Evidence map›Paper›PMID 24334727›Full record

ArticleOncotarget2014

MYCN is a novel oncogenic target in pediatric T-cell acute lymphoblastic leukemia.

Annalisa Astolfi, Francesca Vendemini, Milena Urbini, Fraia Melchionda, Riccardo Masetti, Monica Franzoni, Virginia Libri, Salvatore Serravalle, Marco Togni, Giuseppina Paone and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Shift of N-MYC Oncogene Expression in AML Patients Carrying the FLT3-ITD Mutation.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. TargetingFrontiers in oncology · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

16 authors at 3 institutions in 1 country.

Annalisa Astolfi"Giorgio Prodi" Cancer Research Center, University of Bologna, Bologna, Italy.
Francesca Vendemini
Milena Urbini
Fraia Melchionda
Riccardo Masetti
Monica Franzoni
Virginia Libri
Salvatore Serravalle
Marco Togni
Giuseppina Paone
Luca Montemurro
Daniela Bressanin
Francesca Chiarini
Alberto M Martelli
Roberto Tonelli
Andrea Pession
University of Bologna · ITPoliclinico S.Orsola-Malpighi · ITIstituto Ortopedico Rizzoli · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MYCN is an oncogene frequently overexpressed in pediatric solid tumors whereas few evidences suggest his involvement in the pathogenesis of haematologic malignancies. Here we show that MYCN is overexpressed in a relevant proportion (40 to 50%) of adult and pediatric T-cell acute lymphoblastic leukemias (T-ALL). Focusing on pediatric T-ALL, MYCN-expressing samples were found almost exclusively in the TAL1-positive subgroup. Moreover, TAL1 knockdown in T-ALL cell lines resulted in a reduction of MYCN expression, and TAL1 directly binds to MYCN promoter region, suggesting that TAL1 pathway activation could sustain the up-regulation of MYCN. The role of MYCN in T-ALL was investigated by peptide nucleic acid (PNA-MYCN)-mediated transcriptional silencing of MYCN and by siRNAs. MYCN knockdown in T-ALL cell lines resulted in a reduction of cell viability, up to 50%, while no effect was elicited with a mismatch PNA. The inhibitory effect of PNA-MYCN on cell viability was due to a significant increase in apoptosis. PNA-MYCN treatment in pediatric T-ALL samples reduced cell viability of leukemic cells from patients with high MYCN expression, while no effect was obtained in MYCN-negative blast cells. These results showed that MYCN is frequently overexpressed in pediatric T-ALL and suggested his role as a candidate for molecularly-directed therapies.

Indexed as

Basic Helix-Loop-Helix ProteinsCase-Control StudiesCell Line, TumorChildChild, PreschoolFemaleGene Expression ProfilingGene Expression Regulation, LeukemicGene Knockdown TechniquesGene SilencingHumansMaleMolecular Targeted TherapyN-Myc Proto-Oncogene ProteinNuclear ProteinsOncogene ProteinsBasic Helix-Loop-Helix ProteinsMYCN protein, humanN-Myc Proto-Oncogene ProteinNuclear ProteinsOncogene ProteinsProto-Oncogene ProteinsTAL1 protein, humanT-Cell Acute Lymphocytic Leukemia Protein 1Transcription Factors

Identifiers

PMID24334727
PMCPMC3960194
OpenAlexW1677078557

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.