Evidence map›Paper›PMID 21386967›Full record

ArticlePloS one2011

Frequent and simultaneous epigenetic inactivation of TP53 pathway genes in acute lymphoblastic leukemia.

Amaia Vilas-Zornoza, Xabier Agirre, Vanesa Martín-Palanco, José Ignacio Martín-Subero, Edurne San José-Eneriz, Leire Garate, Sara Álvarez, Estíbaliz Miranda, Paula Rodríguez-Otero, José Rifón and 5 more

Open access · goldAbstract readValidation Study
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
11.0field-weighted citation impact, top 1% 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

20 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Acute lymphoid leukemia etiopathogenesis.Molecular biology reports · 2021
    Review
  3. Article
  4. Deregulation ofOncotarget · 2018
    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

15 authors at 5 institutions in 1 country.

Amaia Vilas-ZornozaHematology Service and Area of Cell Therapy, Clínica Universidad de Navarra, Foundation for Applied Medical Research, University of Navarra, Pamplona, Spain.
Xabier Agirre
Vanesa Martín-Palanco
José Ignacio Martín-Subero
Edurne San José-Eneriz
Leire Garate
Sara Álvarez
Estíbaliz Miranda
Paula Rodríguez-Otero
José Rifón
Antonio Torres
María José Calasanz
Juan Cruz Cigudosa
José Román-Gómez
Felipe Prósper
Universidad de Navarra · ESClinica Universidad de Navarra · ESHospital Universitario Reina Sofía · ESCentre for Biomedical Network Research on Rare Diseases · ESUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant DNA methylation is one of the most frequent alterations in patients with Acute Lymphoblastic Leukemia (ALL). Using methylation bead arrays we analyzed the methylation status of 807 genes implicated in cancer in a group of ALL samples at diagnosis (n = 48). We found that 154 genes were methylated in more than 10% of ALL samples. Interestingly, the expression of 13 genes implicated in the TP53 pathway was downregulated by hypermethylation. Direct or indirect activation of TP53 pathway with 5-aza-2'-deoxycitidine, Curcumin or Nutlin-3 induced an increase in apoptosis of ALL cells. The results obtained with the initial group of 48 patients was validated retrospectively in a second cohort of 200 newly diagnosed ALL patients. Methylation of at least 1 of the 13 genes implicated in the TP53 pathway was observed in 78% of the patients, which significantly correlated with a higher relapse (p = 0.001) and mortality (p<0.001) rate being an independent prognostic factor for disease-free survival (DFS) (p = 0.006) and overall survival (OS) (p = 0.005) in the multivariate analysis. All these findings indicate that TP53 pathway is altered by epigenetic mechanisms in the majority of ALL patients and correlates with prognosis. Treatments with compounds that may reverse the epigenetic abnormalities or activate directly the p53 pathway represent a new therapeutic alternative for patients with ALL.

Indexed as

AdolescentAdultAgedAged, 80 and overCell Line, TumorChildChild, PreschoolCohort StudiesEpigenesis, GeneticFemaleGene Expression Regulation, LeukemicGene FrequencyGene SilencingHumansInfantMaleTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID21386967
PMCPMC3046174
OpenAlexW2033537445

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.