spain.
Aleksandra SparavierCentre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology (BIST), Barcelona 08003, Spain.
Marc A Marti-RenomCentre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology (BIST), Barcelona 08003, Spain.ORCID 0000-0002-0151-4279
Saverio MinucciDepartment of Experimental Oncology, European Institute of Oncology (IEO), Milan 20139, Italy.
Luciano Di CroceCentre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology (BIST), Barcelona 08003, Spain.ORCID 0000-0003-3488-6228
Centre for Genomic Regulation · ESUniversity of Milan · ITInstitució Catalana de Recerca i Estudis Avançats · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome organization plays a pivotal role in transcription, but how transcription factors (TFs) rewire the structure of the genome to initiate and maintain the programs that lead to oncogenic transformation remains poorly understood. Acute promyelocytic leukemia (APL) is a fatal subtype of leukemia driven by a chromosomal translocation between the promyelocytic leukemia (PML) and retinoic acid receptor α (RARα) genes. We used primary hematopoietic stem and progenitor cells (HSPCs) and leukemic blasts that express the fusion protein PML-RARα as a paradigm to temporally dissect the dynamic changes in the epigenome, transcriptome, and genome architecture induced during oncogenic transformation. We found that PML-RARα initiates a continuum of topologic alterations, including switches from A to B compartments, transcriptional repression, loss of active histone marks, and gain of repressive histone marks. Our multiomics-integrated analysis identifies

Indexed as

Leukemia, Promyelocytic, AcuteCell DifferentiationCell Transformation, NeoplasticHumansKruppel-Like Factor 4Oncogene Proteins, FusionTranscription FactorsTretinoinKlf4 protein, mouseKruppel-Like Factor 4Oncogene Proteins, FusionTranscription FactorsTretinoinchromatinchromatin topologygene regulationleukemia

Identifiers

PMID35450883
PMCPMC9067408
OpenAlexW4224213165

What Socratic 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 Socratic graph.