Evidence map›Paper›PMID 24675889›Full record

ArticleCell cycle (Georgetown, Tex.)2014

Lineage-specific function of Engrailed-2 in the progression of chronic myelogenous leukemia to T-cell blast crisis.

Fernando Abollo-Jiménez, Elena Campos-Sánchez, Amparo Toboso-Navasa, Carolina Vicente-Dueñas, Inés González-Herrero, Esther Alonso-Escudero, Marcos González, Víctor Segura, Oscar Blanco, José Angel Martínez-Climent and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Biological function and mechanism of miR-33a in prostate cancer survival and metastasis: via downregulating Engrailed-2.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2017
    Article
  6. 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

12 authors at 7 institutions in 5 countries.

Fernando Abollo-JiménezExperimental Therapeutics and Translational Oncology Program, Instituto de Biología Molecular y Celular del Cáncer; CSIC/ Universidad de Salamanca; Campus M. de Unamuno; Institute of Biomedical Research of Salamanca (IBSAL); Salamanca, Spain.
Elena Campos-SánchezCentro de Biología Molecular Severo Ochoa; CSIC/Universidad Autónoma de Madrid; Campus de Cantoblanco; Madrid, Spain.
Amparo Toboso-NavasaCentro de Biología Molecular Severo Ochoa; CSIC/Universidad Autónoma de Madrid; Campus de Cantoblanco; Madrid, Spain; Current affiliation: Immunity and Cancer Laboratory; London Research Institute; Cancer Research UK; London, UK.
Carolina Vicente-DueñasExperimental Therapeutics and Translational Oncology Program, Instituto de Biología Molecular y Celular del Cáncer; CSIC/ Universidad de Salamanca; Campus M. de Unamuno; Institute of Biomedical Research of Salamanca (IBSAL); Salamanca, Spain.
Inés González-HerreroExperimental Therapeutics and Translational Oncology Program, Instituto de Biología Molecular y Celular del Cáncer; CSIC/ Universidad de Salamanca; Campus M. de Unamuno; Institute of Biomedical Research of Salamanca (IBSAL); Salamanca, Spain.
Esther Alonso-EscuderoExperimental Therapeutics and Translational Oncology Program, Instituto de Biología Molecular y Celular del Cáncer; CSIC/ Universidad de Salamanca; Campus M. de Unamuno; Institute of Biomedical Research of Salamanca (IBSAL); Salamanca, Spain.
Marcos GonzálezDepartment of Hematology, University Hospital of Salamanca; Institute of Biomedical Research of Salamanca; Salamanca, Spain.
Víctor SeguraBioinformatics Unit; Center for Applied Medical Research; University of Navarra; Pamplona, Spain.
Oscar BlancoDepartamento de Anatomía Patológica; Universidad de Salamanca; Salamanca, Spain.
José Angel Martínez-ClimentDivision of Oncology; Center for Applied Medical Research (CIMA); University of Navarra; Pamplona, Spain.
Isidro Sánchez-GarcíaExperimental Therapeutics and Translational Oncology Program, Instituto de Biología Molecular y Celular del Cáncer; CSIC/ Universidad de Salamanca; Campus M. de Unamuno; Institute of Biomedical Research of Salamanca (IBSAL); Salamanca, Spain.
César CobaledaCentro de Biología Molecular Severo Ochoa; CSIC/Universidad Autónoma de Madrid; Campus de Cantoblanco; Madrid, Spain.
Instituto de Investigación Biomédica de Salamanca · ESConsejo Superior de Investigaciones Científicas · ESInstituto de Biologia Molecular e CelularUniversidad de Salamanca · ESBioinformatics Institute · SGCancer Research UK · GBUniversidad de Navarra · ES

Funding

Significance and Function of HGAL in LymphomaR01CA109335 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI LOSSOS, IZIDORE S · 2005 to 2013
$2.1M
NCI NIH HHS R01 CA109335
6 · The paper itself

Abstract

In hematopoietic malignancies, oncogenic alterations interfere with cellular differentiation and lead to tumoral development. Identification of the proteins regulating differentiation is essential to understand how they are altered in malignancies. Chronic myelogenous leukemia (CML) is a biphasic disease initiated by an alteration taking place in hematopoietic stem cells. CML progresses to a blast crisis (BC) due to a secondary differentiation block in any of the hematopoietic lineages. However, the molecular mechanisms of CML evolution to T-cell BC remain unclear. Here, we have profiled the changes in DNA methylation patterns in human samples from BC-CML, in order to identify genes whose expression is epigenetically silenced during progression to T-cell lineage-specific BC. We have found that the CpG-island of the ENGRAILED-2 (EN2) gene becomes methylated in this progression. Afterwards, we demonstrate that En2 is expressed during T-cell development in mice and humans. Finally, we further show that genetic deletion of En2 in a CML transgenic mouse model induces a T-cell lineage BC that recapitulates human disease. These results identify En2 as a new regulator of T-cell differentiation whose disruption induces a malignant T-cell fate in CML progression, and validate the strategy used to identify new developmental regulators of hematopoiesis.

Indexed as

AnimalsBlast CrisisCell DifferentiationCpG IslandsDisease ProgressionDNA MethylationDNA PrimersEngrailed 2 ProteinFlow CytometryGene Expression Regulation, NeoplasticHomeodomain ProteinsHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMiceMice, TransgenicMicroarray AnalysisDNA PrimersEngrailed 2 ProteinHomeodomain ProteinsNerve Tissue Proteinsblast crisischronic myelogenous leukemiaDNA methylationengrailed-2T-cell development

Identifiers

PMID24675889
PMCPMC4111718
OpenAlexW2069492357

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.