Evidence map›Paper›PMID 19995953›Full record

ArticleThe Journal of experimental medicine2009

Bone marrow mesenchymal stem cells from infants with MLL-AF4+ acute leukemia harbor and express the MLL-AF4 fusion gene.

Pablo Menendez, Purificación Catalina, René Rodríguez, Gustavo J Melen, Clara Bueno, Mar Arriero, Félix García-Sánchez, Alvaro Lassaletta, Ramón García-Sanz, Javier García-Castro

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.

  1. Pooled it
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  7. Childhood B cell leukemia: Intercepting the paths to progression.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024
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10 more citing papers are in PubMed but not listed here.

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

10 authors at 5 institutions in 1 country.

Pablo MenendezAndalusian Stem Cell Bank, Centro de Investigación Biomédica, Consejería de Salud-Universidad de Granada, 18100 Granada, Spain. pablo.menendez@juntadeandalucia.es
Purificación Catalina
René Rodríguez
Gustavo J Melen
Clara Bueno
Mar Arriero
Félix García-Sánchez
Alvaro Lassaletta
Ramón García-Sanz
Javier García-Castro
Parque Tecnológico de la Salud · ESUniversidad de Granada · ESHospital Infantil Universitario Niño Jesús · ESComunidad de Madrid · ESUniversidad de Salamanca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MLL-AF4 fusion is a hallmark genetic abnormality in infant B-acute lymphoblastic leukemia (B-ALL) known to arise in utero. The cellular origin of leukemic fusion genes during human development is difficult to ascertain. The bone marrow (BM) microenvironment plays an important role in the pathogenesis of several hematological malignances. BM mesenchymal stem cells (BM-MSC) from 38 children diagnosed with cytogenetically different acute leukemias were screened for leukemic fusion genes. Fusion genes were absent in BM-MSCs of childhood leukemias carrying TEL-AML1, BCR-ABL, AML1-ETO, MLL-AF9, MLL-AF10, MLL-ENL or hyperdiploidy. However, MLL-AF4 was detected and expressed in BM-MSCs from all cases of MLL-AF4(+) B-ALL. Unlike leukemic blasts, MLL-AF4(+) BM-MSCs did not display monoclonal Ig gene rearrangements. Endogenous or ectopic expression of MLL-AF4 exerted no effect on MSC culture homeostasis. These findings suggest that MSCs may be in part tumor-related, highlighting an unrecognized role of the BM milieu on the pathogenesis of MLL-AF4(+) B-ALL. MLL-AF4 itself is not sufficient for MSC transformation and the expression of MLL-AF4 in MSCs is compatible with a mesenchymal phenotype, suggesting a differential impact in the hematopoietic system and mesenchyme. The absence of monoclonal rearrangements in MLL-AF4(+) BM-MSCs precludes the possibility of cellular plasticity or de-differentiation of B-ALL blasts and suggests that MLL-AF4 might arise in a population of prehematopoietic precursors.

Indexed as

Cells, CulturedChildChild, PreschoolCore Binding Factor Alpha 2 SubunitETS Translocation Variant 6 ProteinGene RearrangementHomeostasisHumansInfantMesenchymal Stem CellsMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, FusionPrecursor Cell Lymphoblastic Leukemia-LymphomaCore Binding Factor Alpha 2 SubunitETS Translocation Variant 6 ProteinMLL-AF4 fusion protein, humanMLL-AF9 fusion protein, humanMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, FusionTEL-AML1 fusion protein

Identifiers

PMID19995953
PMCPMC2806455
OpenAlexW2161096609

What OpenQuestion holds

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LicenceCC BY-NC-SA
Read underepoch 390

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.