Evidence map›Paper›PMID 27341078›Full record

ArticleBlood cancer journal2016

A data-driven network model of primary myelofibrosis: transcriptional and post-transcriptional alterations in CD34+ cells.

E Calura, S Pizzini, A Bisognin, A Coppe, G Sales, E Gaffo, T Fanelli, C Mannarelli, R Zini, R Norfo and 6 more

Open access · goldAbstract read
In one paragraph

Article in Blood cancer journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Immunoproteasome Genes Are Modulated in CD34International journal of molecular sciences · 2020
    Article
  6. Article
  7. Review
  8. Review
  9. Article
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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

16 authors at 3 institutions in 1 country.

E CaluraDepartment of Biology, University of Padova, Padova, Italy.
S PizziniDepartment of Biology, University of Padova, Padova, Italy.ORCID 0000-0001-6541-6590
A BisogninDepartment of Molecular Medicine, University of Padova, Padova, Italy.
A CoppeDepartment of Molecular Medicine, University of Padova, Padova, Italy.
G SalesDepartment of Biology, University of Padova, Padova, Italy.
E GaffoDepartment of Molecular Medicine, University of Padova, Padova, Italy.
T FanelliDepartment of Experimental and Clinical Medicine, University of Florence, Florence, Italy.
C MannarelliDepartment of Experimental and Clinical Medicine, University of Florence, Florence, Italy.
R ZiniDepartment of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy.
R NorfoDepartment of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy.
V PennucciDepartment of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy.
R ManfrediniDepartment of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy.
C RomualdiDepartment of Biology, University of Padova, Padova, Italy.
P GuglielmelliDepartment of Experimental and Clinical Medicine, University of Florence, Florence, Italy.
A M VannucchiDepartment of Experimental and Clinical Medicine, University of Florence, Florence, Italy.
S BortoluzziDepartment of Molecular Medicine, University of Padova, Padova, Italy.
University of Padua · ITUniversity of Florence · ITUniversity of Modena and Reggio Emilia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

microRNAs (miRNAs) are relevant in the pathogenesis of primary myelofibrosis (PMF) but our understanding is limited to specific target genes and the overall systemic scenario islacking. By both knowledge-based and ab initio approaches for comparative analysis of CD34+ cells of PMF patients and healthy controls, we identified the deregulated pathways involving miRNAs and genes and new transcriptional and post-transcriptional regulatory circuits in PMF cells. These converge in a unique and integrated cellular process, in which the role of specific miRNAs is to wire, co-regulate and allow a fine crosstalk between the involved processes. The PMF pathway includes Akt signaling, linked to Rho GTPases, CDC42, PLD2, PTEN crosstalk with the hypoxia response and Calcium-linked cellular processes connected to cyclic AMP signaling. Nested on the depicted transcriptional scenario, predicted circuits are reported, opening new hypotheses. Links between miRNAs (miR-106a-5p, miR-20b-5p, miR-20a-5p, miR-17-5p, miR-19b-3p and let-7d-5p) and key transcription factors (MYCN, ATF, CEBPA, REL, IRF and FOXJ2) and their common target genes tantalizingly suggest new path to approach the disease. The study provides a global overview of transcriptional and post-transcriptional deregulations in PMF, and, unifying consolidated and predicted data, could be helpful to identify new combinatorial therapeutic strategy. Interactive PMF network model: http://compgen.bio.unipd.it/pmf-net/.

Indexed as

RNA Processing, Post-TranscriptionalAgedAged, 80 and overAntigens, CD34FemaleGene Expression Regulation, NeoplasticHumansMaleMicroRNAsMiddle AgedNeoplasm ProteinsPrimary MyelofibrosisSignal TransductionTranscription, GeneticAntigens, CD34MicroRNAsNeoplasm Proteins

Identifiers

PMID27341078
PMCPMC5141361
OpenAlexW2474096934

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.